Bio 328 Test 2

Front 1

what does the heart function as

Back 1

a pump to circulate blood through the vasculature

Front 2

3 components to the cardiovascular system

Back 2

1.pump:heart
2.tubing:blood vessels (vascular system)
3.control system: autonomic nervous system, hormone systems

Front 3

how many chambers in heart

Back 3

4

Front 4

what is heart composed of

Back 4

left & right atrium, left & right ventricle

Front 5

where does left side of the heart pump blood through

Back 5

systemic circulation

Front 6

where does right side of the heart pump blood through

Back 6

pulmonary circulation

Front 7

direction arteries carry blood

Back 7

away from heart

Front 8

direction veins carry blood

Back 8

toward the heart

Front 9

myocytes

Back 9

cardiac muscle cells that make up the heart walls->contract and do the work of pumping the blood

Front 10

myocardium

Back 10

the collective tissue that contracts and pumps blood

Front 11

endothelium

Back 11

inner layer of endothelial cells

Front 12

pericardium

Back 12

fibrous sac that contains the heart

Front 13

which ventricle pumps the most force? what's the value?

Back 13

left value; 120 mmHg

Front 14

what percent of ventricular filling is due to atrial contraction

Back 14

15-35%

Front 15

4 valves & what they separate

Back 15

-two atrioventricular valves known as the tricuspid valve (right side) and mitral or bicuspid valves (left side) separate the atria and ventricles
-pulmonary and aortic valves separate the ventricles from the pulmonary and systemic circuits

Front 16

what are cardiac myocytes called, why?

Back 16

striated muscle cells cuz of the stripes seen in these cells

Front 17

what are myocytes connected end to end by

Back 17

intercalated disks

Front 18

gap junction

Back 18

regions at the intercalated disk that contain high concentration of specialized channels called gap junction channels

Front 19

what can gap junction channels pass

Back 19

ions and small intracellular metabolites

Front 20

how are gap junction channels formed

Back 20

each cell of a connected pair contributes
one hemichannel that combines to form the complete channel. There are 6 connexins (subunits) per connexon
(hemichannel) making a total of twelve subunits in the complete channel

Front 21

why is there electrical continuity between all the myocytes in the myocardium

Back 21

the pores of the gap junction channels are permeant to all ions

Front 22

what allows electrical excitation to pass easily from cell to cell

Back 22

high degree of electrical connectivity

Front 23

rate of heart contraction at rest of normal human heart

Back 23

60-70 bpm

Front 24

main cell types in the heart

Back 24

-pacemaker cells
-conducting cells
-working myocardium

Front 25

pacemaker cells

Back 25

primarily in sinoatrial (SA) node

Front 26

conducting cells

Back 26

-atrioventricular (AV) node
-bundle of His
-Purkinje fibers

Front 27

working myocardium

Back 27

-bulk of atrial cells
-bulk of ventricular cells

Front 28

which cells establish the "heartbeat", the rate at which the heart normally contracts

Back 28

SA node cells

Front 29

ectopic pacemakers

Back 29

regions of pacemaking tissue outside of the SA node

Front 30

sequence of excitation in the heart

Back 30

1. SA node initiates electrical excitation
2. internodal pathways
3. AV node conducts electrical excitation very slowly allowing atrial contraction to almost complete b4 excitation reaches the ventricle
4. bundle of his- excitation passes through a non-conducting layer of connective tissue that separates the atria and ventricle
5. bundle branches
6. purkinje fibers
7. bulk of ventricle muscle- when excitation reaches the working myocardium ventricular contraction begins

Front 31

primary difference between the action potential seen in nerve & muscle cells

Back 31

cardiac action potential has a long plateau phase, resulting in a much larger overall AP duration

Front 32

duration the cardiac action potential

Back 32

250-300 ms

Front 33

cardiac action potential phases

Back 33

Na channels open, Na channels close, Ca channels open & fast K channels close, Ca channels close & slow K channels open, resting membrane potential

Front 34

what is the duration of the cardiac muscle contraction controlled by

Back 34

duration of the cardiac action potential

Front 35

2 stable states of ventricular cells

Back 35

depolarized (during the plateau phase) and hyperpolarized (resting membrane potential)

Front 36

what occurs each time the heart flips betw the depolarized and hyperpolarized states

Back 36

it induces small currents flowing throughout the body, which can be recorded using electrodes on the skin

Front 37

what do the systematic rhythmic changes that the ECG undergo relate to

Back 37

the underlying changes in
the membrane voltage of the cardiac myocytes

Front 38

P wave

Back 38

atrial depolarization

Front 39

QRS complex

Back 39

ventricular depolarization

Front 40

T wave

Back 40

ventricular repolarization

Front 41

Q-T interval

Back 41

duration of ventricular action

Front 42

what is automaticity and what cells display this

Back 42

SA node cells- inherent electrical rhythm and beat spontaneously in
isolation

Front 43

pacemaker potential

Back 43

depolarizing ramp towards threshold, inevitably resulting in the triggering of a new action potential

Front 44

primary mechanism underlying the pacemaker potential

Back 44

slow activation of HCN channel

Front 45

HCN channels

Back 45

cation channels (Na and K pass), activated by hyperpolarization and inactivated by depolarization

Front 46

what occurs to HCN channels during atrial action potential

Back 46

they close

Front 47

when do HCN channels open

Back 47

membrane returns to rest
following the action potential

Front 48

what occurs when HCN channels open

Back 48

the membrane potential depolarizes

Front 49

when are voltage gated Ca channels activated and what do they do

Back 49

when membrane potential approaches threshold, create relatively slow and small action potential of SA nodal cells

Front 50

how are SA cells unusual

Back 50

t the action potential is produced by
calcium channels and the cell expresses few or no voltage gated sodium channels.

Front 51

what occurs during the AP

Back 51

potassium channels are activated to repolarize the membrane potential and HCN channels close in preparation to repeat the cycle.

Front 52

what is the nervous system control of the heart heart pacemaker mediated by

Back 52

autonomic nervous system

Front 53

what is SA node innervated by

Back 53

2 neurons from 2 components of the ANS: sympathetic & parasympathetic nervous systems

Front 54

effect of sympathetic nervous system on heart rate

Back 54

increases HR

Front 55

effect of parasympathetic nervous system on heart rate

Back 55

decreases HR

Front 56

what neurotransmitter plays a role in inc. HR and whats the mechanism?

Back 56

noradrenaline- increases the slope of pacemaker potential, activates HCN channels

Front 57

what neurotransmitter plays a role in dec. HR, mechanism?

Back 57

acetylcholine- more neg. starting point at the end of the AP, activates I_K, I_ACh channels

Front 58

heart rate of a heart that's been denervated, what does it mean about HR at rest?

Back 58

100 bpm, at rest the heart is normally under negative control (more parasympathetic input than sympathetic input)

Front 59

what do sympathetic and parasympathetic neurotransmitters work through

Back 59

G-protein linked receptors

Front 60

neuromodulation, whats the use of it

Back 60

when activation of G protein linked receptors modifies the function of ion channels in the cell. It is a common mechanism by which neurotransmitters produce their effects

Front 61

what is a good example of neuromodulation, why?

Back 61

the heart cuz there are 2 independent systems that produce distinct and functionally antagonist effects

Front 62

G protein linked receptor part of parasympathetic response, what is does.

Back 62

muscarinic acetylcholine receptor actovated G-protein G_i, the beta/gamma subunits of which activate a K channel known as I_K,ACh channel. This results in hyperpolarization of the membrane potential

Front 63

effect of parasympathetic input on SA Nodal cells

Back 63

1. ACh binds to M2 muscarinic AChR
2. activates G_i protein
3. beta/gamma subunits bind to I_K, ACh channel
4. activates channel
5. increases K+ ion conductance
6. hyperpolarizes membrane potential
7. dec. HR

Front 64

main effect of acetylcholine

Back 64

hyperpolarize the membrane potential

Front 65

what does noradrenaline act on, what occurs

Back 65

G protein linked receptor called beta-adrenergic receptor, this activates G_s G-protein and the alpha subunit activates adenylyl cyclase to produce cAMP. increased cAMP levels activated HCN channel, increases I_f current and inc slope of pacemaker potential

Front 66

effect of sympathetic input on SA Nodal cells

Back 66

1. NA bind to beta-adrenergic receptor
2. activates G_s protein
3. alpha subunit binds to and activates adenylyl cyclase
4. inc CAMP concentration
5. activates HCN channel
6. inc slop of pacemaker potential
7. inc heart rate

Front 67

what are humans acutely sensitive to

Back 67

individual differences

Front 68

what percent of genes show significant variation

Back 68

8%

Front 69

channelopathies

Back 69

diseases which involve mutations in ion channel genes

Front 70

basic building block of our genetic heritage

Back 70

chromosomes

Front 71

total number of human chromosomes

Back 71

46

Front 72

sex chromosomes

Back 72

females- 2 X chromosomes
males- X & Y chromosome

Front 73

how did males get shortchanged genetically

Back 73

cuz the Y chromosome is very short and contains junk DNA

Front 74

primary function of chromosomes

Back 74

protect the DNA yet allow access
for enzymes involved in gene transcription and DNA replication.

Front 75

scaffold proteins

Back 75

proteins which create a structure into which the DNA can pack

Front 76

number of genes

Back 76

20,500

Front 77

what percent of the genome codes for proteins

Back 77

less than 1.5%

Front 78

what percent do junk sequences (repetitive DNA) make up in the genome?

Back 78

50%

Front 79

what role did repetitive sequences play

Back 79

reshaping the genome by rearranging it: creating new genes, and modifying existing genes.

Front 80

goal of genome project

Back 80

create genetic maps

Front 81

single nucleotide polymorphisms (SNPs), what do they account for

Back 81

single base pair changes, large fraction of individual differences found in human populations

Front 82

how does evolution work with SNPs

Back 82

by increasing or
decreasing the frequency with which these SNPs occur in the population.

Front 83

how many SNPs have been identified

Back 83

3.5 million

Front 84

exons

Back 84

protein coding regions of the gene

Front 85

altering bases in the triplet code, which DNA uses to encode amino acids, altering bases

Back 85

1st position:changes in the 88
amino acid that is encoded for all but two amino acids
2nd position:Fewer codons are affected
3rd position: a large number of codons are unaffected

Front 86

2 kinds of genetic diseases

Back 86

single gene disorders
multifactorial disorders

Front 87

single gene disorders

Back 87

display simple Mendelian inheritance. They can have either a dominant or recessive phenotype.

Front 88

incomplete penetrance

Back 88

genetic background of the carrier can affect expression of the disease phenotype

Front 89

multifactorial disorders

Back 89

no single gene causes disorder

Front 90

example of multifactorial disorder

Back 90

hypertension- mutations in several different genes can each contribute a small amount to the disease phenotype.

Front 91

susceptibility genes

Back 91

several different genes that can each contribute a small amount to the disease phenotype

Front 92

most common channelopathy

Back 92

cystic fibrosis

Front 93

cystic fibrosis

Back 93

a recessive mutation in a chloride channel, which affects mucous formation in the lung increasing
the susceptibility to life threatening infections of the lung

Front 94

heterozygote advantage

Back 94

mutation confers some selective advantage for the heterozygous carriers, possibly resistance to a common infectious disease.

Front 95

diseases that have heterozygote advantage

Back 95

autosomal recessive disease sickle-cell anemia & cystic fibrosis

Front 96

what does long QT syndrome (LQTS) cause

Back 96

sudden death due to cardiac failure in young and otherwise healthy individuals.

Front 97

how to produce same clinical phenotype as in long QT syndrome, effect?

Back 97

-Mutations in several different ion channel genes
-The mutations produce defects in cardiac action potential repolarization.

Front 98

benign clinical phenotype of LQTS

Back 98

prolongation of QT interval

Front 99

torsades de pointes

Back 99

severe phenotype, first stage to ventricular arrhythmia and ventricular fibrillation

Front 100

ventricular fibrillation

Back 100

electrical activity is completely disordered (known as arrhythmia) and the ability of the 89
heart to pump blood is compromised leading to sudden death.

Front 101

treatment for ventricular fibrillation

Back 101

defibrillators can be used in order to
reset the normal electrical rhythm of the heart by giving the heart an electrical shock

Front 102

common kind of arrhythmia, where is it found

Back 102

reentrant arrhythmia, seen in ischemic damage

Front 103

reentrant arrythmia

Back 103

-electrical activity follows a circular path in the wall of the ventricle constantly reexciting the tissue.
-If a significant fraction of the ventricle is captured by a reentrant arrhythmia the
heart ceases to be an effective pump and sudden death soon follows

Front 104

effective treatment for LQTS mutations

Back 104

anti-adrenergic drugs which block sympathetic nervous system input to the heart during physical
or emotional stress

Front 105

problem for treatment of LQTS syndrome

Back 105

first symptom is sudden death

Front 106

why is treatment with β-adrenergic blockers not effective for LQTS syndrome

Back 106

genotypic
heterogeneity (the patients can have a number of different mutations)

Front 107

3 ion currents affected by mutations in LQTS

Back 107

I_Ks, I_Kr, I_Na current

Front 108

I_Ks

Back 108

slow, delayed rectifier K+ channel

Front 109

I_Kr

Back 109

rapid, delayed rectifer K+ channel

Front 110

I_Na

Back 110

fast sodium channel

Front 111

multimeric proteins

Back 111

ion channels made up of more than 1 subunit

Front 112

heteromeric proteins

Back 112

made up of 2 or more different kinds of subunits

Front 113

typical ion channel structure

Back 113

large α subunit and several β subunits

Front 114

most common genotype for LQTS syndrome, hows it treated?

Back 114

LQT1 mutation (a mutation in the
KCNQ1 gene), is particularly sensitive to triggers that activate the sympathetic nervous system, such as exercise and emotional stress. responds best to treatment with β-blockers

Front 115

LQT3 mutation treatment

Back 115

use of an implantable defibrillator

Front 116

how many copies of gene on autosome

Back 116

2 copies

Front 117

null mutation

Back 117

only one copy of the gene
is functionally inactivated

Front 118

what can a genetic defect in a single copy of the gene produce

Back 118

null mutation or dominant mutation

Front 119

two forms that dominant mutations can take

Back 119

gain of function mutations
dominant negative mutation

Front 120

gain of function mutations

Back 120

e function of
the channel is modified, thereby destabilizing electrophysiological function

Front 121

dominant negative
mutation

Back 121

bad subunits combine
with the good subunits to make bad channels thereby largely inactivating the products of the good gene

Front 122

what makes the biological system fail under stress

Back 122

Just a 50% reduction in the level of gene dosage

Front 123

null mutations in
the KCNQ1 gene

Back 123

post-transcriptional control of channel expression (subsequent regulation by the protein synthesis and assembly apparatus) cannot compensate for the loss of one allele and a dominant
mutation results.

Front 124

epilepsy

Back 124

global, synchronized
electrical activity

Front 125

most common cause of epilepsy

Back 125

brain trauma

Front 126

what form is of epilepsy is Benign familial neonatal convulsions (BFNC)

Back 126

inherited epilepsy, epileptic fits start two to three weeks after birth and cease after several months

Front 127

is BFNC dominant or recessive

Back 127

dominant

Front 128

two genes that can be mutated in
BFNC

Back 128

KCNQ2 and KCNQ3,

Front 129

what do KCNQ2 and KCNQ subunits combine to form

Back 129

M current

Front 130

what is M current important for

Back 130

important controller of membrane potential and reduces electrical excitability.

Front 131

effect of XE-991, what does it resemble

Back 131

blocks M-channels (KCNQ2-3 heteromultimers) and increases excitability of neurons, BFNC epilepsy

Front 132

ways by which new or modified genes can be introduced into the somatic tissues

Back 132

1.viral vectors
2.nonviral vectors
3.stem cells

Front 133

examples of viral vectors

Back 133

-adenovirus based vectors
-adeno-associated virus (AAV) based vectors

Front 134

ex. of nonviral vectors

Back 134

liposome based vectors

Front 135

stem cell gene therapy

Back 135

- integrate into some tissues and deliver modified gene

Front 136

what is genetic screening useful for

Back 136

-to optimize drug treatment
-treatment of genetic diseases such as LQTS,

Front 137

huntington's disease

Back 137

neurodegenerative disease that results in dementia and is frequently associated
with seizures

Front 138

homeostasis

Back 138

maintaining a similar condition

Front 139

William Cannon's descriptions of homeostasis

Back 139

1. constancy in an open system, requires mechanisms that act to maintain this constancy
2. steady-state conditions require that any tendency toward change automatically meets with factors that resist change
3. the regulating system that determins the homeostatic state consists of a number of cooperating mechanisms acting simultaneously
4. homeostasis doesn't occur by change, its a result of organized self-government

Front 140

parameters that are homeostatically regulated

Back 140

-body temperature
-osmolarity
-pH
-Na
-Ca
-other inorganic ions
-blood O2
-blood CO2
-blood glucose
-blood pressure

Front 141

open loop system

Back 141

has difficulty maintaining stable parameters

Front 142

closed loop system

Back 142

introduces feedback to control output

Front 143

purpose of negative feedback loop

Back 143

act to maintain the regulated variable at or near a set point

Front 144

negative feedback loop

Back 144

stimulus->sensor or receptor->afferent pathway->integrating center->efferent pathway->target of effector->response

Front 145

single sided control

Back 145

heater only

Front 146

antagonistic control

Back 146

heater and air-conditioner

Front 147

switching control

Back 147

response not identical to stimulus

Front 148

proportional control

Back 148

response identical to stimulus

Front 149

tonic AP

Back 149

slow adaptation

Front 150

phasic AP

Back 150

rapid adaptation

Front 151

control of body temperature

Back 151

dec room temp->inc heat loss from body->dec body temp->body's response (constriction of skin blood vessels, curling up, shivering)->dec. heat loss from body, heat production-> return of body temp to original value

Front 152

what does feedforward regulation do

Back 152

anticipates changes in a regulated variable and improves the speed of the body's homoeostatic response in order to minimize fluctuations in the variable being regulated.

Front 153

anticipatory responses

Back 153

-response to changes in environmental temperature
-brain initiated secretion of insulin and other hormones prior to eating a meal reduces glucose overload

Front 154

adjustments in behavior in response to phosphate deficiency

Back 154

1. inc kidney retention of phosphate
2. inc ingestion of phosphate-rich food

Front 155

hierarchical control,ex?

Back 155

multiple nested feedback loop
ex: one loop controls body temp. another loop controls the circadian rhythm in the body temperature set point

Front 156

trade-off of complex system

Back 156

robust but fragile

Front 157

classic way to build robustness into system

Back 157

redundancy

Front 158

downside to redundancy

Back 158

requires more resources

Front 159

2 basic ideas relating to the mechanisms evolved to maintain stability

Back 159

1. control theory, feedback loops, homeostasis
2. robust networks

Front 160

what can the complexity of bodies lead to

Back 160

instability

Front 161

where is this idea evident: body must achieve and maintain a balance

Back 161

buddhism & traditional chinese medicine

Front 162

who recognized first description of homeostasis and what was it

Back 162

Claude Bernard, the constancy of the internal environment is the condition for a free and independent life

Front 163

what is the function of the body's cells, (physiological and biochemical functions) dependent on

Back 163

the maintenance of a stable internal state

Front 164

what is associated with the control theory, what is it

Back 164

concept of homeostasis, its a branch of engineering

Front 165

when is the system considered to be an open loop

Back 165

in the absence of a control system

Front 166

do open loops work well usually?

Back 166

NO

Front 167

closed loop system

Back 167

has some kind of feedback to help regulate the output

Front 168

what do negative feedback loops act for

Back 168

to maintain the regulated variable at or near a given setpoint

Front 169

parts of neg. feedback loop in a biological system

Back 169

1. controlled variable
2. sensor to detect or measure this variable
3. wiring to transmit sensory signals from sensor to integrating sensor (which does computations required to produce output signal)
4. wiring to transmit the effector signal form the integrating center to the effector
5. effector that can produce a response to modify the controlled variable

Front 170

simple example of neg. feedback loop

Back 170

heating a fish tank- primary function is maintenance of set point using a heater

Front 171

what is the property of hysteresis

Back 171

The point at which the thermostat turns the heater
on or off depends on the prior history of the temperature.

Front 172

dead-band

Back 172

region of oscillation

Front 173

what do you not want the dead-band to be, why

Back 173

too narrow, cuz then the heater would be constantly turning on and off which would tend to wear out the components relatively
quickly.

Front 174

what kind of control does a complex system use

Back 174

antagonistic control, Temperature regulation of an office building
uses both heating and air-conditioning

Front 175

what kind of output do most biological sensors produce as part of feedback loop

Back 175

proportional output

Front 176

PID Control (proportional-integral-differential control)

Back 176

form of control commonly used in engineered control loops. proportional feedback from the sensor the integral and the differential of the sensor signal are also fed back

Front 177

integral term in a PID controller

Back 177

sum of instantaneous error over time

Front 178

integral term in a PID controller

Back 178

-sum of instantaneous error over time
-accelerates the movement of the process towards the set-point and eliminates the residual steadystate error that occurs with a pure proportional controller.

Front 179

what do non-idealities in the motor system result in

Back 179

physiological muscle tremor

Front 180

controlled variable in the control of body temperature?

Back 180

core body temperature that is monitored by temperature sensors

Front 181

error signal

Back 181

different betw setpoint and the actual core body temperature

Front 182

what minimizes the error signal

Back 182

negative feedback loop

Front 183

how does a decrease in the amplification the system has effect accuracy of the control of setpoint

Back 183

it decreases the accuracy of the control of setpoint

Front 184

how does gain affect accuracy the setpoint

Back 184

the larger the gain of the amplifier, the more accurately it will match the setpoint

Front 185

can a setpoint be controlled by other feedback loops? ex?

Back 185

YES
-diurnal change in body temp.
-acclimatization
-fever

Front 186

describe diurnal change in body temp

Back 186

. Even if the environmental
temperature remained absolutely stable throughout the day, the core body temperature will oscillate on a
daily cycle. Cooling during the night and then heating up during the day. T

Front 187

how does the response act in the neg feedback loop

Back 187

it acts to reduce the stimulus (error signal)

Front 188

how does the response act in the positive feedback loop

Back 188

the response makes the signal bigger eliciting a greater response
resulting in a increasing buildup of response

Front 189

ex. positive feedback loop

Back 189

in child birth:
movement of fetus down the birth canal starts to stretch the cervix. This releases oxytocin, which stimulates contractions of the uterus. This causes more stretching of the cervix
and so on. The cycle continues to escalate until the baby is forced out of the birth canal and the stimulus, stretching of the cervix is eliminated

Front 190

pathological condition resulting from pos. feedback loop

Back 190

congestive heart failure. The inability of the heart to pump blood causes more blood to accumulate in the ventricles
stretching the ventricle walls, which further impairs the heart's pumping ability resulting in a positive feedback cycle.

Front 191

what does feedforward regulation do

Back 191

anticipates changes in a regulated variable and improves the speed of the
body's homoeostatic response in order to minimize fluctuations in the variable being regulated.

Front 192

ex. of feedforward regulation

Back 192

regulation of core body temperature

Front 193

what is most feedforward regulation mediated by

Back 193

he nervous system and learning by the nervous
system is usually necessary in order to create these kinds of anticipatory behavior

Front 194

important homeostatically regulated variable

Back 194

blood glucose levels

Front 195

classic example of the role of learning in feedforward control

Back 195

beginning to salivate in expectation of the presentation of food

Front 196

another ex. of the role of learning in feedforward control

Back 196

anticipatory responses that occur before exercise

Front 197

Adjustments in behavior can have a large impact on the homeostatic regulation of what?

Back 197

sodium and calcium levels

Front 198

what is the simplest control system

Back 198

open loop, also known as ballistic control

Front 199

x

Back 199

the desired value, equivalent to set point

Front 200

Q

Back 200

control center, creates a command c

Front 201

command c

Back 201

the input to the plant p

Front 202

plant p

Back 202

what creates the output, y

Front 203

what is the controller in biological systems

Back 203

nervous system

Front 204

what is the plant in biological systems

Back 204

muscles, organs, glands

Front 205

job of control center

Back 205

convert the set point value into a suitable command, taking
account of any phase lag or gain limitations in the plant.

Front 206

parametric feedforward

Back 206

Monitor the noise and adjust the parameters of Q to compensate.

Front 207

ex. of parametric feedforward

Back 207

the stimulation of insulin release by the taste of food, which
anticipates the influx of glucose from a meal.

Front 208

parametric feedback

Back 208

Instead of monitoring the disturbance you can monitor its effects.

Front 209

error signal

Back 209

desired results-effects

Front 210

direct feedback

Back 210

the error signal is used to change the input to the controller by modifying the original input, x.

Front 211

disadvantage of direct feedback

Back 211

it introduces phase lag at higher frequencies

Front 212

how to overcome the problem of delays in feedback loops

Back 212

use an internal model of the
plant

Front 213

advantage of internal feedback

Back 213

e predicted error may be available long before there is
any information about the actual output. This helps eliminate problems of instability that are caused by
the long phase lags characteristic of biological systems.

Front 214

disadvantage of internal feedback

Back 214

it is not a real error signal and cannot compensate for unexpected
disturbances in the outside world

Front 215

problem with internal model

Back 215

if it falls out of registration with actual plant

Front 216

second or subsidiary feedback loop

Back 216

compares the
actual output y with the prediction y' and uses this prediction error as parametric feedback to update the parameters of the model.

Front 217

hierarchies of control in directing a gun at a targer

Back 217

Local loop controls muscle lengths and then another loop controlling joint angle and finally visual
feedback controlling the entire system

Front 218

complex branched control

Back 218

many muscles around a joint can contribute to joint angle so that zero
joint error may be achieved with various combinations of muscle lengths

Front 219

what is robustness paid for with

Back 219

fragility

Front 220

what does the bode theorem state

Back 220

that an improvement of sensitivity gained by a negative feedback
amplifier in the low-frequency range has unavoidable tradeoff of increased instability in the highfrequency range

Front 221

what does the bode theorem state

Back 221

that an improvement of sensitivity gained by a negative feedback
amplifier in the low-frequency range has unavoidable tradeoff of increased instability in the highfrequency range

Front 222

effect of increasing gain to increase robustness to a specific perturbation

Back 222

reduces range of stability

Front 223

stability

Back 223

personality, perceptions, and memories remain relatively stable throughout adult life even though the underlying physical substrate will have changed

Front 224

plasticity

Back 224

you can learn new skills and form new memories throughout life suggesting that the nervous system retains ability able to reorganize certain aspects of its function

Front 225

sources of stability at species level

Back 225

1.purifying selection acting on protein sequence/function
2.purifying selection acting on gene expression
3.evolution & robust networks underlying developmental, biochemical & physiological function
4.evolution of homeostatic feedback loops regulating development, biochemical & physiological function

Front 226

sources of stability at organismal level

Back 226

1. robust networks
2. homeostatic feedback loops (during development & in the adult)

Front 227

structural evolution

Back 227

evolution of gene coding sequences

Front 228

regulatory evolution

Back 228

evolution of gene coding sequences

Front 229

regulatory region

Back 229

-core promoter (transcription start site)
-regulatory modules (enhancers, repressors)

Front 230

2 components to gene regulation

Back 230

1.cis regulatory sequences (regions of DNA to which transcription factors bind)
2. transcription factor network (proteins that bind directly or indirectly to DNA to alter rates of gene transcription)

Front 231

transcription unit

Back 231

starts at transcription start site and encompasses all of the introns and exons of the gene

Front 232

enhancers

Back 232

transcription factors that bind to regulatory modules and inc. the rate of transcription

Front 233

repressors

Back 233

transcription factors that bind to regulatory modules and dec. the rate of transcription

Front 234

what is the regulatory region often restricted to

Back 234

regions immediately upstream of the transcription start
site

Front 235

what does the core promoter region encompass

Back 235

transcription start site

Front 236

size of regulatory regions in yeast and simple eukaryotes

Back 236

compact

Front 237

size of regulatory regions in mammals

Back 237

large and scattered

Front 238

where in the mouse BMP gene are large regulatory regions found

Back 238

a long way downstream from the end of the coding region.

Front 239

what is regulatory evolution most important in

Back 239

evolution of body morphology

Front 240

constraints on ion channel structural evolution

Back 240

1.structural constraints
2.epistatic constraint
3.pleiotropic constraint

Front 241

structural constraints on ion channel structural evolution

Back 241

-pore
-defective protein folding/retention in the ER
-assembly
-trafficking to Golgi and surface membrane

Front 242

epistatic constraint on ion channel structural evolution

Back 242

interactions with other channels

Front 243

pleiotropic constraint on ion channel structural evolution

Back 243

broad expression pattern of multipurpose channels

Front 244

efficient AP generation

Back 244

1. minimize overlap betw. Na and K currents
2. minimize overall current levels

Front 245

what is the source of most the protein motifs found in all multicellular species

Back 245

bacteria

Front 246

how do multicellular animals have greatly reduced degrees of freedom?

Back 246

The same protein is used in multiple different cells types and modifying the protein to improve the function of one cell is
likely to compromise its function in another cell, so that there are now more constraints on the protein function.

Front 247

what kind of effects occur when changing the function of transcription factor networks

Back 247

pleiotropic effects

Front 248

what does the regulatory network in sea urchin display

Back 248

changing the function of a given transcription factor is likely to produce pleiotropic effects, constraining the evolution of these proteins.

Front 249

how does the modular nature of cis-regulatory region effect evolution of cis regulatory regions

Back 249

makes them more specific

Front 250

Toolkit of developmental genes that can be used flexibly to construct new morphologies

Back 250

-hox gene cluster
-tinman/Nkx2.5
-eyeless/Pax6

Front 251

hox gene cluster

Back 251

specify anterior-posterior axis and segment identity in all metazoans

Front 252

Tinman/Nkx2.5

Back 252

heart determination

Front 253

eyeless/Pax6

Back 253

eye determination

Front 254

how can a toolkit of genes be used to construct diff animal morphologies and physiologies

Back 254

changing the timing and extent of expression of different genes during development.

Front 255

examples of structural evolution in physiological systems

Back 255

opsins-changes in light sensitivty
olfactory receptors-olfaction
lens crystallins- light focusing
melanocortin receptor- skin patterning/ camouflage
hemoglobin-high altitude adaptation
antifreeze proteins-resistance to freezing
channels-toxin resistance

Front 256

how many members in ion channel gene family

Back 256

143 members

Front 257

where is a wide variety of ion channel genes expressed

Back 257

in electrically excitable cells such as different types of neurons, muscle cells and hormone releasing cell. Also in cells that are not electrically excitable, such as kidney, liver and immune system cells.

Front 258

how are significant change in AP in heart produced

Back 258

by varying the relative
expression levels of a relatively fixed set of ion channel genes

Front 259

how is the typical ion channel gene expressed in the brain

Back 259

in literally hundreds of different
phenotypically differentiated types of neurons in the nervous system.

Front 260

what is the CatSper family

Back 260

a cation channel that is only expressed in one part of sperm cell

Front 261

where is the sperm cell expressed

Back 261

in the principle piece of the sperm

Front 262

how are most ion channels expressed

Back 262

broadly and multi-purpose;they underlie a wide range of different electrophysiological functions

Front 263

one exceptional thing about morphology of mammals

Back 263

their enormous diversity in body size

Front 264

what does heart size scale directly with

Back 264

body size over the entire range of animals

Front 265

what changes between cardiac myocytes of different species

Back 265

the duration of the cell proliferation phase

Front 266

how does mouse pressure differ from human pressures

Back 266

mouse pressures change about 10 times faster

Front 267

what are the physiological properties of the cardiovascular system classified as

Back 267

fundamental or derived

Front 268

fundamental properties of cardiovascular system

Back 268

mean arterial pressure, pulse
pressure and the minimum diastolic pressure

Front 269

what underlies the constraint on fundamental properties

Back 269

The need to maintain adequate perfusion of key tissues such as the brain and kidneys

Front 270

what are derived properties? ex?

Back 270

properties that change systematically with mammalian body weight in order to maintain the fundamental physiological properties of the system independent of body
size. ex: HR, ventricular AP duration, rate of calcium uptake

Front 271

what is the primary constraint

Back 271

physical properties of vasculature function

Front 272

what is the vasculature modeled as

Back 272

capacitor and resistor in series

Front 273

what does the decay of arterial pressure look like

Back 273

exponential curve

Front 274

is the decay rate faster for large or small animals

Back 274

small animals

Front 275

how does the time constant (τ) for decay of arterial pressure during diastole relate to body mass

Back 275

it decreases with decreasing body mass

Front 276

duration of diastole related to body mass

Back 276

duration must be shorter in smaller animals

Front 277

ventricular AP related to body mass

Back 277

shorter in smaller animals

Front 278

2 key parameters in the electrical function of the heart

Back 278

the duration of the cycle of contraction and relaxation, and the duration of systole, the period of contraction that scale almost identically.

Front 279

why is there a strong constraint on the duration of diastole

Back 279

because this is the low pressure period during which coronary perfusion takes place and this period cannot become too short

Front 280

one key difference betw. small animals and larger animals

Back 280

a change in the action potential morphology

Front 281

AP morphology in large animals

Back 281

classic spike and dome morphology

Front 282

AP morphology in small animals

Back 282

triangular waveforms

Front 283

why is there a difference in AP morphology in large and small animals

Back 283

changes in potassium channel expression

Front 284

what happens to the waveform as large I_to is added

Back 284

converted to triangular waveform

Front 285

what do larger species not express

Back 285

I_Kur

Front 286

pattern of Kv2.1 expression

Back 286

a step function from small to large species, reflecting the pattern of IKur expression.

Front 287

pattern of Kv4.2 expression

Back 287

a step function reflecting Ito expression

Front 288

what do the differences in gene regulatory function correlate well with

Back 288

changes in mRNA expression

Front 289

two forms of ventricular action potential morphology

Back 289

triangular or spike & dome

Front 290

what is the difference in the 2 forms of ventricular AP morphology due to

Back 290

greatly increased expression of two potassium currents Ito and IKur in small mammals.

Front 291

what do changes in Kv2.1 and Kv4.2 potassium channel gene expression and promoter function show

Back 291

that evolution of cis-regulatory elements is the primary determinant of this trait.

Front 292

what are the repolarizing currents for guinea pig and larger species

Back 292

I_Ks and I_Kr

Front 293

what genes encode I_Ks and I_Kr

Back 293

KCNQ1 and KCNH2

Front 294

what 2 channel properties remain the same betw. human and mouse

Back 294

KCNQ1 and KCNH2

Front 295

another current that has a large impact on the AP duration in larger animals

Back 295

calcium channel

Front 296

is structural evolution of importance

Back 296

NO

Front 297

how will a small species effect expression of Ca channel

Back 297

there will be a paradoxical increase in the expression of this channel

Front 298

how does Ca current effect AP duration

Back 298

it will increase AP duration

Front 299

most important function of Ca channel

Back 299

to form the link between electrical excitation and mechanical contraction

Front 300

second constraint on the size of the Ca current

Back 300

the need to avoid calcium overload

Front 301

2 main calcium uptake mechanisms

Back 301

Ca-ATPase and Na-Ca exchanger

Front 302

size of the time constant of recovery of internal calcium levels in smaller animals

Back 302

faster

Front 303

what is the plateau period of increased calcium levels in smaller animals

Back 303

decreased

Front 304

effect of smaller species on expression of the gene
encoding the Ca-ATPase

Back 304

dramatically increases

Front 305

effect of smaller species on expression of the gene encoding Na-Ca transporter

Back 305

unchanged

Front 306

2 ways to pump Ca out

Back 306

1. ATPase pumps it back to cytoplasmic reticulum
2. Na-Ca exchanger

Front 307

competing constraints

Back 307

- scaling of AP duration
-maintain excitation-contraction coupling
-avoid calcium overload

Front 308

what is the predominant mechanism by which scaling of electrophysiology is achieved

Back 308

regulatory evolution

Front 309

what 2 features do physiological and developmental system share

Back 309

1. Changes in protein sequence/function are greatly constrained by the pleiotropy constraint.
2. Both systems have a large computational component.

Front 310

2 kinds of tasks physiological systems perform

Back 310

1. primarily physical tasks
2. primarily computational tasks

Front 311

ex. of physical tasks the physiological systems perform

Back 311

modify substrates, sense physical stimuli, etc.

Front 312

what does the relative balance between tasks the physiological system performs effect

Back 312

whether the system evolves by regulatory or structural evolution.

Front 313

what kind of evolution will physical tasks require

Back 313

structural evolution

Front 314

what kind of evolution will result in computational tasks

Back 314

structural or regulatory evolution

Front 315

what kind of function occurs as physiological systems become more complex and control structures form an increasingly large component of the overall system

Back 315

computational function

Front 316

stability

Back 316

personality, perceptions, and memories remain relatively stable throughout adult life even though the underlying physical substrate will have changed

Front 317

plasticity

Back 317

you can learn new skills and form new memories throughout life suggesting that the nervous system retains the ability to reorganize certain aspects of its function

Front 318

sources of stability at the species level

Back 318

1.purifying selection acting on protein sequence/function
2.purifying selection acting on gene expression
3.evolution of robust networks underlying developmental, biochemical, and physiological function
4.evolution of homeostatic feedback loops regulating developmental, biochemical and physiological function

Front 319

sources of stability at the organismal level

Back 319

1.robust network (unmonitored)
2.homeostatic feedback loops (monitored)

Front 320

effects of denervation on skeletal muscle

Back 320

1.atrophy
2.denervation supersensitivity
3.changes in Na channel isoform expression (change in TTX sensitivity)
4.changes in contractile protein expression (myosin isoform expression)

Front 321

what occurs in atrophy

Back 321

reduced muscle fiber mass

Front 322

denervation supersensitivity

Back 322

rapid increase in the expression of AChRs in the extrajunctional regions

Front 323

what kinds of changes in Na channel isoform expression occur?

Back 323

Nav1.5 is up-regulated but Nav1.4 remains same

Front 324

what are denervation effects due to

Back 324

1.loss of trophic input
2.loss of electrical input

Front 325

what did TTX cuff experiment show, how?

Back 325

that electrical activity by itself was important. By placing TTX cuff around the nerve, leaving trophic support intact and showed that this produced effects of denervation. blocking synaptic transmission w/toxin or an AChR antagonist does same thing

Front 326

what does electrical activity regulate

Back 326

AChR expression
expression of Na channel isoforms

Front 327

how do repeated burst of stimulation (tetanic stimulation) affect synaptic current

Back 327

increase excitatory synaptic current->LTP (long term potentiation)

Front 328

how does electrical activity result in LTP

Back 328

it controls the number of AMPA receptors at the synapse

Front 329

what does LTP do

Back 329

enhances weak and/or silent synapses

Front 330

what does the typical protocol for eliciting LTP involve

Back 330

prolonged repetitive low-frequency stimulation (900 stimuli at 1Hz)

Front 331

predominant current hypothesis for LTD

Back 331

quantitative properties of the postsynaptic calcium signal within dendritic spines dictates whether LTP or LTD is triggered, with LTD requiring a modest inc in calcium, whereras LTP requires an inc beyond some critical threshold value

Front 332

why are the temporal characteristics of the inc in calcium important

Back 332

since changing the relative timing betw. pre- and postsynaptic activation by just a few tens of milliseconds can reverse the direction of synaptic modification

Front 333

how does LTP & LTD affect AMPA receptors

Back 333

changes the rate of insertion or removal

Front 334

what does LTP affect

Back 334

receptor trafficking and is restricted to specific synapses

Front 335

what is the problem with LTP

Back 335

it creates a positive feedback cycle->synaptic strengths become increasingly strengthened resulting in saturation of synaptic inputs and neural activity

Front 336

what does synaptic scaling do

Back 336

reduces the strength of all synapses to maintain neuronal activity within an acceptable range

Front 337

form of synaptic plasticity

Back 337

non-associative LTP->occurs at synapses in CNS

Front 338

where is habituation common in

Back 338

CNS

Front 339

what do we habituate to

Back 339

loud noises, touch of clothing, many other kinds of sensory stimuli

Front 340

Gill Siphon Withdrawal Reflex

Back 340

defensive reflex occurs in response to a threatening stimulus like a gentle tap on the siphon or mantle shelf, which causes animal to withdraw its siphon and gill

Front 341

what causes habituation in the siphon short term

Back 341

reduction in synaptic efficiency at multiple synapses in the underlying circuit in the short term

Front 342

what causes habituation in the siphon long term

Back 342

changes in synaptic morphology, with a reduction in synaptic connections

Front 343

what is sensitization

Back 343

when a sensitizing stimulus acts to amplify synaptic transmission betw. sensory & motor neurons, amplifying reflex

Front 344

what is sensitization mediated by

Back 344

serotonergic interneurons

Front 345

actions of serotonin

Back 345

1.inhibition of K channels results in spike broadening, inc Ca influx & neurotransmitter release
2.vesicles are mobilized to the release site and probability of release is increased
3.the L-type Ca channel is activated, inc Ca ion influx during AP

Front 346

targets of sensitization

Back 346

K channel, Ca channel, NT release

Front 347

what are long term effects of sensitization mediated by

Back 347

changes in gene expression

Front 348

What does repeated activation of A kinase lead to

Back 348

changes in the biochemistry of the cell & the pattern of gene expression

Front 349

what does the dynamic equilibrium do

Back 349

it maintains synaptic connections

Front 350

example of the role of electrical activity in the regulation of neuronal phenotype

Back 350

ocular dominance

Front 351

what affects cell differentiation

Back 351

presence & pattern of electrical activity

Front 352

two types of skeletal muscle

Back 352

slow-twitch and fast-twitch

Front 353

what are slow twitch muscles involved in

Back 353

maintenance of posture and receive a slow steady electrical input

Front 354

what are fast twitch muscles involved in

Back 354

more active movement and receive sporadic bursts of electrical activity

Front 355

what is the switch in contractile properties produced by

Back 355

changes in myosin isoform expression

Front 356

what do cross innervation experiments show

Back 356

the nature of the innervating nerve determines the muscle properties

Front 357

what do experiments using direct electrical stimulation show

Back 357

that much of this differentiation is due to different patterns of electrical activity generated by different types of innervating motor neurons

Front 358

what is the phenotype of the muscle cells determined by

Back 358

the pattern of electrical activity produced by the innervating motor neuron

Front 359

what are the effects of Ca mediated through

Back 359

regulation of a Ca regulated protein phosphatase calcineurin and the transcription factor NFAT

Front 360

what is calciuneurin

Back 360

protein phosphotase

Front 361

what is NFAT

Back 361

a transcription factor

Front 362

effect of high steady-state Ca levels

Back 362

calciuneurin is active, dephosphorylated form of NFAT enters nucleus and activates slow muscle fiber transcriptional program

Front 363

effect of low steady-state Ca levels

Back 363

low NFAT fails to enter the nucleus permitting expression of the fast fiber program

Front 364

what can electrical activity modulate

Back 364

the phenotype of electrically excitable cells

Front 365

besides for the amount of electrical activity, what is important in modulating the phenotype

Back 365

the pattern

Front 366

what is the only known linkage btw electrical activity and regulation of phenotype

Back 366

changes in internal Ca levels

Front 367

what is Munc18-1 essential for

Back 367

synaptic transmission

Front 368

why do Munc18-1 knockout mice die

Back 368

they cant initiate breathing

Front 369

Munc18-1 knockout mice

Back 369

no synaptic activity in either the cortex or NMJ. neurotransmitter receptors are present

Front 370

what occurs after initial brain development in Munc18-1 knockout mice

Back 370

there was extensive cell death of mature neurons

Front 371

what does the brain follow during wiring up

Back 371

genetic program

Front 372

what is maintenance of neurons dependent on

Back 372

synaptic function

Front 373

what occurs in the absence of electrical activity

Back 373

neurons go into programmed cell death, apoptosis

Front 374

what 2 signals does creation of synapses require

Back 374

1.molecular guidance cues for circuit assembly during development
2.activity-dependent regulation

Front 375

where is it shown that the expression levels of most ion channels are relatively fixed

Back 375

in heterozygote null mutations that produce haploinsufficiencies

Front 376

haploinsufficiency

Back 376

one copy of a gene is functionally inactivated in such a way that it is null

Front 377

which genes produce haploinsufficiencies

Back 377

null mutation in both KCNQ1 gene that encodes alpha subunit of I_Ks channel & KCNH2 gene that encodes alpha subunit of I_Kr gene

Front 378

response to feedback of haploinsufficiency

Back 378

inc in gene expression or inc in effectiveness of biosynthetic pathway

Front 379

how many ion channel gene mutations produce haploinsuffiencies

Back 379

four

Front 380

which genes in heterozygous KOs produce a graded reduction in current expression

Back 380

scn5a and KChIP2

Front 381

how many cardiac currents produce haploinsuffiency mutations

Back 381

five

Front 382

channel biosynthesis pathway

Back 382

gene transcription->mRNA processing->translation->protein processing->assembly of subunits->transport to cell membrane->assembly into channel complex->functional channels in plasma membrane ->cellular electrophysiological phenotype

Front 383

what model does homeostatic regulation follow

Back 383

hard-wired model=feedback pathways in adult heart & nervous system are either quite limited or dont exist

Front 384

well established linkage between electrical excitation and the genome

Back 384

fluctuations in internal calcium concentrations

Front 385

limitations of homeostatic regulation

Back 385

-its computationally difficult to turn a simple 1-D signal from the Ca transients into info that can be used to regulate expression of a large multi-dimension array of genes
-there may not be much evolutionary pressure to produce homeostatic feedback pathways to compensate for haploinsufficiency mutations

Front 386

how can development occur

Back 386

-with all info required for its trajectory inscribed into the genome at the start of the flight
-homeostatic regulatory pathways feedback during course of development

Front 387

canalization

Back 387

homeostatic regulatory pathways feedback during the course of development making the arrival at the final destination a more likely and accurate occurance

Front 388

other way to establish phenotypic stability

Back 388

evolve robust networks

Front 389

what do u do if calcium channel is regulated by calcium fluxes

Back 389

u remove most the info available about electrical activity to the system cuz a decrease in Ca flux results in upregulation of the channel resulting in maintained Ca flux

Front 390

what does the floxed gene allow

Back 390

you to knockout the gene in the tissue of choice to some degree at the time of choice depending of the nature of the transgenic mice to which the floxed mouse is bred

Front 391

what does mice dying rapidly reflect

Back 391

the time course of loss of the Cav1.2 protein and mRNA

Front 392

what occurs to contractility before death, why

Back 392

ir declines, reflecting the loss of functional Cav1.2 channels in the ventricular myocytes

Front 393

is there a general purpose homeostatic system that can respond to changes in experimentally induced changes in gene number

Back 393

NO

Front 394

is there an effective response in life threatening situation where there's a reasonable solution to up-regulate Cav1.3 and or another Cav1 channel

Back 394

NO

Front 395

when homeostatic system exist what do they evolve for

Back 395

to deal with common problems that affect fitness

Front 396

what occurs to Cav1.2 mRNA in heterozygous KO mice

Back 396

large reduction

Front 397

what occurs to peak current size in heterozygous KO mice

Back 397

no change!

Front 398

what does compensation reflect

Back 398

a non-linear biosynthetic pathway

Front 399

is compensation post-transcriptional

Back 399

YES

Front 400

what is Ca's role in membrane potential and intracellular events

Back 400

it is the linkage between membrane potential and intracellular events

Front 401

types of glial (neuroglial)

Back 401

astrocyte
oligodendrocyte
microglial cell

Front 402

astrocyte

Back 402

maintain chemical environment
blood-brain barrier
reuptake of neurotransmitters

Front 403

oligodendrocytes

Back 403

myelin formation
(schwann cells in PNS)

Front 404

microglial cells

Back 404

scavenger (related to macrophages)

Front 405

cellular constituents of the CNS

Back 405

neurons
glial (neuroglial)
ependymal cells

Front 406

ependymal cells

Back 406

epithelial cells that line cavities in the brain

Front 407

what is choroid plexus, what does it do

Back 407

ependymal cell specialization, manufacture and secrete CSF

Front 408

arachnoid granulations

Back 408

outpouching of arachnoid, turns over CSF (CSF exits here)

Front 409

where does the CSF exit to

Back 409

venous sinus (large venous vessel)

Front 410

where does the CSF exit to

Back 410

venous sinus (large venous vessel)

Front 411

CSF

Back 411

shock absorber for the brain

Front 412

meninges

Back 412

brain coverings: dura, arachnoid, pia

Front 413

ganglion

Back 413

group of neurons

Front 414

topographic organization

Back 414

orderly point-to-point representation of the periphery in the brain

Front 415

gray matter

Back 415

location of cell bodies in the spinal cord

Front 416

white matter

Back 416

location of myelinated axons

Front 417

dorsal roots

Back 417

sensory nerve fibers from skin, muscle, internal visceral organs

Front 418

ventral roots

Back 418

motor nerve fibers to skeletal muscle and autonomic output to blood vessels, glands and internal visceral organs

Front 419

somatomotor neurons

Back 419

alpha motor neurons that innervate skeletal muscle

Front 420

how big is spinal cord

Back 420

18 inches

Front 421

2 dilations in spinal cord

Back 421

cervical and lumbar

Front 422

what does the lumbar nerves region control

Back 422

every movement with the legs, also gets sensory input form there

Front 423

brain stem

Back 423

midbrain, pons, medulla oblongata

Front 424

midbrain

Back 424

substantia nigra and its role in the initiation of motor movements, regulates eye movements, controls pupil diameter, movement of eyelids, relays auditory and visual information to cerebral cortex, descending control of skeletal muscles

Front 425

pons

Back 425

coordinates respiration, control of lateral eye movements, relays info to and from cerebral cortex and cerebellum

Front 426

medulla

Back 426

regulates blood pressure, HR, control of respiration, walking, and standing

Front 427

cerebellum

Back 427

-integrates sensory and cortical information critical for maintenance of an upright posture (orthostasis)
-planning and coordinating movements

Front 428

diencephalon

Back 428

thalamus & hypothalamus

Front 429

thalamus

Back 429

-sensory relay for all senses
-sleep-wakefulness

Front 430

hypothalamus

Back 430

thermoregulation
salt & water balance
satiety
endocrine functions
sexually dimorphic nuclei
stress responses
circadian rhythms

Front 431

cerebrum (cerebrum cortices)

Back 431

has 4 lobes-> frontal, parietal, occipital, temporal

Front 432

hills on the invaginated part of the cortex

Back 432

gyri, sulci

Front 433

frontal lobe

Back 433

motor, speech, personality, emotive, association

Front 434

parietal lobe

Back 434

sensory integration, association cortex,damage leads to deficits in attention and perceptual awareness

Front 435

occipital lobe

Back 435

vision

Front 436

temporal lobe

Back 436

audition, learning, memory, facial recognition, language

Front 437

Peripheral nervous system

Back 437

somatic & autonomic

Front 438

somatic part of PNS

Back 438

-consists of a single neuron betw. CNS & skeletal muscle cells
-innervates skeletal muscle ONLY
-can lead only to muscle excitation

Front 439

autonomic nervous system

Back 439

-maintains the ability of our body's internal environment
-involuntary nervous system: reflects subconscious control
-innervates heart, lungs, blood vessels, skin, bladder, eyes, glands, stomach, intestines, pancreas, gallbladder, liver

Front 440

3 divisions of ANS

Back 440

sympathetic NS, parasympathetic NS, enteric nervous system (gut glandular secretions, GI tract motility)

Front 441

autonomic part of PNS

Back 441

-has 2 neuron chain (connected by a synapse) betw, CNS & effector organ
-innervates smooth & cardiac muscle, glands, and GI neurons
-can be either excitatory or inhibitory

Front 442

upper motor neurons

Back 442

structure above spinal cord
-motor cortex (planning, initiating, directing voluntary movements)
-brainstem centers (basic movements and postural control)

Front 443

lower motor neurons

Back 443

spinal cord

Front 444

3 receptors that innervate sensory neurons

Back 444

-receptors in tendons
-skeletal muscle sensory receptors
-nociceptor sensory receptors in skin

Front 445

what is each region of the spinal cord associated with

Back 445

pairs of sensory inputs and motor outputs to appropriate regions in the body

Front 446

cervical enlargement

Back 446

controls arms & hands

Front 447

thoracic region

Back 447

controls stomach

Front 448

lumbar enlargement

Back 448

controls legs

Front 449

intermediate spinal grey

Back 449

region in between ventral & dorsal horn, contains neurons involved in integration of info.

Front 450

lateral horn

Back 450

contains cell bodies for ANS

Front 451

sciatica

Back 451

compression & loss of motor function

Front 452

free nerve ending receptor function

Back 452

pain, temperature, crude touch

Front 453

muscle spindle receptor axons

Back 453

Ia and II (sensory axons)

Front 454

golgi tendon organs axons

Back 454

Ib (sensory axons)

Front 455

where do alpha and gamma motor neurons travel

Back 455

in the peripheral nerve

Front 456

axon for alpha-motor neurons

Back 456

A-alpha

Front 457

axon for gamma-motor neurons

Back 457

A-gamma

Front 458

target of innervation for alpha-motor neurons

Back 458

innervation of skeletal muscle

Front 459

target of innervation of gamma- motor neurons

Back 459

innervation of intrafusal fibers (sensory organ)

Front 460

reflex

Back 460

a stereotyped (involuntary) motor response elicited by a defined sensory stimulus

Front 461

classification of neural reflexes

Back 461

-efferent division that controls effector
-integrating region within CNS
-time at which reflex develops
-number of neurons in reflex loop

Front 462

efferent division that controls effector

Back 462

-somatic motor neurons control skeletal muscles
-autonomic neurons control smooth & cardiac muscle, glands, and adipose tissue

Front 463

integrating region within the CNS

Back 463

-spinal reflexes don't require input from the brain
-cranial reflexes are integrated within the brain

Front 464

time at which reflex develops

Back 464

-innate (inborn) reflexes are genetically determined
-learned (conditioned) reflexes are acquired through experience

Front 465

the number of neurons in reflex loop

Back 465

-monosynaptic inputs have only 2 neurons (Afferent and efferent)
-polysynaptic reflexes add one or more interneurons betw, the afferent & efferent neurons

Front 466

what are all autonomic reflexes, why

Back 466

polysynaptic cuz they have 3 neurons: 1 afferent, 2 efferent

Front 467

pathway for skeletal muscle sensory receptors

Back 467

sensory neurons->spinal cord
->efferent neurons->somatic motor neurons->inc/dec. excitation-contraction coupling->skeletal muscles->contraction or relaxation

Front 468

what is special about the muscle stretch reflex (knee jerk, myotatic, patellar tendon)

Back 468

its the only monosynaptic reflex circuit in spinal cord

Front 469

muscle spindle

Back 469

sensory receptor that conveys info about muscle length, in parallel with skeletal muscle fibers
-stimulus for peripheral receptor to generate AP in afferent fibers

Front 470

another name for skeletal muscle fiber

Back 470

extrafusal muscle fiber

Front 471

another name for muscle spindle

Back 471

intrafusal muscle fiber

Front 472

basics of knee jerk reflex

Back 472

quadriceps muscle (extensor) contracts and hamstring (flexor) relaxes

Front 473

properties of stretch reflex

Back 473

-monosynaptic excitatory reflex pathway
-polysynaptic inhibitory reflex pathway
-local sign (ipsilateral)
-no afterdischarge
-reflex is responsible for maintenance of muscle tone
-import. for maintenance of upright posture

Front 474

explain monosynaptic excitatory reflex pathway

Back 474

contraction of same & synergist muscles: monosynaptic excitation of motoneurons innervating quadricep muscles

Front 475

explain polysynaptic inhibitory reflex pathway

Back 475

relaxation of antagonist muscles: reciprocal inhibition of motoneurons innervating hamstring muscles

Front 476

explain local sign (ipsilateral)

Back 476

negative feedback, designed to maintain muscle length at a desired value

Front 477

explain no afterdischarge

Back 477

no sustained contraction of quadricep muscles

Front 478

what does alpha refer to

Back 478

alpha motor neurons

Front 479

what does gamma refer to

Back 479

gamma motor neurons

Front 480

what do gamma motor neurons do

Back 480

innervate muscle spindle-puts tension back on it and allows it to get the new muscle length

Front 481

what is the crossed extensor (flexor withdrawal) flex involve

Back 481

polysynaptic pathway
protective reflex

Front 482

basics of crossed extensor reflex

Back 482

extensor muscles (that felt painful stimulus) relax and flexors contract, moving foot away from painful stimulus. in the other leg, the flexor muscles relax

Front 483

properties of flexor withdrawal reflex

Back 483

-polysynaptic excitation of alpha-motoneurons innervating ipsilateral flexor muscles
-polysynaptic reciprocal relaxation of ipsilateral extensor muscles
-local sign
-afterdischarge of neural reflex circuitry
-crossed polysynaptic excitation of alpha motoneurons innervating extensor muscles
-crossed polysynaptic inhibition of alpha motoneurons innervating flexor muscles
-protective reflex

Front 484

what do golgi tendon organs do

Back 484

they encode information about muscle tension

Front 485

placement of golgi tension in relation to skeletal muscle fibers

Back 485

in series

Front 486

what occurs in the inverse myotatic reflex

Back 486

-inhibition of the motor neurons that innervate this muscle
-excitation in the opposing flexor's motor neurons

Front 487

sequence of events in inverse myotatic reflex

Back 487

-neuron from golgi tendon organ fires
-motor neuron is inhibited
-muscle relaxes
-load is released

Front 488

functions of golgi tendon organ reflex

Back 488

-neg. feedback system designed to monitor and maintain muscle force
-relatively insensitive to muscle stretch
-relaxation of muscles attached to stretched tendon
-excitation of muscle's antagonist
-exquisitely sensitive to muscle tension
-in the extreme prevents tearing of muscles from tendon insertions
-helps preserve muscle integrity
-protective reflex
-normally is believed to slow muscle contraction as tension increases (import for performance of fine motor acts)

Front 489

principles of sensory system organization

Back 489

-specific sensory receptor types are sensitive to certain modalities and submodalities
-a specific sensory pathway codes for a particular modality or submodality
-the specific ascending pathways are crossed so that sensory info is generally processed by the side of the brain opposite the stimulated side of the body
-most specific ascending pathways synapse in the thalamus on their way to the cortex

Front 490

map of sensory dermatomes

Back 490

outlines regions of the body surface that project into dorsal roots of specific segments

Front 491

what is the cortical area proportional to

Back 491

sensory sensitivity

Front 492

1st order neurons

Back 492

sensory, cell bodies are in the PNS, located in dorsal root ganglia

Front 493

2nd order neurons

Back 493

central nervous system neurons whose cell bodies are located in spinal cord or medulla

Front 494

3rd order neurons

Back 494

CNS neurons whose cell bodies are located in the contralateral (opp side of nervous system from the incoming sensory stimulus) thalamus

Front 495

do ascending systems cross? explain

Back 495

yes, sensory info from left side of the body is transmitted to the right somatosensory cerebral cortex (and right side of body to left somatosensory cerebral cortex)

Front 496

mechanosensory system

Back 496

dorsal column(kind of sensory info. system is transmitting)-medial lemniscal system(pathways within NS being accessed)

Front 497

somatic sensory receptors in the skin

Back 497

-merkel's disk (touch)
-free nerve ending (pain)
-meissner's corpuscle (light touch)
-pacinian corpuscle (vibration & deep pressure)

Front 498

1st order sensory receptors

Back 498

touch, pressure, vibration, joint mechanoreceptors that provide important information about limb placements (proprioception)

Front 499

how do axons of 1st order neurons travels

Back 499

in the ipsilateral dorsal columns

Front 500

where are dorsal column nuclei

Back 500

in medulla

Front 501

where do 1st order axons synapse

Back 501

on 2nd order neurons in caudal medulla

Front 502

where do 2nd order medullary neuron axons project to, how?

Back 502

the contralateral thalamus via the fiber called medial lemniscus

Front 503

where do 3rd order axons project to

Back 503

ipsilateral (same side) somatosensory cortex

Front 504

how are the target neurons in somatosensory cortex organized

Back 504

somatotopically organized (activation of touch receptors in the right index finger activate thalamic neurons in the right index finger region of somatosensory cortex)

Front 505

where are the receptors for the pain (and temperature) pathway/spinothalamic/anterolateral

Back 505

on free nerve endings

Front 506

where are 1st order sensory cell bodies located

Back 506

in dorsal root ganglia

Front 507

which reflex is associated with activation of a nociceptor

Back 507

flexor withdrawal reflex

Front 508

what are peripheral sensory endings specialized for

Back 508

to sense tissue damaging stimulus (nociceptive)

Front 509

where do 1st order sensory axons synapse

Back 509

on 2nd order neurons in the ipsilateral dorsal horn

Front 510

what happens to axons of 2nd order neurons

Back 510

they cross to the contralateral side of the spinal cord and travel in the anterolateral white matter

Front 511

what forms spinothalamic tract

Back 511

axons in the anterolateral white matter

Front 512

where are 3rd order neurons located

Back 512

in thalamus

Front 513

where do 3rd order neurons project to

Back 513

neurons in the ipsilateral somatosensory cortex

Front 514

what are thalamocortical projections

Back 514

somatotopic

Front 515

pathway in the anterolateral system

Back 515

afferent neuron from pain or temperature receptor->anterolateral column of spinal cord->brainstem->collaterals to reticular formation->thalamus

Front 516

pathway in the dorsal column system

Back 516

receptors for body movement, limb positions, fine touch discrimination, pressure->dorsal column of spinal cord->brainstem nucleus->brainstem->collaterals to reticular formation->thalamus

Front 517

for the fine touch, proprioception, and vibration stimulus, where does the primary sensory neuron terminate

Back 517

in the medulla, ipsilateral

Front 518

for the irritants, temperature, coarse touch stimulus, where does the primary sensory neuron terminate

Back 518

in the dorsal horn of the spinal cord

Front 519

for the fine touch, proprioception, and vibration stimulus, where does the secondary sensory neuron terminate

Back 519

in thalamus, contralateral

Front 520

for the fine touch, proprioception, and vibration stimulus, where does the tertiary sensory neuron terminate in

Back 520

somatosensory cortex

Front 521

for the irritants, temperature, coarse touch stimulus, where does the secondary sensory neuron terminate

Back 521

thalamus contralateral

Front 522

for the irritants, temperature, coarse touch stimulus, where does the tertiary sensory neuron terminate

Back 522

somatosensory cortex

Front 523

through which nerve do mechanosensory and pain pathways from the face use different pathways

Back 523

through cranial nerve (trigeminal nerve)

Front 524

referred pain

Back 524

visceral pain sensations are referred to the skin

Front 525

how does one have phantom limb pain

Back 525

central pathways & representations can be active in the absence of peripheral sensory stimuli

Front 526

common problem described in phantom limb pain

Back 526

tingling and/or burning sensation in the missing limb

Front 527

spinal cord hemisection

Back 527

damage spinal cord in one section

Front 528

where do pyramidal cells synapse

Back 528

from cortex to motor neuron

Front 529

pyramidal tract

Back 529

motor cortex->corticospinal tract ->spinal cord

Front 530

rubrospinal tract

Back 530

motor cortex->red nucleus->spinal cord

Front 531

lower motor neuron control

Back 531

spinal cord motor neurons in ventral horn

Front 532

upper motor neuron control

Back 532

direct & indirect pathway

Front 533

direct pathways for upper motor neuron control

Back 533

-corticospinal (pyramidal) pathway arising from neurons in motor cortex
-rubrospinal pathway arising from neurons in the red nucleus located in midbrain

Front 534

indirect pathways in upper motor neuron control

Back 534

many and generally classified as "extrapyramidal" pathways

Front 535

what does removal of motor cortex result in

Back 535

the loss of fine, fractionated movements of the fingers

Front 536

what do lesions of lateral pathways (rubrospinal & cortocospinal) result in

Back 536

-permanant weakness of distal flexors and inability to move fingers independently
-inability to make fractioned movements of the arms & hands
-inability to move shoulders, arms, and hands independantly
-DOESNT result in deficits in posture, ability to stand upright or sit

Front 537

what are indirect pathways associated with

Back 537

descending innervation to core muscles

Front 538

what do indirect descending motor pathways influence

Back 538

medial motoneurons

Front 539

where do indirect (extrapyramidal) pathways arise from

Back 539

circuits originating in cortex, brainstem, and cerebellum

Front 540

where do indirect pathways synapse on

Back 540

neuron in brainstem

Front 541

where do brainstem neurons project to

Back 541

neurons in cranial nerve nuclei and spinal cord

Front 542

what are the indirect pathways involved in

Back 542

maintenance of upright posture and coordinated head and eye movements

Front 543

motor effects of spinal cord deficit

Back 543

spastic paralysis- muscles continue to be stimulated by spinal reflex activity, there's loss of descending modulation of spinal cord motor neurons, inc. resistance to passive movements, unable to make fractioned movements

Front 544

flaccid paralysis

Back 544

loss of motor function

Front 545

what disease is associated with sensory & motor deficits following a spinal cord hemisection

Back 545

brown-sequard syndrome

Front 546

ratio of neuroglial to neurons

Back 546

10:1

Front 547

foramen of magendie (median aperture)

Back 547

holes that allow for leakage of CSF, its the pathway to the subarachanoid space