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633 Cards in this Set

  • Front
  • Back
Fifth and Sixth best selling drugs
Abilify and Seroquel; antippsychotics
Positive symptoms of Schizophrenia
delusions, hallucinations, inappropriate affect, incoherent speech or thought, odd behavior

gain of function
Negative symptoms of Schizophrenia
affective flattening, alogia, avolition, anhedonia

loss of function
affective flattening
negative symptom; no emotion
negative symptom of Schizophrenia; no speech
no motivation; negative symptom of Schizophrenia
no pleasure; negative symptom of schizophrenia
inappropriate affect
positive symptom of schizophrenia; inapproriately behaving in regards to emotion; overreacting
Dopamine Receptor hypothesis of Schizophrenia Version 1
believed excess transmission at dopamine receptors, so blocking receptors could treat psychosis

antipsychotic drugs increase metabolism of dopamine
antipsychotic and anti hypertensive drug

blocks reuptake of dopamine, breaks down vesicles that store dopamine
increase monoamine levels; can induce psychotic symptoms
Downfalls to Dopamine receptor hypothesis Version 1
no relation to positive/negative symptoms

no link to genetic and neurodevelopmental deficits

no relation to location of abnormalities in living brain
Version 2 Dopamine Receptor Hypothesis
dopamine receptors show differential brain distribution

prefrontal hypodopaminergia and subcortical hyperdopaminergia
dopamine receptor in the cortical region of the brain
dopamine receptor in the subcortical region of the brain
Downfalls of Version 2 hypothesis
no relation to positive/negative symptoms

no direct evidence
Version 3 Dopamine Receptor Hypothesis
striatal dopamine dysregulation

this alters the appraisal of stimuli which induces psychosis
NT's linked to Schizophrenia
serotonin, glutamate, NMDA receptors
PCP and Ketamine
anesthetics that induce negative symptoms and cognitive dysfunction due to schizophrenia
Glutamate Hypothesis for Schizophrenia
symptoms might reflect dysfunction or dysregulation of NMDA receptors and neurotransmission
Brain damage in Schizophrenia
global atrophy of grey matter

ventricular enlargement

alterations in fronto-temporal regions

volume decrease in temporal structures: superior temporal gyrus, and inferior frontal cortex
Affective (Mood) Disorders



Neurochemical imbalance theory of depression
synthesis and secretion of norepinephrine and serotonin
Monoamine theory of depression
impairment in central monoaminergic function

serotonin, norepinephrine, and dopamine disruption

depression associated with underactivity of serotonergic and noradrenergic synapses
Meds for monoamine theory
agonists of serotonin, norepinephrine, or both

Norepinephrine and serotonin receptors have been found to be more numerous in the brains of deceased clinically depressed individuals (up-regulation)
Deficiency of norepinephrine
can result in depressed mood

low levels can= depression

NE projects to frontal cortex and limbic hypothalamus
Deficiency of serotonin
also called 5-HT

Projects to frontal cortex, basla ganglia (limbic regions), and hypothalamus
Drugs used to treat Depression (MDD)
Monoamine oxidase inhibitors

Tricyclic antidepressants

selective monoamine-repuptake inhibitors

mood stabilizers
Monoamine oxidase inhibitors
Example: Iproniazid (developed for treatment of TB)

Monoamine agonist

increases levels of monoamines by inhibiting the activity of monoamine oxidase (MAO)
side effects of monoamine oxidase inhibitors
cheese effect: cheese, wine, and other food containing amine tyramine

elevates blood pressure
Tricyclic antidepressants
Example: Imipramine

Blocks reuptake of 5HT and NE

safer than MAO inhibitors
Selective Monoamine-reuptake Inhibitors

serotonin agonists

block reuptake of serotonin from synapses

increases activation of serotonin receptors

Other examples: Fluoxetine, Paxil, Zoloft

few side effects
Selective Norepinephrine Reuptake Inhibitors

Reboxetine: example
blocks reuptake of more than one monoamine NT
Sleep Alterations in Depression
older antidepressants disrupted REM sleep

some enhance REM sleep

5-HT modulates sleep and wakefulness
Pathophysiology of Depression
adaptation of plasticity of neural systems

decrease in number of length of branch points of apical dendrites of CA3 neurons in hippocampus

decrease in plasticity in depression and chronic stress
Glucocorticoids and Depression
increase levels of basal cortisol

corticosteroids influence NT, CORT secretion likely regulated by monoamines

Hippocampus and prefrontal cortex have high levels of CORT receptors
HPA axis
hypothalamo-pituitary adrenal axis

associated with glucocorticoids

Hypothalamus secretes CRF (corticotropin releasing factor) which targets the anterior pituitary, which secretes ACTH (adrenocorticatropic hormone) which targets the adrenal cortex and that secretes GCORT

patients with MDD have high levels of CORT
Other effects of depression
Impairs neuroplasticity

hippocampal volume reduction, HPA axis, and depression link?

Hippocampal atrophy could result i further neuroendocrine dysfunction, and hence a run-away system
HPA overactivity
leads to increased sympathetic tone, which promotes release of cyto cines from macrophages
Kindling hypothesis
depressive episodes become more easily triggered over time

as the number of depressive episodes increases, future episodes predicted more by the number of prior episodes rather than life stress
Neuropathology seen in Depression
abnormalities in prefrontal cortex, basal ganglia, hippocampus, thalamus, cerebellum, and temporal lobe
Prefrontal cortex abnormalities in depression
medial PFC size reduced

reduction in number of glial cells

increase in activity posterior orbital PFC, amygdala, and anterior cingulate cortex
Treatments for treatment-resistant cases
Deep Brain stimulation

Electroconvulsive Therapy
Deep Brain stimulation

electrical stimulation of the medial PFC and anterior cingulate

60% showed improvement
Electroconvulsive Therapy
intentionally triggering a brief seizure

changes neurochemistry

2-3 times a week for a couple of weeks

memory loss right around that event
Mood stabilizers
antidepressants can trigger bouts of mania, but these do not


act on signal transduction mechanism

trigger long-term changes in neuronal signaling patters that account for its prophylactic properties
Anxiety Disorders
all associated with anxiety and physiological stress reactions
symptoms of Anxiety Disorders
tachycardia, hypertension, breathing difficulties, nausea, high glucocorticoid levels
genetic component

Anxiolytics (anti-anxiety)

Serotonin agonists

agonistic action at GABA-A receptors

sedation, ataxia, nausea, withdrawal reaction that induces rebound anxiety

good for short-term use
Serotonin agonists

Selective agonists effects at 5-HT1A receptor

no ataxia and sedation
Anxiety Disorders and Depression
show comorbidity

both involve heightened emotional response to stress

SSRIs are often effective against anxiety disorder
Neural bases of anxiety disorders
possible role of GABAergic and serotonergic transmission

Brain areas involved and affected:
amygdala (heightened activity)
anterior cingulate cortex
Reticular theory
nervous tissue is a continuous web of unbroken network and information can blow between the this web; Golgi's proposal
Neuron Doctrine
each neuron is an independent unit, the nervous system is made up of nervous systems
Unipolar neuron
the cell body is set off from the trunk of the axon

single branch coming from cell body which extends in two directions

find these in touch receptors

sensory receptor
Bipolar neuron
cell body isn't off set, still has two extensions

important in vision and olfaction

sensory systems
multipolar neuron
what most neurons of the vertebrate brain are

single axon; many dendrites
multipolar interneuron
really small axon that has no myelin

found in the spinal cord

point to point communicator
specialized input zones

shorter than axons

many in one neuron
specialized output zones

range from nonexistent to several meters long

axon hillock present
axon hillock
where an action potential is initiated
at the terminal button; where NT are able to bind to the dendrites
presynaptic membrane
synaptic vesicles contained in presynaptic axon terminal; contain NT
postsynaptic membrane
contains receptors for NT

where the soma and the dendrites are
axonal transport
the process by which the materials and nutrients move across the axon
anterograde transport
movement of materials from the soma toward the terminal button

kinesin is motor protein involved in this

Functions to supply nerve terminal with necessary components
retrograde transport
movement of any material from the axon terminal back toward the soma

dymine is the motor protein involved
type of retrograde transport

return of "used up" material from the nerve terminal to the soma for degradation or reuse
type of retrograde transport

postsynaptic messengers or regulatory substances

terminal button can give back info to the soma about what is going on
glia cell

in the CNS

can myelinate multiple axons of multiple cells at one time

faster communication speed because of myelin
schwann cells
located in the PNS

can only myelinate one part of one cell
in the CNS


connect brain to vascular system

buffer ion concentrations in extracellular spaces

involved in NT uptake
small glia cells

clean up dead or injured cells in the brain
lines the ventricles of the brain and produces the CSF
Golgi staining
looks at dendritic spines

more spines means more complexity of information
Nissl stain
stain cell bodies

can't see as much detail
Myelin stain
stain myelin

useful to look at axon pathways
Electron microscopy
get very high resolution

can look at microtubules, synapses, or layers of myelin wrapping
also called rostral

front of the nose
also called caudal

back of the head
top of the head
bottom of the head
same side
opposite side
what most structures of the brain are
towards the center
towards the side
close to
away from
towards the reference point

towards the brain
away from the reference point

away from the brain
sagittal cross section
lateral sectioning
coronal cross section
cutting like a loaf of bread
horizontal cross section
sectioning it horizontally
Peripheral Nervous System
Contains the somatic nervous system
Sensory nerves
afferent neurons
Motor nerves
efferent neurons
spinal nerves
innovatie musculature within that region
ventral roots
carry motor information
dorsal roots
carry sensory information
Autonomic nervous system
sympathetic nervous system and parasympathetic nervous system
Central Nervous system
brain and spinal cord
gray matter
contains interneurons
white matter
contains axons
spinal cord
white matter on the outside, grey matter on the inside

central canal contains the CSF
The Meninges
dura mater


pia mater
dura mater
outter most; tough tissue of brain and spinal cord
web-like; contains CSF and arachnoid villa
pia mater
inner most; delicate
Cerebrospinal fluid (CSF)
contained in the ventricular system

produced by the choroid plexus and ependymal cells
Lateral ventricles
ventricles 1&2
all connected to each other. where the CSF is located
defect in how the CSF leaves the brain, so it builds up. Ventricles enlarge, and the cortical tissue gets smooshed out.
Olfactory nerve
cranial nerve #1

function: sensory; smell
Optic nerve
cranial nerve #2

function: sensory; vision
oculomotor nerve
cranial nerve #3

function: motor and sensory; eye movement and pupillary constriction; sensory signals from certain eye muscles
trochlear nerve
cranial nerve #4

function: motor and sensory; eye movement; sensory signals from certain eye muscles
trigeminal nerve
cranial nerve #5

function: sensory and motor; facial sensations; chewing
cranial nerve #6

function: motor and sensory; eye movement; sensory signals from certain eye muscles
facial nerve
cranial nerve #7

function: sensory and motor; taste from anterior 2/3 of tongue

facial expression, secretion of tears, salivation, cranial blood vessel dilation
auditory-vestibular nerve
cranial nerve #8

function: sensory; audition; sensory signals from the organs of balance in the inner ear
Glossopharyngeal nerve
cranial nerve #9

function: sensory and motor; taste from posterior 1/3 of tongue; salivation, swallowing
Vagus nerve
cranial nerve #10

function: sensory and motor; sensations from abdominal and thoracic organs; control over abdominal and thoracic organs and muscles of the throat
Spinal Accessory Nerve
Cranial nerve #11

function: motor and sensory; movement of neck, shoulders, and head; sensory signals from the muscles of the neck
hypoglossal nerve
cranial nerve #12

function: motor and sensory; tongue movements; sensory signals from tongue muscles
Choroid plexus
lines the ventricles and is continuously secreting CSF

constituted by the ependymal cells
functions of CSF
mechanical stability
chemical transport
removing large molecules
regulation of chemical environment
foramen of luschka and foramen of magendia
openings in the fourth ventricle where the CSF flows in and out
Lumbar puncture
spinal needles is inserted in between the 3rd and 4th lumbar vertebrae

taps into central canal

mononuclear cells
CSF pressure
Abnormalities seen in Lumbar puncture
blood- brains tumors/ subarachnoid hemorrhage
increased inflammatory cells- syphilis/brain tumors
increased protein- myelin fragments, myelin basic protein
internal carotid arteries
artery that supplies blood to the brain
vertebral artery
supplies blood to the brain
Circle of Willis
where the basilar artery joins the carotid artery in a circular shape

provides a safety mechanism
blood brain barrier
functions to protect the brain from toxins and infections

can make drug delivery to the brain more difficult
contains the telencephalon and the diencephalon
contains the mesencephalon
hindbrain and brain stem
contains the metencephalon and the myelencephalon
cerebral cortex
means "bark"

forms the outer surface of the cerebral hemispheres

grey matter outside, white matter inside

primarily composed of cell bodies
small grooves
large grooves
longitudinal fissure
runs along the two cerebral hemispheres
bulges in cortex
columnar organization
columns are mini processing units
paramital neuron
located in regions 4 and 5, has one long axon and many basal dendrites
Von Economo neuron
found in humans, great apes, elephants, and dolphins

related to emotional and social feelings

complex social behavior
Frontal lobe
anterior to the central sulcus and dorsal-medial to the lateral fissure

includes the primary motor cortex

contains prefrontal cortex
prefrontal cortex
associated with executive function
central sulcus
important boundary that separates the frontal lobe from the parietal lobe
Sylvian fissure (lateral fissure)
separates the frontal lobe form the temporal lobe
Parietal lobe
behind the central sulcus and in front of the occipital lobe, and dorsal-medial to the lateral fissure

includes the primary somatosensory cortex

auditory and visual info
temporal lobe
below lateral fissure and in front of occipital lobe

includes the primary auditory cortex
occipital lobe
includes primary visual cortes and secondary visual cortex

below the parietal and temporal lobes
Corpus Callosum
band of white matter fibers

seen through midsagittal section

very organized

communicates info from one hemisphere to the other
anterior commissure
toward the front of the brain
posterior commissure
toward the hindbrain
Limbic system
associated with emotion

contains the hippocampus, amygdala, olfactory bulbs, and cingulate gyrus
functions in memory
involved in detection of stimlui that can be perceived as danger or a threat
olfacotry bulbs
cranial nerve #1

initial input of olfactory stimuli

most primitive sense
cingulate gyrus
band superior to the corpus callosum

emotion responses

involved in the processing of the info sent by emotions
basal ganglia
collection of subcortical nuclei that lie just under the anterior aspect of the lateral ventricles

consists of: globus pallidus, caudate nucleus, putamen, and the substantia nigra
in the forebrain

contains the thalamus and hypothalamus

contains nuclei that receive sensory info and transmit it to the cortex

sensory relay station

all senses except parts of olfaction go through the thalamus
nuclei involved in integration of species typical behaviors, control of the autonomic nervous system and pituitary

3 f's: feeding, fighting, and sexual behavior
located in the midbrain

contains the tectum and the tegmentum
dorsal portion of midbrain
superior and inferior colliculi
involved in visual and auditory systems; in the tectum
superior colliculi
involved in visual systems
inferior colliculi
involved in auditory systems
portion of midbrain located under the tectum and contains:

rostral end of reticular formation
perlaqueductal gray
red nucleus
substantia nigra
ventral tegmental area
in the hindbrain

involved in the control of sleep and arousal
involved in motor control

timing, tension switching
contains the medulla oblongata
medulla oblongata
most caudal portion of brain

rostral to spinal cord

contains part of the reticular formation

involved in respiration
Neuronal signaling
1. receives signal (chemical or physical)
2. signal causes ionic fluctuations in the neuron's plasma membrane
3. creates an electrical current flow in the neuron
4. current flow travels down the axon
5. when current reaches terminal button, NTs are released into synapse
Axodendritic synape
most common

axons synapse onto dendritic spines of the postsynaptic neuron
Types of synapses
axon on axons

dendrites on dendrites

Membrane Potential
the difference in electrical charge from the distribution of positively and negatively charged ions between the inside and outside of a cell
ions want to flow from an area of high concetration to an area of low concentration

imbalance= concentration gradient
selective permeability
membrane can be impermeable to both ions

membrane can select for which ion can cross the membrane
electrical potential
difference in charges across the membrane
Resting Membrane Potential
neuronal membrane is mostly impermeable; responsible for maintaining the resting potential

selectively permeable (not equally) to K+, Cl-, and Na+

More Na+ on the outside, more K+ on the inside, and more Cl- on the outside
Voltage difference
difference between the intracellular fluid and the extracellular space

at resting potential it is -70mV

doesn't require any active support by the neuron to have things move across
Ion pump
Sodium- Potassium Pump
uses ATP to move 3 Na+ out and bring in 2 K+

uses a lot of energy

where most of the neurons energy goes to
Non-gated channels
permit the passage of Na+ in and K+ out. More K+ leaks out than Na+ leaks in because the membrane is more permeable to K+
Mechano-sensitive channels
affected by distortions in the membrane around it

convert external mechanical forces into signals
Voltage-sensitive channels
Whether the gate is open/closed is determined by the voltage is around it
Ligand-sensitive channels
affected by chemical agents

found on dendrites in the postsynaptic cells
Graded potentials
small voltage fluctuations

restricted to portion of axon where ion concentrations change
due to an efflux of K+ or influx of Cl- voltage inside axon becomes more negative
due to an influx of Na+, voltage inside axon becomes more positive
about -65mV
threshold of excitation
the point of voltage that will result in an action potential
action potential
brief, large reversal in the polarity of an axon's membrane

all sodium voltage gated channels open

intracellular side becomes positive
then reverses again
hyperpolarizes then restores to resting potential
Hodgin-Huxley cycle
Depolarization of membrane => opens Na+ channels => Na+ flows into neuro=> depolarization of membrane
absolute refractory period
when it starts to come down to restore itself

membrane hits 40mV, all the Na+ voltage-gated channels close and K+ voltage-gated channels open
Myelinated axons
nodes of ranvier contain the voltage-gated Na+ channels

allows Na+ to rush in

sodium potential jumps down the length of the axon much faster
postsynaptic potentials
graded potentials causing a depolarization or hyperpolarization
Excitatory postsynaptic potential (EPSP)
brief depolarization of nueron membrane

more likely to produce action potential
Inhibitory postsynaptic potential (IPSP)
brief hyper polarization of neuron membrane

less likely to produce an action potential
Integration of PSPs and Generation of an AP
One EPSP typically will not cause a neuron to fire need summation
adding or combining a number of individual signals into one overall signal
spatial summation
integration of events happening at different places but at the same time
temporal summation
integration of events happening at different times
Loewi's classic experiment
have a donor heart and recipient heart

stimulate donor heart and heart rate slows down

removed fluid sample from donor and put in recipient heart

caused the heart rate of recipient heart to slow down

secreted vagusstoff (acetylcholine)
Synaptic transmission in 4 steps
1. NT synthesized and stored in axon terminal
2. NT release
3. Receptor-site activation
4. NT deactivation
Step 1 of synaptic transmission

NT synthesized and stored in axon terminal
transporters pump substances across the cell membrane

requires substances acquired from the blood supply

synthesized and packaged all down the axon terminal
NT synthesized in soma
transported on microtubules to axon terminal (anterograde transport)
Step 2: NT release
In response to Action potential, NT released across the membrane by exocytosis

Ca2+ channels open

Ca2+ bind to protein calmodulin

complex binds to vesicles, inducing some vesicles to bind to presynaptic membrane

docking complex brings them together and they fuse
Step 3: receptor-site activation
Nt binds to receptor embedded in postsynaptic membrane


initiate other chemical reactions that modulate either of the previous effects
self-receptor in neural membrane that responds to the transmitter released by the neuron
Ionotropic receptors
associated with ligand-activated ion channels

fast communication

NT binds and ion channel opens or closes, causing a PSP
Na+ channels are opened, EPSP
K+ channels are opened, IPSP
Metabotropic receptors
associated with signal proteins and G proteins

NT messenger binds
G protein subunit breaks away
Ion channel opens/ closes OR 2nd messenger is synthesized

slower, longer-lasting

found in learning membrane areas
long-term potentiation
the neurological changes that happen while learning
quantity that produces a just observable change in postsynaptic potential
Number of quanta factors
amount of Ca2+ that enters the axon terminal

number of vesicles docked at the membrane
Step 4: NT deactivation
Reuptake or Enzymatic degradation
transporter pumps in the presynaptic that bring the NTs back up into the button of the presynaptic neuron; could grab the NT before it binds to receptor
Enzymatic degradation
deactivating enzyme that is specific to the NT attach and deactivate the NT by breaking it down

Amino Acid NTs
usually found at fast-acting directed synapses in the CNS

Aspartate and glycine
most widespread excitatory NT in the brain

two types of receptors: AMPA and NMDA

activated by MSG
AMPA receptor
ionotropic receptor of Glutamate
NMDA receptor
metabotropic receptor of Glutamate

important in memory
widespread inhibitory NT in brain and spinal cord

opens chloride channels and works on K+ channels
widespread in spinal cord

inhibitory NT

lower parts of the brain; hindbrain regions

important in locomotive behavior

if blocked, see continuous contraction

tetnis can block glycine
found in pathways essential for sensory and motor functions; cognitive functions

not as many

specific and limited neural pathways

have huge effects on cognitive and motor function
synthesized from tyrosine

can produce excitatory and inhibitory postsynaptic potential

Two main pathways:
mesolimbocortical pathway
mesostriatal pathway

involved in mood regulation

inbalances in schizophrenia
mesolimbocortical pathway
originates in ventral tegmental area to nucleus accumbens, cortex, and hippocampus

feeds into limbic system structures
mesostriatal pathway
substantia nigra to striatum

important in initiation of movement
noradrenergic pathways:
locus coeruleus
lateral tegmental area

related in regulation of mood and arousal (CNS)

in the sympathetic nervous system has an excitatory effect
Locus coeruleus
In the region of the pons to the hippocampus, basal ganglia, and cortex.

Involved in alertness and awakeness
lateral tegmental area
projects to the spinal cord, pons, and cerebellum
also known as adrenaline

synthesized from norepinephrine; location tends to be in adrenal medulla (adrenal gland)

also a hormone

in brain, it's NT

released from adrenal medulla in response to stress
synthesized from tryptophan

synthesized by the raphe nuclei

projections to hippocampus, spinal cord, cerebellum

mesencephalic seroteonergic cells project to thalamus, hypothalamus, basal ganglia, and cortex

involved in eating, regulation of sleep and arousal, and also involved in regulation of pain and mood.

regulates REM sleep and dreams

LSD acts on serotonin receptors
Acetyl group + choline

Excitatory effect on skeletal muscles

inhibitory effect on muscle fibers of the heart

involved in initiation of REM sleep

basal forebrain

only NT destroyed by enzyme

Peduculopontine pathway
cholinergic pathway in brain

nucleus and laterodorsal tegmental nucleus
Basal Forebrain pathway
cholinergic pathway in brain

nucleus basalis, medial septal nucleus, and nucleus of diagonal band
nicotinic receptor
acteylcholinergic receptor

ionotropic, excitatory

muscle fibers only
muscarinic receptor
acetylcholinergic receptor

metabotropic, excitatory or inhibitory

slower and longer lasting

CNS contains mostly muscarinic receptors
Unconventional NTs
soluble gases
soluble gases
unconventional NT

nitric oxide and carbon monoxide

retrograde transmission

diffuse through cell walls
anandamide is one of the two known
large molecules

Substance P, Neuropeptide Y


Endogenous opioids
Substance P
involved in pain reception
Neuropeptide Y
involved in circadian rhythm and eating patterns
Endogenous opioids
body's natural pain relievers

produce analgesia
mass action
whole brain is involved in all functions
localization of function
means specific areas of the brain were involved in certain functions
Broca's area
third convolution of the left frontal lobe
Neuropsychological testing of humans
very time intensive
Finger tapping frequency
motor tasks test

used in parkinson disease
peg board
insert the pegs and then told to retrieve them out and it is timed. Then do it with other hand.

Motor task test

used for Parkinson's
Sequential finger learning
used for Parkinson's

motor task test
intelligence test

memory, language, language lateralization
Wisconsin card sort task
memory (short term/long term, elicit/implicit)
frontal lobe function
people with frontal lobe lesions adapt poorly to rule changes in this test
Open-field test
three measures of emotionality:
thigmotaxis (don't venture from the walls of the enclosure- hesitant to go into open space)
defecation (number of bowels)
Aggression and defense analysis of species-common behavior
predatory aggression
maternal aggression
sexual aggression
Sexual behavior: analysis of species-common behavior
lordosis quotient: proportion of mounts that produce lordosis

number of mounts to intermission
number of intermissions to ejaculation
time to reinitiate mounting after ejaculation
Static Imaging Techniques
CT (computerized tomography)
Narrow x-ray beam passed through the brain at many different angles

Images combined to create 3D image of brain

Not good resolution, a bit fuzzy

Not used for research purposes

more rapidly triage patients requiring emergency surgery
MRI (magnetic resonance imaging)
hydrogen atoms behave like spinning bar magnets in the presence of magnetic field

non ionizing radiation

density differences in hydrogen atoms in different regions

in magnetic field, hydrogen atoms line up in parallel

radio pulses applied

structural MRI

preferred in brain tumors and infection
Dynamic Brain Imaging
Resting State fMRI
Transcranial Magnetic Stimulation (TMS)
positron emision tomography

small amount of radioactively labeled substance injected into subject

active areas of the brain use more blood and thus have more radioactive labels

look at distribution of what areas are more active than the others in the brain
function MRI

increases in functional activity of brain, increase in blood flow to those regions

Blood oxygen level dependent

Temporal resolution may not be very accurate compared to structural MRI

must be motionless and alert

no radiation

measures changes in brain activity in more or less real time compared to PET
Resting state MRI
mesures brain activity when you are at rest

Shows high levels of brain activity when you are not task engaged, but when you become task engaged, see a decrease in this.
Transcranial Magnetic Stimulation (TMS)
becoming one of the most important research tools
stereotaxic surgery
means by which experimental devices are precisely positioned in the depths of the brain. An atlas is required to provide directions to the target site and an instrument for getting there.

place an experimental device in the brain in a precise and accurate location
can administer drug
can inject a chemical that can cause a lesion
Three principles of the sensorimotor function
1. Hierarchically organized
2. Motor output is guided by sensory input
3. Learning changes the nature and locus of sensorimotor control
Functional segregation
each level of the hierarchy tends to be composed of different neural structures, each of which performs a different function
Ballistic movements
brief, all-or-none, high speed movements

aren't influenced by sensory feedback
knowing where your arms and legs are and being aware of surroundings
Proprioceptive disorder
no movement is automatic. Have to think every little step through in order to move
Initial stages of motor learning
each individual response is under conscious control
After practicing motor learning
responses become organized into continuous integrated sequences of action
1. Association cortex
2. Secondary motor Cortex
3. primary motor cortex
4. brain stem nuclei
5. spinal motor circuits
Association cortex
contains the posterior parietal association cortex and dorsolateral prefrontal association cortex
parietal association cortex
integrates info about body part location and external objects

receives visual, auditory, and somatosensory info from visual cortex auditory cortex, and somatosensory cortex

directs behavior by providing spatial info and directing attention

motor cortex
dorsolateral prefrontal cortex
secondary motor cortex
frontal eye field

conscious intention and motor awareness arise from increased parietal activity BEFORE movement execution
frontal eye field
small area of prefrontal cortex that controls eye movements
disorder of voluntary movement

only evident when instructed to perform an action

damage to the left posterior parietal cortex
contralateral neglect
unable to respond to stimuli contralateral to the side of the lesion

seen with large lesions on the right
Dorsolateral prefrontal association cortex
input: posterior parietal cortex
output: secondary motor cortex, primary motor cortex, and frontal eye field

evaluation of external stimuli and initiation of voluntary reactions
Secondary Motor Cortex
Input: association cortex

areas included:
Supplementary motor area (SMA and preSMA)
premotor area
cingulate motor areas

output: primary motor cortex

involved in programming patterns of movements in response to input from dorsolateral prefrontal cortex

active when imagining/planning movements
Primary Motor Cortex
Located in precentral gyrus of frontal lobe

Major point of convergence of cortical sensorimotor signals

Major point of departure of signals from cortex

somatotopic- more cortex devoted to body parts


motor humunculus

Function: initiating body movements
Motor humunculus
control of hands
recognizing by touch

interplay of sensory and motor systems
PMC lesions
disrupt ability to move one body part independently of another
not being able to move hands
Brain Stem Motor Nuclei
controls muscles of head and neck

caudal pons
ponto-medullary junction
cervical cord
reticular formation
reticular formation
In medulla and pons:
important in modulation respiration, heart rate, and blood pressure

In rostral pons and midbrains:
critical for maintenance of consciousness
reticular nuclei
important for mediating eye movement
Spinal motoneurons
All muscles outside of head and neck

sends commands to spinal cord => muscles

2 dorsolateral:
2 ventromedial:
cortico-brainstem-spinal tract
Corticospinal pathway
the direct pathway for dorsolateral and ventromedial pathways of the spinal motoneurons
indirect dorsolateral pathway of spinal motoneurons
cortico-brainstem-spinal tract
indirect ventromedial pathway of the spinal motoneurons
primary and secondary motor cortex
brain stem nuclei
somatosensory and vestibular systems

involved in fine-tuning and motor learning
layers of the cerebellum
molecular layer
purkinje cell layer
granular layer
molecular layer of the cerebellum
outter most

axons for the granular cells; few cell bodies

dendrites of purkinje cells
purkinje cell layer
middle layer

output cells

output of the cerebellum
granular layer
inner most layer of cerebellum

dense cell bodies

processing cells- most processing done here
Cerebellar loops
prefrontal loop
motor loop
prefrontal loop of cerebellum
dentate nucleus=> prefrontal regions of cortex => pontine nucleus => cerebellar cortex
pontine nucleus
part of the pons involved in motor activity
dentate nucleus
within cerebellar hemisphere
damage to cerebellum
movement deficits of timing, force, range, and direction

impairment of equilibrium during walking

deficits in voluntary eye movement

problems in motor learning
Basal Ganglia
collection of nuclei

receives cortical input and send output back via thalamus

modulate motor output and cognitive functions

involved in parkinson's, Huntington's, OCD, ADHD, and schizophrenia
brake hypothesis
puts on the brake or releases the break

example: sitting down

regulated by basal ganglia
Direct pathway of basal ganglia
Glutamatergic excitation from cortex to neostriatum

then GABAergic inhibition from neostriatum to GPi
Substantia nigra
SNpr and SNpc
substantia nigra pars reticulate

eye movements
substantia nigra pars compacta

large DA-containing cells
Parkinson's Disease
resting tremor that's lost during intended movements
difficulty initiating movements

60% neuron loss

DA neurons degenerate

loss DA results in decrease in striatal activity, so less inhibition of GP

increasing GP reduces firing of thalamus, which decreases excitatory input to motor cortex

results in hypokinesis
diminished motor function
super demerol

found through teenagers doing drug that came in with parkisonian symptoms

synthetic opioid; like heroid
converted to MPP+ by monoamine oxidase

MPP+ is toxic to DA neurons of substantia nigra
blocks nMDA receptors
eases the pain of muscles spasms
Cerebellar ataxia
difficulty with eye movements

can't complete standard sobriety tests

balance is off
Indirect pathway of Basal Ganglia
cortex=> neostriatum => globus pallidus external => subthalamic nucleus => globus pallidus internal => thalamus => cortex

Globus pallidus inhibited then wil not inhibit subthalamic nucleus; inhibits thalamus so not excitation of cortex

GABAergic inhibition from striatum to GPe
GPe inhibited => subthalmic nucleus has glutamatergic excitation to GPi
thalamus inhibited so no excitation of cortex
Huntington's chorea
spontaneous, disruptive movements, uncontrolled

inherited, progressive neurodegenerative disorder

genetic mutation in coding for "Huntington" protein

striatal neurons projecting to and inhibiting GPe degenerate

GPe isn't inhibited, so it fires. then inhibits subthalamic nucleus from exciting GPi, which then fires less. Thalamus not inhibited by GPi and fires

Results in thalamus exciting motor cortex => hyperkinesia
uncontrollable spontaneous movement
Plasticity of the brain
changeable; ability to adapt to experience
growth of new neurons; occurs in adults as well; does decline with age
Phases of development
1. induction of neural plate
2. neural proliferation
3. migration and aggregation
4. axon growth and synapse formation
5. neuron death and synapse rearrangement
6. synaptogenesis
7. myelination
Induction of neural plate
A path of tissue on the dorsal surface of embryo becomes the neural plate

development induced by chemical signals from mesoderm

visible three weeks after conception

neural plate cells= embryonic stem cells

neural tube closes at anterior end first
18 days of development
neural plate develops

tall, columnar cells develop, get thickened neural plate
Day 21 of development
neural groove becomes present
Day 24 of development
neural tube fuses
Neural crest cells
come from neural plate; neural plate cells that escaped

become the neurons of the PNS
anterior end of neural tube
becomes brain

cells proliferate much faster here than posterior end
posterior end of neural tube
becomes spinal cord
spina bifida
some of the vertebrae overlying the spinal cord aren't fully formed; remain unfused and open

folic acid during pregnancy best way to prevent
Neural tube
becomes the CNS
neural cavity
becomes the ventricles of the brain and central canal of spinal cord
Poliferation of Neurons and Glia
2nd stage of development

occurs in the ventricular zone, next to neural cavity
Part of 3rd stage of development

Migrating cells are immature; lack axons and dendrites

Two types of migration:
radial migration
tangential migration

Methods of migration:
glial-mediated migration
radial migration
toward the outer wall of the tube
tangential migration
parallel to the tube wall
Somal migration
extension develops that leads migration, cell body flows

think snail
Glial-mediated migration
cell moves along a radial glial network
radial glia
form guide wires; network
part of 3rd stage of development

Cells align themselves with other cells and form structures

Gap junctions pass cytoplasm between cells
Cell-adhesion molecules (CAMs)
aid in migration and aggregation

recognize and adhere to molecules on other cells
Axon Growth
part of 4th stage of development

axons and dendrites differentiate

extensions emerge from growth cones at tips of axons and dendrites
finger extensions coming from the growth cone
at the base of the growth cone

extensions that can help direct the developing axon in a specific direction
Chemoaffinity hypothesis
For axon growth

target cells are releasing some sort of chemical that attract the developing growth cone to it

target cells also release chemical repellents to keep other growth cones away

uses chemoattractants and chemorepellents
Bowe Print hypothesis
for axon growth

each neuron is built with internal blue print on where to go
Topographic gradient hypothesis
for axon growth

keeping spatial relationships with neighbors

two intersecting signal gradients (ephrins)
Synapse formation
part of 4th stage of development

depends on presence of glial cells (astrocytes)

high levels of cholesterol are needed

chemical signal exchange between pre and postsynaptic neurons is needed
6th stage of development

synapses form rapidly on dendrites and dendritic spines

spines proliferate after birth, connections affected by experience
Determinants of Neuron Survival
produce more neurons than we need

two conditions:
must form synapse with target cell and receive a neurotrophin from that cell

must be stimulated to release NT into synapse
producing more neurons than we need
Neuron death and synapse rearrangement
5th stage of development
programmed cell death that occurs when synapses receive little neurotrophins
passive cell death
synapse rearrangement
space left after apoptosis is filed by sprouting axon terminals of surviving neurons

leads to increased selectivity of transmission

occurs caudal to rostral

prefrontal cortex is last
final stage in development

occurs about 24 weeks postconception

sensory regions myelinate before motor regions

continues throughout life

spinal cord, hindbrain, midbrain, forebrain
Adult neurogenesis
declines with age

declines in dentate gyrus of hippocampus from old age
Early life stress effects on developing brain
alteration of GABA receptors
decreased size
decreased neurogenesis
hereditary disorder of protein metabolism

lacks enzyme to metabolize phenylalanine (amino acid in food)

phenylalanine builds up and becomes toxic
Down Syndrome
extra chromosome 21

impaired synaptogenesis

degeneration of branching out of dendrites
Fragile X syndrome
more common in males

Fragile X Gene= FMR1; prone to breaking

FMRP protein dysfunction

abnormal dendritic spines
Autism Spectrum Disorder
Neurodevelopmental disorder

social impairment
communication problems
abnormal behavioral movements
decreased area of corpus callosum
fewer neurons in amygdala but increased activity when looking at faces

more common in males

brain develops more slowly

overgrowth of gray matter
Fusiform face area
gyrus in the temporal lobe
decrease in activity
recognition of faces
catgraphs syndrome
can't tell who anybody's face is
"Wiring up"
child brain development

synapse formation and rearrangement, myelination, wiring and rewiring, getting things ready
Betz cell
motor cortex

#s decline around 50 years, many gone by 80 years

large neuron in cortical layers 4 and 5

associated with descending motor information
Inferior olive
located on medulla
associated with and located within the auditory system
Shrinkage in brain aging
frontal cortex
dementia and alzheimer's

sulci widen

corpus callosum area decreases
Dementia with Lewy bodies
progressive cognitive decline

pronounced fluctuations in alertness and attention

recurrent visual hallucinations

parkinsonian motor symptoms
Lewy Body
circular deposit of protein

alpha-synuclein protein
Frontotemporal dementia
severely disrupts personality and social skills

damages anterior cingulate cortex, orbitofrontal cortex, temporal lobe, and frontal insula

widened sulci

often misdiagnosed as Alheimer's disease

von Economo neurons are targeted
Alzheimer's disease
Mild or Moderate
hippocampus shrinks
initial cortical atrophy in parietal and temporal areas first then frontal lobe

Autopsy shows:
extensive neural degeneration
amyloid beta plaques

acetylcholine levels low
Mild AD
mild memory problems for new events and new info
increased difficulty thinking of words
if noticed by other people, considered minor
Moderate AD
other people will notice
anxiety, depression, paranoia
spatial difficulty
problems with math and organization
difficulty understanding time, date, and place
Pittsburgh Blue (PiB)
PET technique
imaging compound
tries to determine accumulation of beta amyloid plaques
Medications for AD
Cholinesterase inhibitors
NMDA receptor antagonist
Choloinesterase inhibitors
medicine for AD
aricept, exelon

keep acetylcholine levels high
NMDA receptor antagonist

regulates activity of glutamate by blocking areas in the brain that are overexcited by glutamate
Brain tumors
astrocytic tumors
oligodendroglial tumors
encapsulated and tend to be benign
has boundaries
spreading throughout
astrocytic tumors
astrocytomas and anaplastic astrocytomas
most aggressive type of primary brain tumor
sudden onset, cerebrovascular event
cerebral ischemia
type of stroke

insufficient blood flow to the brain


cerebral hypoxia

damage is consequences of glutamateric excitotoxicity
blood clot; typically forming in the brain
blood clot that forms somewhere else and gets dislodged and moves to the brain and lodges
cerebral hypoxia
death of brain tissue
cerebral hemorrhage

abnormal widening or ballooning of a portion of an artery

due to weakness in the wall of the blood vessel
brain hits the front of the skull
brain hits the back of the skull
Amyloid-beta peptide
normal product of cellular metabolism
essential for normal brain functioning
regulates synaptic transmission in the hippocampus
involved in cholesterol transport
infection of the CNS

inflammation of the brain parenchyma

symptoms: headaches, flu-like symptoms, fever

West Nile or Varicella-zoster virus
Inflammation of the meninges
Viral infections (most common)
bacterial meningitis
parasitic menigitis
Bacterial meningitis
much less common

Streptococcus pneumonia: most common source of infection

rapid onset

can be fatal
Parasitic meningitis
Naegleria fowleri enters the body through the nose

not common in US
Fungal meningitis
Inhaling fungal spores
cryptococcus- inhaling soil contaminated with bird droppings
histoplasma- environments heavy with bat feces
Transverse myelitis
spinal cord inflammation

destroy/damage myelin which results in scars that interfere with motor neuron communication

Results from:
viral infection
abnormal immune reactions
complication of syphilis, measles, Lyme disease
Brain abscess
accumulation of infectious materials within the CNS
Teponema pallidum bacteria is cause

occurs in individuals with untreated syphilis for many years

infects brain/spinal cord

cognitive decline, seizures ocular disorders
Creutzfeld-Jakob disease (CJD)
caused by a prion
lack of coordination, cognitive dysfunction, rapid progression, fatal

Classic and Variant types

may be related to Kuru
causes proteins to fold abnormally
Classic CJD
Sporadic or Familial
Sporadic CJD
happens but we don't know why
Familial CJD
hereditary form
Variant CJD
related to mad cow disease

caused by exposure to contaminated products
seen in New guinea women who ate brains of dead relatives as funeral ritual
permanent changes in brain tissue cause the brain to be too excitable

causes: stroke, TBI, dementia, infections, brain tumor some medications

symptoms: repeated, unpredictable seizures; staring spells; violent shaking (convulsions); subtle changes of thought, mood, or behavior
Partial epilepsy
doesn't involve entire brain

simple partial epilepsy
symptoms are primarily sensory or motor or both

spread as epileptic discharge spreads

spreads regionally
complex partial epilepsy
restricted to temporal lobes

engages in automatisms: compulsive and repetitive simple behaviors
Generalized epilepsy
involves entire brain

Grand mal
Petit mal
Grand mal epilepsy
loss of consciousness and equilibrium

Tonic-conic convulsions: rigidity (tonus) and tremors (clonus)

resulting hypoxia
Petit mal epilepsy
not associated with convulsions

disruption of consciousness associated with a cessation of ongoing behavior
biological components involved in hunger
blood sugar, insulin, hormones
set point
breaking down food and absorbing its constituents
secreted from the pancreas
regulates the way the body uses glucose
controls glucose production and release from liver

levels high => glucagon levels low
levels low => glucagon levels high
stored in the liver as glycogen
when glucose levels drop, liver converts glycogen to glucose
glucose levels high => liver stops conversion of glycogen to glucose; converts glucose into glycogen for storage

levels drop prior to a meal
secreted by pancreas
converts glycogen to glucose
Energy storage in the body
Energy is stored in fats, glycogen, and proteins

fats are most efficient
Three phases of energy metabolism
Cephalic phase
Absorptive phase
Fasting phase
Cephalic phase
preparatory phase; preparation for eating
initiated by sight, smell, expectation of food

insulin levels are high
Absorptive phase
insulin levels are high

blood glucose is being utilized as form of energy

excess glucose is converted into glycogen

glycogen is stored in the liver
Fasting phase
glucagon levels are high, insulin levels are low

energy that body needs is going to be drawn from the energy stores you made by eating

converting fats into free fatty acids

converting glycogen into glucose
Dual-center theory
the hypothalamus contains two different regions

one acting to initiate eating and one to stop it
Lateral hypothalamus (LH)
feeding center; hunger center

stimulation increases eating

deactivated by glucose
Ventromedial hypothalamic nucleus (VMH)
satiety center

stimulation decreases eating

stimulated by glucose/ glucoreceptors
hunger pangs and feeling of fullness

contractions => hunger

distension => satiety
gut peptides
satiety signal

cholecystokinin (CCK)
secreted by fat cells

sensed by hypothalamus

inhibits appetite
Neuropeptide Y
manufactured in hypothalamus and gut; stimulates appetite
Set point
homeostatic brain mechanism defends some level of body weight
metabolic rate
rate at which body burns energy when at rest
Environmental factors of hunger
Food's pleasure
learning component
taste preferences
taste aversions
Adaptive species-typical preferences
sweet and fatty foods = high energy
salty = sodium-rich
Adaptive species-typical aversions
bitter= toxins
Orbital prefrontal cortex
If lesioned, causes you to eat less
input from olfactory system/bulb
Types of Chemical Communication
autocrine funciton
paracrine function
pheromone funciton
allomone function
endocrine funciton
neurocrine function
pheromone function
chemical indicators between individuals in the same species
allomone function
chemical communication between diff species
endocrine function
long distance communicator
goes into bloodstream, can go everywhere
Features of the endocrine system
1. endocrine glands are ductless
2. have a rich blood supply
3. hormones secreted into bloodstream
4. hormones can travel to every cell in the body
5. hormone receptors interact with particular hormones
Neurosecretory cells
receives info synaptically just like a neuron
release hormones instead of NT
link between nervous system and circulatory system
Hormones vs. NTs
released into blood
act at sites far from point of release
graded responses

release into synapse
act locally
all/none response
Functions of hormones
modulate cell activity
promote growth, proliferation, and differentiation of cells
modulate rate of function
influence the probability of behavior
Types of hormones
Protein/peptide hormones
amine hormones
steroid hormones
Protein/Peptide hormones
bind to receptors on outside of membrane
most rapid effects of all hormones

ocytocin and ACTH
Amine hormones
same relatively fast receptor response as protein hormones
Steroid hormones
bind to receptors within the cell
sexual actions and sexual development

gonadal and adrenal hormones
releases releasing hormones
paraventricular nucleus and subraoptic nucleus

releases CRH
releases TRH
releases GnRH
releases GnRI

signals endocrine gland to secrete horomone, hormones effects target cells, target produces a response, this response feeds back to the hypothalamus to regulate continued secretion of hormone
pituitary gland
one of the most regulated systems in endocrine system
connected to hypothalamus

two parts:
anterior pituitary

derived during embryological development from the roof of the mouth

connected to hypothalamus by hypohyseal protal system


FSH and LH

posterior pituitary

derived from nervous tissue

two protein hormones released:

synthesized in paraventricular and supraoptic nucleus

has axons

Leydig cells, T
progestins, estrogens
Human chorionic gonadotropin, estrogen, progesterone
Corpus luteum secretes progesterone

egg not fertilized=> levels of progesterone decrease
egg fertilized=> progesterone stays high
Egg not fertilized
Progesterone and estrogen levels decrease
uterine lining sluffs off

tells hypothalamus to secrete FSH and cycle happens all over again
Egg is fertilized
progesterone levels stay high
uterine lining stays thick
fertilizd egg secretes the human coreonic gonadotrpic hormone
coreonic gonadotropic hormone
hormone looked for in pregnancy tests
Toward ends of pregnancy- placenta secretes large amounts CRH
then mom and fetus produce ACTH
ACTH acts on adrenal cortex which secretes DHEA
DHEA converted to estrogen by placenta, which results in increase levels of estrogen
This causes smooth muscles of uterus to form gap junctions, contract together
Oxtytocin is expressed
Prostaglandins are synthesized- cause contractions
Organizational effects of hormones
early in development
"sensitive period"
enable later behavior
determine male or female development
activational effects of hormones
occur late in life, related to developmental period

transient effects

occur when hormones enables certain types of behaviors to be more likely
Chromosomal sex
determined at conception

XY- male
Gonadal sex
determined later in development
Y chromosome controls development of glands that produce male sex hormones
Before 6 weeks post fertilization
undifferentiated fetus
bipotential gonads
Fetus has two sets of undeveloped internal reproductive ducts
Wolffian duct system
undeveloped male system
Mullerian duct system
undeveloped female system
SRY Gene
on Y chromosome, produces tesits-determining factor

gonads develop into testes

secrete testosterone, MIH
No SRY Gene
Ovary development
Mullerian duct develops into fallopian tubes, uterus, and inner vagina
Aromatization Hypothesis
androgens masculinize nervous system
enzyme that converts testosterone to estradiol
binds to estrogen and this complex can't cross the blood brain barrier
prevents estrogen from entering the brain so it doesn't masculinize
sexually dimorphic nucleus of pre-optic area
nuclei larger in males
nucleus in hypothalamus
involved in male copulatory behavior
Testosterone in a male
right around birth, testosterone increase then decreases until puberty; large SDN-POA
Testosterone in a female
no rise in testosterone around birth or puberty; small SDN-POA
Brain and Hormone Activity in Male Mating
Input from estrous female, causes activity in olfactory bulbs and MPOA
causes surge in GnRH
leads to rise in testosterone
this facilitates sexual behavior
copulation occurs
Neurotransmitters involved in sexual behavior
Dopamine plays central role
Mesostriatal tract
controls muscular response for mounting

controls genital response
Mesolimbocortical tract
controls sexual motivation
Medial Preoptic Area (MPOA)
body postures associated with sex
Oxytocin and Vasopressin
central players in regulation of species-specific social and reproductive behavior
female sexual behavior, parturition, lactation, maternal attachment, pair bonding
male erection and ejaculation, mediates aggression, territoriality, pair-bonding
ventral pallidum
contains vasopressin receptors
Androgen insensitivity
defect on the X chromosome of a male individual
mutation on the X chromosome of the AR gene (codes for androgen receptors)
body does not masculinize
no significant effect in females
can't occur in chromosomal female
Congenital Adrenal Hyperphasia (CAH)
genetic detect of the adrenal gland that can't produce vital hormones known as corticosteroids
smallest unit in the sound system of language
smalles grammatical unit of language
the way that different linguistic elements are combined together in phrases or in sentences
sensitive period
critical time to be exposed to languages for optimal learning
Broca's area
Brodmann areas 44 and 45

area 44= posterior inferior frontal gyrus; phonological
verbal fluency
processing, language production

area 45= anterior inferior frontal gyrus; semantics
arcuate fasiculus
connects Broca's area and Wernicke's area
Wernicke's area
Brodmann area 22
Three subarea
1st subarea of Wernicke's area
responds to spoken words (self and others) and other sounds
2nd subarea of Wernicke's area
words spoken by someone else, when recalling a list of words
3rd subare of Wernicke's area
producing speech
planum temporale
located on superior temporal gyrus
superior portion of area 22
lies between primary auditory cortex
angular gyrus
area 39
semantic processing
supramarginal gyrus
area 40
phonological and articulatory processing of words
When you hear a spoken word
processed first by primary auditory cortex
then Wernicke's area

associates structure of word with representation of words stored in memory
When you read a word aloud
processed first by visual cortex
then angular gyrus
then Wernicke's area
When you hear someone speak a word
Wernicke's area recognizes the word, then arcuate fasciculus, then Broca's area, then motor learning
Amnesia aphasia
comprehension of language is relatively intact
difficulty in finding names of objects
Two kinds:
one with noun
one with verbs
Wernicke's apashia
fluent aphasia
lack of comprehension
"word salad"
speech is fluent but doesn't make sense
damage to left hemisphere in temporal parietal junction
Auditory Agnosia
difficult recognizing spoken words
can't perform repetitive tasks or repeat instructions

Two types:
verbal: comprehension
nonverbal: only environmental sounds
surface dyslexia
difficult identifying words as a whole

errors in trying to pronounce complex or irregular words

damage to left temporal lobe, fusiform gyrus, left inferior parietal lobe, angular and supramarginal gyro

rely on pronunciation rules
Advantages of lateralization
increased neural efficiency to concentrate function in one hemisphere
Two cognitive processes may be more readily performed simultanesouly
can recognize objects not faces
acquired form brain trauma; fusiform gyrus
Right hemisphere
perception of music
people that are profession key board players have larger corpus callosums relative to brain size
Left hemisphere
planum temporale

perfect pitch
Anatomic hemispherectomy
frontal, parietal, temporal, and occipital lobes removed

basal ganglia and thalamus left in place
Functional hemispherectomy
smaller area of the affect hemisphere removed
split-brain individuals
corpus callosum severed

communication between left and right severed
Motor Theory of evolution of hemispheric asymmetry
Left controls fine movements

left damage can produce motor and speech deficits
Language theory of evolution of hemispheric asymmetry
primary role of left hemisphere is language
locked-in syndrome
high levels of awareness and arousal

completely paralyzed except being able to move eyelids

result of massive brainstem lesion (stroke)
low arousal
low awareness
vegetative state
high arousal
low/no awareness
minimally conscious state
high arousal
low awareness that fluctuates
persistent vegetative state
in vegetative state more than a month
permanent vegetative state
no awareness
high arousal
3 months for non-traumatic brain injury

1 year for traumatic brain injury
thought to be dependent upon the functional integrity of the cerebral cortex and its subcortical connections
Bedside examination
look for eye tracking, motor and verbal responses
not recommended
Glasgow coma scale
40% misdiagnosed
electroencephalogram and event-related potential

looking to see if there are action potentials responding to stimuli given
Fronto-parietal network for consciousness
prefrontal cortex => parietal cortex => thalamus => prefrontal cortex
"hub" in the network
where consciousness is located

located in the posterior parietal cortex
also important to consciousness
Circadian rhythm
24 hours
temperature, heart, respiration, metabolism in humans
Ultradian rhythm
90 minutes
infradian rhythm
more than 1 day
menstrual cycle
circannial cycle
phase shift
alter when you give cue for experiment
endogenous clock
superchiasmatic nucleus
rhythm gets set to external cues
external cue
superchiasmatic nucleus
recieves visual info directly from the eye

lies just above the optic chiasm

projects to the paraventricular nucleus
SCN clock cells
glucose metabolism increases during the day more than night

Each cell has own clock

act in synchronized fashion
Nature of clock cells
produce protein upon reaching critical level, inhibits own production


activate retinal ganglion cells
retinohypothalamic pathway
consists of retinal ganglion cells that project to the SCN
paraventricular nucleus
connects with the pineal gland and secretes melatonin
secreted more the longer the night

suppresses reproductive gonadal output

only applies to seasonal breeders
Shift Work
phase advance/phase delay

can lessen by:
rapidly rotating shifts
better; one/two shifts max then diff time
slow rotating shifts
rotate shifts on weekly/monthly basis
phase advance
rising early/going to bed early
phase delay
going to bed late/getting up late
Jet lag
East => West (better adjustment); day lengthened
West => East (1 day per 1 hour); day shortened
NREM sleep
slow, high amplitude brain waves

initiated and maintained by forebrain
REM sleep
fast, low amplitude waves, rapid eye movements

reduced muscle tone

generated by brain stem
Electroencephalograph (EEG)
used to study sleep

widespread cortical and subcortical systems generate the electrical rhythms of diff states/stages
Waking Stage of Sleep
Alpha and Beta waves

beta activity associated with alertness
Alpha waves
10-12 hertz
beta waves
13-40 hertz
Stage 1 of sleep
slow wave sleep

Vertex spike

transition between wakefulness and sleep

lasts about 10 minutes

very easily awakened

heart rate slows; muscle tension decrease

theta waves
theta waves
3.5-7.5 hertz
Stage 2 of seep
slow wave sleep

irregular brain waves

bursts of activity

sleep spindles

about 15 minutes long

if awakened would deny being asleep

important for learning of motor tasks
sleep spindles
bursts of activity

12-24 hertz

last about 0.5 seconds
Stage 3 of sleep
slow wave sleep

delta waves

important for memory and learned facts
delta waves
3.5 hertz

large amplitude
Stage 4 sleep
Delta waves

hard to waken

slow wave sleep

important for memory and learned facts
Slow wave sleep
important for memory

increase of glucose metabolism in frontal lobe

more delta activity in frontal lobe when there is more brain power used during the day
REM sleep
beta activity

lack of muscle tones


80% report dreaming if awakened
Polyphasic sleep cycles
infants and elderly
no REM or deep sleep

only get stage 1/2
Forebrain in sleep
produces a state of SWS
encephale isole
isolated brain

incision between medulla and spinal cord

EEG alternates b/t periods of wakefulness and periods of sleep

shows patterns of sleep are regulated by structures in the brain
cerveau isole
isolated forebrain

incision in midbrain

EEG rostral to incision shows constant
basal forebrain in sleep
generates SWS

when lesioned => no SWS

releases GABA which suppresses activity in tuberomamillary nucleus in hypothalamus

suppresses wakefulness
Reticular formation in sleep
extends from medulla to forebrain

when stimulated, it activates the forebrain from sleep

lesioned => persistent SWS
Raphe nucleus in sleep
serotonin is synthesized here

serotonin release promotes SWS

promotes SWS

inhibits REM during SWS and wakefulness
Pontine System in sleep

Triggers REM sleep

stimulating pons induces REM sleep

pontogeniculociiptae waves (PGO waves)
What happens during REM
acetylcholinergic neurons in pons are activated

Neurons project to:
lateral geniculate nucleus
nuclei of medulla
neurons in basal forebrain
tectum in sleep
rapid eye movement
lateral geniculate nucleus in sleep
PGO waves
nuclei of medulla in sleep
muscular paralysis, GABA, glycine
neurons in basal forebrain area in sleep
cortical activation
Hypothalamic center in sleep
secretes protein Hypocretin

controls transitions between stages

Neurons project to:
basal forebrain
reticular formation
nuclei of medulla
tuberommaillary nucleus
loss of hypocretin

extreme drowsiness every 3-4 hours
dream-like hallucinations
sleep paralysis
cataplexy (loss of muscle tone)

intrusion of REM into wakefulness
protein secreted by the hypothalamic center that prevents transition from wakefulness directly into REM sleep
sleep attacks in narcolepsy
last about 15 minutes

typically occur after eating

wake up and feel refreshed

can happen at anytime
sudden loss of muscle tone while awake

inability to move

strong emotions can bring this on

usually less than 30 seconds long
Treatments for narcolepsy
lifestyle adjustments

antidepressants and narcolepsy
used to reduce episodes of cataplexy, sleep paralysis, and hallucinations
stimulants and narcolepsy

preferred because it is less likely to be abused
trouble falling asleep/staying asleep

poor sleep, lifestyle habits, medications, alcohol, caffiene
Medications for Insomnia
Ambien (Zolpidem)
used for Insomnia
trouble falling asleep

GABA-BZ receptor complex

preserves deep sleep
for middle of the night wakefulness in Insomniacs

same as ambien just less
mild effect for reducing time to fall asleep in insomniacs
Sleep apnea
one/more pauses in breathing or shallow breaths while you sleep, lasting a few seconds/minutes
Obstructive sleep apnea
blockage of narrow airway during sleep

surgery can be performed to remove excess tissue

more common in overweight

most common form of sleep apnea
Central sleep apnea
less common

brain regions responsible for controlling breathing isn't working properly

more common in some types of medical conditions
Periodic movement limb disorder/ Restless leg syndrome
altered dopaminergic mechanisms

REM behavior disorder
act out dreams

physically move limbs

result of damage to brainstem regions that are involved in inhibiting cranial and spinal nerves

not sleepwalking
sleepwalking and night terrors
occur in stages 3 or 4.
Agonistic Drug Effects
1. increase synthesis of NT
2. increase # of NT by destroying degrading enzymes
3. increase release of NT from terminal buttons
4. binds to autoreceptors and blocks their inhibitory effect on NT release
5. binds to postsynaptic receptors and activates or increases effect of NT
6. blocks deactivation of NT by blocking degradation/ reuptake
Antagonistic Drug Effects
1. block synthesis of NT
2. causes NT to leak from vesicles then destroyed by enzyme
3. blocks release of NT from terminal buttons
4. activates autoreceptors and inhibits NT release
5. receptor blocker
Oral injection of drugs
dissolved in stomach, carried to intestines, absorbed in bloodstream
advantages of oral injection of drugs
easy to administer
disadvantages of oral injection of drugs
influenced by amount and type of food in stomach, some metabolized in stomach, or can't pass membrane
Injection of drugs

exact dosage known

too much/allergy- not much can be done
Inhalation of drugs
absorbed in bloodstream via capillaries in lungs

hard to regulate dosage, lungs may be damaged
Therapuetic index
ratio b/t dose that produces desired effect in 50% of animals and dose that produces toxic effect in 50% of animals
Factors determining effet of drug
setting in which drug is used
time of day
drug tolerance
decreased sensitivity due to repeated exposure
one drug can produce tolerance to similar drugs
Functional drug tolerance
decreased responsiveness at site of action
decrease receptors
decrease efficiency of binding at receptors
receptors less responsive
Conditioned drug tolerance
tolerance effects maximized when drug is taken in same environment as previously taken
Physical dependance theory
Biopsychological theory of addiction

not right because:
addicts relapse after detox
begin drug use not explained
addictions develop to drugs without severe withdrawal symptoms
Incentive-sensitization theory
Biopsychological theory of depression

anticipated pleasure associated with taking drug
Hedonic value- actual value

as the positive incentive value increases, the hedonic value decreases

crave more; enjoy less
Nicotine is main ingredient

changes number of receptors in nicotinic cholinergic receptors in CNS

stimulates release of DA from NA

decrease in monoamine oxidase
targets acetylcholine

blocks nicotinic receptors at neuromuscular joint

muscle relaxer
muscarinic receptors

decrease in parasympathetic activity of muscles, glands

decrease glandular secretions, breathing difficulty, blocks vagus nerve
blocks NMDA receptors

AMPA receptors (ligand gated)

NMDA receptors (ligand and voltage)

decreases GABA levels

acts as an anxiolytic

increases DA release in NA
Wernicke-Korsakoff Syndrome
associated with alcohol

degenerative brain disorder caused by lack of vitamin B1 (thiamine)
dietary deficiencies can result in this

memory disorder
amnesia, disoriented, attention deficits
confabulation (making up something)
difficulty in retreiving memories
difficulty acquiring new info

Wernicke is initial stage then Korsakoff is chronic part
THC is main active ingredient

acts on CB1 receptor in NS

acts on substantial nigra, hippocampus, cerebellar cortex, cerebral cortex

stimulates release of DA from NA

contains endocannabinoids
function as retrograde messengers


alterations of memory formation, appetite stiumlation, reduced pain sensitivity

binds to DA re-uptake transporters on presynaptic membranes of DA neurons

inhibits removal of DA from synaptic cleft and degradation by monoamine oxidase

blocks reuptake transports for serotonin

ventral tegmental area, NA, and caudate nucleus

increases alertness, feelings of well-being, energy, and motor activity

Tachycardia, hallucinations and elevated blood pressure => excessive prolonged use
Ecstasy (MDMA)
binds to serotonin reuptake transporter

enters the serotonergic neuron via transporter, causing excessive release of serotonin

similar effects on norepinephrine

causes of release of DA
heroin, morphine, codeine

effective analgesics

act on delta, kappa, and mu opioid receptors
all are metabotropic

heroin is converted to morphine in the brain

agonists at the receptors
club drugs
GHB, Rohypnol, Ketamine, MDMA
CNS depressant
treat narcolepsy
metabolite of GABE
exists naturally in brain at low levels
Acts on GABA receptor
date rape drug

Acts at GABA receptor
sedation, muscle relaxation, reduction of anxiety

not approved in US
special K

dissociative anesthetic

distorts perception of sight and sound

used in Vets

NMDA receptor target

related to PCP