Neuro 1

Front 1

Modalities of DCML (4)and from what part of the body are these sensations

Back 1

1. two point discrimination tactile localization
2. tactile localization
3. vibration
4. conscious propioception
FROM the limbs and trunk

Front 2

Definition: conscious propioception

Back 2

sense of the relative position of neighboring body parts

Front 3

synonyms of Spinothalamic tract and from what part of the body are these sensations

Back 3

anterolateral system
from the limbs and trunk

Front 4

modlities of spinothalamic/anterolateral tract (which is anterior, which is lateral)

Back 4

pain and temperature (lateral), crude/light touch (anterior)

Front 5

peripheral process of the 1st neuron in sensory pathways

Back 5

has the sensory receptor at the end and leads up to the spinal ganglion (normally the DRG)

Front 6

central process of the 1st neuron in sensory pathways

Back 6

runs from the cell body of the 1st neuron and synapses on the body of the 2nd neuron, these make up the dorsal roots

Front 7

dorsal funiculus

Back 7

also called dorsal columns, dorsal-medial area of the spinal cord, central processes of the 1st neuron of the DCML enter here

Front 8

definition of ganglia

Back 8

collections of neurons in the PNS

Front 9

definition of nuclei

Back 9

collections of neurons in the CNS

Front 10

synonym and definition of tract

Back 10

fasiculus, collection of axons which serve the same function

Front 11

synonym and definition of column

Back 11

funiculus, several fasiculi, each with their own function, bundled together

Front 12

foramen magnum

Back 12

transition point between the spinal cord and brainstem

Front 13

tonsil

Back 13

part of the cerebellum that sits right above the foramen magnum and be herniated through the opening with increased ICP

Front 14

reticular formation

Back 14

which is concerned with wakefulness, alertness and attention, damage can lead to loss of consciousness or coma

Front 15

Thalamus (location and 3 functions)

Back 15

rostral to the brainstem, processes all sensory information except olfaction, transmits info to the sensory cortex, plays a central role in the motor functions of the cerebellum and basal nuclei

Front 16

Hypothalamus

Back 16

placed below and anterior to the thalamus, includes mamillary bodies and gives attachment to the pituitary stalk, maintains homeostasis and has reproductive functions

Front 17

cerebellum

Back 17

gray matter as the folia on the outside and white matter and nuclei on the inside, coordinates motor activity and maintains balance

Front 18

insula

Back 18

in the depth of the lateral sulci

Front 19

Broca's area

Back 19

controls the expression of language

Front 20

Wernicke’s area

Back 20

comprehends and composes language

Front 21

Basal nuclei

Back 21

masses of gray matter located within the subcortical white matter that regulate motor function by working closely with the motor cortex

Front 22

coronal section

Back 22

like a crown

Front 23

sagittal

Back 23

splits body in R and L halves

Front 24

Interventricular foramen

Back 24

connects the lateral ventricles to the 3rd ventricle and separates the diencephalon for each half of the brain, rostral (anterior) boundary is the fornix

Front 25

Fourth ventricle

Back 25

lies between the cerebellum and the caudal brainstem, is continuous with the subarachnoid space outside the brain and the central canal of the spinal cord

Front 26

Folia

Back 26

gyri of the cerebellum

Front 27

Lateral fissure

Back 27

separates the temporal lobes from the parietal and frontal lobes

Front 28

Central sulcus

Back 28

separates the frontal lobe from the parietal lobe, drops down laterally but does not quite reach the lateral fissures

Front 29

Precentral gyrus

Back 29

gyrus immediately rostral to the central sulcus (in front of it)

Front 30

Postcentral gyrus

Back 30

gyrus immediately caudal to the central sulcus

Front 31

Parieto-occipital sulcus

Back 31

can only be seen on the medial surface, separates the parietal lobe from the occipital lobe

Front 32

Pre-occipital notch

Back 32

if you draw a line on the lateral surface between the most superior part of the P-O sulcus and this notch, you form the boundary between the occipital lobe and the parietal lobe as well as the occipital lobe and the temporal lobe more inferiorly

Front 33

Limbic lobe

Back 33

consists of the cingulated gyrus (the gyrus just superior to the corpus collosum) as well as other gyri

Front 34

Corpus collosum

Back 34

massive bundle of axons that interconnects the cortical layers of the 2 cerebral hemispheres (is a commisure

Front 35

Genu

Back 35

enlarged rostral (anterior) bend of the Corpus collosum

Front 36

Splenium

Back 36

enlarged portion of the caudal (posterior) portion of the Corpus collosum

Front 37

Anterior commisure

Back 37

adjacent to the fornix and laminal terminalis, located anteriorly to the 3rd ventricle, interconnects the 2 temporal lobes and the inferior portion of the 2 frontal lobes

Front 38

Septum pellucidum

Back 38

membranous structure that extends from the Corpus collosum superiorly to the fornix inferiorly, each hemisphere has its own septum which is closely apposed or even fused to the opposite hemispheres septum in the mid-sagittal plane (looks paired in coronal sections)

Front 39

Fornix

Back 39

originates deep in the temporal lobe, curves dorsally (superiorly) and medially to form the rostral boundary of the interventricular foramen, then dives below the surface to end in the hypothalamus

Front 40

Third ventricle

Back 40

slit like cavity between the 2 thalami and the 2 halves of the hypothalamus

Front 41

Lamina terminalis

Back 41

forms the rostral (anterior) wall of the 3rd ventricle, runs from the anterior commisure down to the optic chiasm

Front 42

Hypothalamic sulcus

Back 42

groove on the medial surface of the diencephalon, boundary between the thalamus and the ventrally (inferior) placed hypothalamus

Front 43

massa intermedia

Back 43

fused zone between the 2 thalami, not always present

Front 44

Pineal body

Back 44

is attached to the dorso-caudo aspect of the thalamus (posterior/superior, is often calcified and serves as a landmark for imaging

Front 45

Open medulla

Back 45

rostral portion (superior), ventral (anterior) to the cerebellum

Front 46

Closed medulla

Back 46

caudal portion (inferior)

Front 47

Tela choroidea

Back 47

where the ventricular lining (ependyma) comes into contact with the pia mater

Front 48

Choroid plexus

Back 48

created when BV’s infiltrate the tela choroidea

Front 49

Arachnoid villi

Back 49

extensions of the arachnoid membrane that protrude through the dural layer into the superior sagittal sinus, have thin outer membranes beneath which are bundles of collagenous and elastic fibers, small oval epithelial cells cover the surface of the villi, they act like 1 way valves that are pressure dependent

Front 50

Cistern

Back 50

pools of CSF in the subarachnoid space,

Front 51

Paracentral lobule

Back 51

gyrus surrounding the central sulcus on the medial surface

Front 52

fasciculus gracilis

Back 52

tract carrying fibers of the DCML from the lower limbs and trunk below T6, is located medial to the F.C.

Front 53

fasciculus cuneatus

Back 53

tract carrying fibers of the DCML from the upper limbs and trunk above T6, is located lateral to the F.G.

Front 54

nucleus gracilis (include location, name of axons from here)

Back 54

1st neurons of the DCML (from the lower limbs/lower trunk)synapse in this nucleus, located in the lower medulla, axons from these are called internal arcuate fibers

Front 55

nucelus cuneatus (include location, name of axons from here)

Back 55

1st neurons of the SCML (from the upper limbs/trunk) synapse in this nucleus, located in the lower/middle medulla, axons from these are called internal arcuate fibers

Front 56

internal arcuate fibers

Back 56

axons from the second neurons (N.C. and N.G.) of the DCML, immediately decussate (in the mid-medulla)

Front 57

medial lemniscus

Back 57

ascending fibers of the 2nd nueclei of the DCML (internal arcuate fibers) ascend through the brainstem as a bundle, terminates in the thalamus, vertical in the upper medulla, horizontal in the pons and triangle in the midbrain

Front 58

terminal nuclei of the DCML

Back 58

located in the VPL, axons from here project through the posterior limb of the internal capsule and terminate in SS1 and (SS2?)

Front 59

primary sensory cortex

Back 59

also called Brodmann's areas 1, 2 and 3
correspond to the postcentral gyrus and posterior part of the paracentral lobule, is the primary receptive area of the somatosensory information

Front 60

sensory ataxia

Back 60

loss of coordination when eyes are closed or when patient cannot physically see what they are doing, due to loss of conscious propioception, injury/lesion to DCML can cause this

Front 61

astereognosis

Back 61

loss of ability to recognize objects, people, smells, etc, can occur with injury/lesion to the DCML

Front 62

nucleus propius

Back 62

central processes of the anterolateral 1st neurons synapse on these dorsal horn neurons, is located at the same level, axons from here decussate obliquely w/in 1-2 segments

Front 63

white commisure

Back 63

axons from the nucleus propius of the ALS decussate obliquely w/in 1-2 segments through this

Front 64

location of decussation of the ALS

Back 64

1-2 spinal cord levels above where the 1st sensory neuron enters the SC

Front 65

muscle stretch reflex

Back 65

also called deep tendon reflex, contraction of a muscle in response to its tendon being stretched, protective to prevent overstretching, ex: knee jerk, ankle jerk, etc

Front 66

level of decussation of DCML

Back 66

mid-medulla

Front 67

Rhombencephalon (location, goes to which 2 structures at 5 weeks and which ventricle structure)

Back 67

Is located most inferiorly
Metencephalon
Myencephalon
4th ventricle

Front 68

Metencephalon

Back 68

pons and cerebellum

Front 69

Myencephalon

Back 69

medulla

Front 70

Mesencepahalon (location, creates which structure and which ventricle structure)

Back 70

located in the middle, midbrain, cerebral aqueduct

Front 71

Prosencephalon (location, goes to which 2 structures at 5 weeks and which ventricle structure)

Back 71

Is the most superior part
2 telencephalons, lateral ventricle, Diencephalon,
3rd ventricle

Front 72

telencephalon

Back 72

cerebral hemispheres (lateral ventricles too)

Front 73

Diencephalon

Back 73

thalamus and hypothalamus and 3rd ventricle

Front 74

C-shaped structures (4)

Back 74

Hippocampus, caudate nucleus, lateral ventricles and choroid plexus

Front 75

Hippocampal formation (location, formation, function, what occurs if it atrophies)

Back 75

area of the temporal lobe where parts of the cerebral cortex have become invaginated into the ventricular cavity during development, essential for forming (consolidating) short-term memory and atrophies in Alzheimer’s

Front 76

what forms the roof of the 3rd ventricle

Back 76

body of the fornix

Front 77

Basal Nuclei (location, function, 4)

Back 77

collections of gray matter within the subcortical white matter involved in regulation of motor function (except amygdyla), includes Caudate nucleus, Lentiform nucleus, Amygdaloid nucleus, Claustrum

Front 78

Caudate nucleus

Back 78

forms a C shaped configuration with its head related to the anterior horn of the lateral ventricle, body to the body of the ventricle and the tail passing into the temporal lobe (located laterally to the ventricle)

Front 79

Lentiform nucleus

Back 79

located lateral to the caudate nucleus, includes the Putamen (lateral structure, connected to the caudate nucleus) and Globus pallidus (medial, associated with the thalamus)

Front 80

Amygdaloid nucleus

Back 80

found at the tip of the tail of the caudate nucleus in the temporal lobe (just superior to the inferior horn of the lateral ventricle) and is involved in the regulation of emotional perception and expression

Front 81

Commisures

Back 81

are axons that interconnect corresponding areas of two sides

Front 82

Corpus callosum

Back 82

connects the frontal (genu), parietal (trunk) and occipital lobes (splenium), its axons form the roof and parts of the lateral walls of the lateral ventricles, Functions in interhemispheric transfer of information

Front 83

Anterior commisure (what is it and where is it on both sagittal and coronal section)

Back 83

interconnects much of the temporal lobes, Is best identified on the medial surface of the hemisphere as a small bundle of axons in front of the column of the fornix, Can also be seen in coronal sections as a white bundle crossing the midline and passing below the lentiform nucleus into the temporal lobes

Front 84

Association fibers

Back 84

axons that interconnect different cortical areas within the same hemisphere, Are the most numerous fibers in the white matter

Front 85

Arcuate fibers

Back 85

short association fibers that run in the depth of the sulci and connect adjacent gyri (ex: connect 1° general sensory cortex with the adjacent sensory association cortex)

Front 86

Superior longitudinal fasciculus

Back 86

made up of long association fibers that interconnect the frontal, parietal, temporal and occipital lobes and allows integration of motor, general sensory and special sensory information

Front 87

Arcuate fasciculus

Back 87

lower part of the Superior longitunial fasciculus, connects Broca’s (frontal) to Wernickes (temporal) and is essential to normal speech

Front 88

Projection fibers

Back 88

form the major afferent and efferent connections of the cortex and run bidirectionally between the cortex and subcortical structures (basal nuclei, thalamus, brainstem and spinal cord)

Front 89

Internal capsule

Back 89

type of projection fiber through which the major sensory and motor pathwyas run, dense collection of axons that can be seen in both coronal and horizontal sections between the caudate nucleus and the lentiform nucleus and between the lentiform nucleus and the thalamus, Is a straight line when it is a coronal section and a boomerang when in a horizontal section

Front 90

interventricular foramen

Back 90

connects lateral ventricles to the 3rd ventricles

Front 91

3rd ventricle (location and limits)

Back 91

narrow slit like cavity between the thalami and hypothalami of the two sides, Is limited above by the body of the fornix, Below, it extends to the optic chiasm and median eminence of the hypothalamus and infundibulum

Front 92

massa intermedia

Back 92

connects the 2 thalami, passes through 3rd ventricle

Front 93

Cerebral aqueduct

Back 93

placed between the sup/inf colliculi posteriorly and the cerebral peduncles anteriorly, Connects the 3rd and 4th ventricles

Front 94

4th ventricle

Back 94

located between the cerebellum posteriorly and the pons and upper medulla anteriorly

Front 95

Lateral apertures (Luschka)

Back 95

located at the tips of the lateral recesses of the 4th ventricle, allows for communication with the subarachnoid space

Front 96

Lateral recesses

Back 96

two narrow extensions from the lateral angels of the floor which extend forward around the medulla

Front 97

Midline aperture (Magendie)

Back 97

located in the middle/anterior part of the 4th ventricle, allows for connection with CSF

Front 98

Cistern magna

Back 98

is a large dilation of subarachnoid space in which the apertures open to, located between the cerebellum and posterior surface of the upper medulla

Front 99

Glomus

Back 99

large clump of choroid plexus in the atrium, can contain calcifications, shifts in the position are usually as a result of changes in the volume or shape of the ventricle indicating a “space occupying lesion”

Front 100

Choroid plexus

Back 100

highly vascular structure made up of pial CT and CAPS and lined on the ventricular surface by specialized ependymal cells, makes CSF

Front 101

major flow of the newly synthesized CSF (6)

Back 101

lateral ventricle → 3rd → cerebral aqueduct → 4th ventricle → median and lateral apertures → subarachnoid space

Front 102

major cource of CSF drainage

Back 102

arachnoid granulations

Front 103

Hydrocephalus

Back 103

abnormal accumulation of CSF in the brain cavity

Front 104

non-communicating obstructions (hydrocephalus)

Back 104

Obstructions within the ventricular system

Front 105

communicating obstructions (hydrocephalus)

Back 105

Obstructions in the subarachnoid space

Front 106

superior and inferior (BS and brain)

Back 106

means up and down in both

Front 107

rostral (BS and brain)

Back 107

is anterior for the brain
is superior for the BS

Front 108

caudal (BS and brain)

Back 108

is posterior for the brain
is inferior for the BS

Front 109

Oligodendroglial cells

Back 109

reside 1° within the white matter where they form myelin, they have small, round nuclei and no apparent cytoplasm on H&E, in the CNS, each cell can myelinate segments of several axons (Schwann cells make the myelin in the PNS)

Front 110

Astrocytes

Back 110

present in gray and white matter, have oval nuclei, have many processes which are only apparent when stained with GFAP, have functions in the BBB, a metabolic role and regulator of the ionic environment of the brain

Front 111

Microglial cells

Back 111

small, elongated, dark staining nuclei; can be activated in response to brain injury or during local immune response, become rod shaped and may upregulate MHC molecules and inflammatory cytokines; Are mesodemal, derived from the BM and infiltrate into the developing brain along with the BV’s, enter the brain during development and have a slow turnover during life

Front 112

red neuron

Back 112

due to ischemia, not visible until 8-24 hours after insult (and patient must be alive for these hours), neuron shrinks and cytoplasm becomes eosinophilic, nucleus shrinks, becomes darkly stained and then is lost, changes are irreversible, due to ATP depletion, intracellular acidosis, impaired glutamate reuptake → excitatory neuron damage, accumulation of intracellular Ca, generation of free radicals

Front 113

Central chromatolysis

Back 113

occurs in neuronal cell body after severe injury to the axon, most commonly seen in large motor neurons, cell body swells, Nissl bodies dissolute and nucleus migrates to the periphery, is reversible but may take months

Front 114

Wallerian degeneration

Back 114

occurs when axon is transected, axon and its myelin sheath, distal to the transaction, degenerates because it is separated from its cell body, shows impaired axonal transport followed by disappearance of neurofibrils and breaking up of axon into short fragments that are phagocytosed and removed, occurs over weeks in PNS, months in CNS, in PNS there may be sprouting → regeneration, doesn’t occur in CNS

Front 115

Neurofibrillary triangle

Back 115

located in cytoplasm, use Argyrophilic stain, associated with Alzheimer’s

Front 116

Lewy body

Back 116

located in the cytoplasm, use eosinophilic stain with halo, associated with Parkinsons

Front 117

what do you stain myelin with?

Back 117

Luxol Fast Blue

Front 118

Progressive multifocal leukoencephalopathy (PML)

Back 118

small plaques of demyelination develop where oligodendroglial cells dies and the myelin they support degenerates

Front 119

Leukodystrophies

Back 119

myelin is abnormally formed due to a genetic abnormality, myelin is unstable and breaks down, oligodendroglial cells show some capacity to proliferate and remyelinate in response to injury

Front 120

Astrogliosis

Back 120

astrocytes respond in this manner to almost any brain injury which includes both proliferation and hypertrophy, when they hypertrophy, the cytoplasm becomes apparent and is eosinophilic due to accumulation of GFAP (called gemistocytes in this form), does not result in fibrosis

Front 121

Microglial nodule

Back 121

may respond to single, damaged neurons in encephalitis by encircling the neuron and phagocytosing it (neurophagia), results in the formation of a microglial nodule, can also be present in white matter, especially in HIV-encephalitis

Front 122

Multinucleated giant cell

Back 122

in HIV encephalitis, groups of microglial cells may accumulate in the white matter, some can fuse to form giant cells, often seen in patients with AIDS dementia

Front 123

Ependymal rosettes

Back 123

when ependyma is disrupted and ependymal cells are lost, there is proliferation of adjacent astrocytes to form small proturberances known as ependymal granulations, disrupted ependymal cells may form small rosettes in the adjacent brain tissue

Front 124

Vasogenic edema

Back 124

BBB is composed of specialized endothelim joined by tight junctions, surrounding basement membrane, feet of astrocytes and microglial cells; Loss of integrity → entrance of excess water and solutes into extracellular space of the brain → collects predominantly in the white matter → ↑ volume and ICP

Front 125

Cytotoxic edema

Back 125

toxic or metabolic events that affect normal neuronal and glial cell membranes → intracellular accumulation of fluid → more likely to affect cells in the gray matter and will not usually result in a mass effect

Front 126

Neural tube closure

Back 126

fusion starts at day 22, anterior rostral neuropore closes at day 24, posterior caudal neuropore (lumbar-sacral region) closes between day 26-28

Front 127

Outgrowth of the telencephalic vesicles

Back 127

arise in the 5th week of development but by 7-8 weeks → formation of 2 hemispheres

Front 128

Cell migration (gestational time)

Back 128

postmitotic neuroblasts migrate away from the ventricular wall to final sites, unused neurons die via apoptosis, cerebral cortex is formed “inside out” from successive waves of migrating neurons, begins at 7 weeks and most have arrived by 16 weeks

Front 129

Gyration

Back 129

external surface of the brain is essentially smooth until after 24 weeks, in the following weeks there is development of gyri → ↑ surface area

Front 130

Myelination (gestational time)

Back 130

begins at about 20 weeks gestation in the BS and SC and progresses in an orderly fashion such that by 18 post-conceptional months, it has begun in almost all telencephalic sites.

Front 131

Neural tube defects

Back 131

also called dysraphism and can be associated with failure of fusion of the bony vertebrae and cranial vault, folic acid deficiency has been implicated, timing and extent of injury can affect how severe the effects are

Front 132

Spina bifida occulta

Back 132

simple bony defect usually in the lumbosaccral region that involves no nervous tissue, may be clinically silent but is often covered by a nevus, hairy patch, lipoma or dimple

Front 133

Meningocele

Back 133

some of the vertebrae remain unfused and the meninges are damaged and pushed out, appears as a sac/cyst filled with CSF, spinal cord and nerves are not involved

Front 134

Myelomeningocele

Back 134

unfused spinal column allows the spinal cord to protrude out of the opening, meninges may or may not form a sac around the SC, nerves of this section of SC are damaged → some degree of paralysis

Front 135

Encephalocele

Back 135

when brain and meninges protrude from an opening in the skull

Front 136

Anecephaly

Back 136

most severe, results from lack of fusion of the anterior neuropore, absent development of overlying skull → mechanical destruction of the malformed developing cerebrum, may be stillborn or alive (but die w/in hours)

Front 137

Holoprosencephaly

Back 137

developmental defect of the forebrain and frequently the midface in humans that involves incomplete development and septation of midline structures, other signs are microcephaly (small head), mild hypotelorism (close set eyes)

Front 138

Alobar HPE

Back 138

most severe form, usually incompatible with life, failure of division of the forbrain into R and L hemispheres, associated with cyclopia, primitive nasal structure and midfacial clefting; teratogens, chromosomal abnormalities and familiar forms have been described

Front 139

Heteropias

Back 139

groups of neurons that have halted their migration and differentiated w/in the white matter proximal to their final destination in the cortex

Front 140

Gyration defects

Back 140

can also occur, gyri may be absent, ↑ in # or broader than normal

Front 141

incidence of anencephaly

Back 141

Was 1/1000 but w/ folic acid supplementation it is 1/5000

Front 142

incidence of
holoprosencephaly

Back 142

is 1/250 in embryogenesis and 1/16,000 newborns

Front 143

Hydrocephalus

Back 143

↑ amount of CSF, usually associated w/ enlarged ventricles and usually under ↑ ICP

Front 144

Obstructive Hydrocephalus

Back 144

due to blockage of CSF flow, most common

Front 145

Non-obstructive Hydrocephalus

Back 145

due to excess CSF, like by a tumor of the choroid plexus

Front 146

Communicating Hydrocephalus

Back 146

if the obstruction is in the subarachnoid space or due to blockage of arachnoid granulations; may be a consequence of subarachnoid hemorrhage, leptominigitis, developmental abnormality or rarely dural sinus thrombosis

Front 147

Non-communicating Hydrocephalus

Back 147

if the blockage occurs in the brain, most common are developmental malformation (aqueduct stenosis), inflammation and neoplasm

Front 148

Mental retardation

Back 148

Significantly sub-average general intelligence (IQ <70) WITH Concurrent deficits in adaptive behavior (ex: communication, social skills, etc) AND Onset during developmental period

Front 149

Cerebral palsy

Back 149

chronic disorders impairing control of movement that appear in the first few years of life and generally do not worsen over time, Caused by faulty development of or damage to motor areas in the brain that disrupts the brains ability to control movement and posture, Symptoms: difficulty w/ fine motor tasks, difficulty maintaining balance and involuntary movements, Can be congenital or acquired after birth

Front 150

Electrochemical potential

Back 150

sum of the electrical and chemical potentials for the component

Front 151

Electrochemical equilibrium

Back 151

normally occurs when the force due to the chemical concentration difference to move an ion one direction is balanced by an equal but oppositely directed force due to the membrane potential to drive the ion the opposite direction → net force is zero

Front 152

Equilibrium Potential

Back 152

(E) is the value of the membrane potential that will prevent ions from moving down concentration gradients, calculated using the Nernst equation

Front 153

Equilibrium potential difference

Back 153

drives ions to move across cell membranes, Both the chemical concentration difference and the membrane (voltage) potential represent forces that drive an ion towards equilibrium

Front 154

Membrane potential (Vm)

Back 154

the electric potential (voltage) across a membrane; Arises from the action of ion transporters which maintain variable ion concentrations inside the cell; Resting membrane potential for most cells is 40-100 mV (in most cells this is due to a net leakage of K+ out of the cell) with the cytoplasm at a negative potential relative to the EC fluid and is present in both excitable and non-excitable cells

Front 155

Conductance (g)

Back 155

ease with which current flows, reciprocal of resistance; Is directly proportional to the # of open ion channels in the membrane; Is much higher for K+ than for Na+ → greater outward K+ current than inward Na+ current (this net efflux of + charges underlies the inside negative resting potential in animal cells)

Front 156

Ohms law

Back 156

determines the magnitude of the current carried by each ion
INa = gNa (VM - ENa)

Front 157

Action potential

Back 157

is generated in either neurons or muscle cells when the membrane conductance to Na+ ↑ and the membrane potential is driven towards ENa

Front 158

Local anesthetics

Back 158

work by blocking transmission of pain by preventing Na channels from opening in pain conducting neurons

Front 159

Node of Ranvier

Back 159

areas without myelin with lots of Na+ channels; Occur b/c the neuronal membrane under the myelin has few Na+ channels

Front 160

Salutatory conduction

Back 160

occurs as the AP jumps from one node of Ranvier to the next

Front 161

Local responses

Back 161

membrane potential changes that occur in response to stimuli that are too small to initiate an AP; The magnitude of the depolarization ↓ exponentially with ↑ distance from stimulus

Front 162

Length constant

Back 162

distance over which the voltage change decreases to 1/e (37%) of its maximum (2-3 mm is typical)

Front 163

Electrotonic conduction

Back 163

mechanism of depolarization spread where small currents flow between adjacent areas of different electrical potential but the depolarization induced by these currents is too small to initiate an AP

Front 164

Receptor or generator potential

Back 164

a graded potential that is the result of a change in ion fluxes across the membrane due to the transduction of stimulus energy

Front 165

Adaptation or desensitization

Back 165

↓ in the frequency of AP’s in a sensory neuron despite maintenance of the stimulus at constant strength, purpose is so that sensory neurons can maintain their responsiveness as the mean level of the stimulus changes

Front 166

Recruitment

Back 166

activated sensory neuron starts to activate sensory units in the areas that are adjacent, weak stimuli will activate receptors with low thresholds and strong stimuli will activate receptors with higher thresholds

Front 167

Sensory modality

Back 167

type of sensory information that is being conveyed

Front 168

Sensory unit

Back 168

describes a sensory axon and all its peripheral branches

Front 169

Receptive field

Back 169

area from which the stimulus produces a response in that unit, over overlap with the fields of other sensory neurons

Front 170

Somatotopy

Back 170

organized arrangement of fibers conveying sensory information from the body which is maintained throughout the CNS and allows the CNS to accurately pinpoint the origin of the particular sensation

Front 171

Phasic receptor

Back 171

rapidly adapting, respond very rapidly to the onset of stimulus → frequency ↓ over time and axons may eventually stop responding; This is in part due to a generator potential that rapidly decays despite continued stimulus and in part due to accommodation in the nerve fiber itself; These are important for indicating when there is a change in the stimulus, such as an ↑ or ↓ in intensity

Front 172

Tonic receptor

Back 172

slowly adapting; found in joints and muscles to convey positional information to the brain, receptors that measure O2 in our blood and receptors that measure cold/hot and maintain their response to a stimulus over time; Due to a slowing decaying generator potential

Front 173

Salutatory conduction

Back 173

occurs as the AP jumps from one node of Ranvier to the next

Front 174

Local responses

Back 174

membrane potential changes that occur in response to stimuli that are too small to initiate an AP; The magnitude of the depolarization ↓ exponentially with ↑ distance from stimulus

Front 175

Length constant

Back 175

distance over which the voltage change decreases to 1/e (37%) of its maximum (2-3 mm is typical)

Front 176

Electrotonic conduction

Back 176

mechanism of depolarization spread where small currents flow between adjacent areas of different electrical potential but the depolarization induced by these currents is too small to initiate an AP

Front 177

1. Stimulus transduction

Back 177

process by which a sensory receptor converts the stimulus into the electrical signal that is carried by sensory axons.

Front 178

lateral inhibition

Back 178

receptors at the edge of the field are inhibited to make the boundaries more distinct

Front 179

Autoregulation of the brain

Back 179

the brain can maintain fairly constant blood flow and pressure, despite rather large changes in system blood flow, is under metabolic control, when BP is <50-70 → autoregulation fails and there is ↓ blood supply to the brain

Front 180

Carotid system

Back 180

supplies the anterior, medial and lateral aspects of the cerebral hemispheres as well as some deep structures

Front 181

Vertebral-basilar system

Back 181

supplies portions of the SC, brainstem, cerebellum and the inferior and posterior aspects of the cerebral hemispheres as well as some of the deep structures

Front 182

Internal carotid artery

Back 182

branch from the common carotid, once they enter the brain, they start to branch bilaterally; After exiting the cavernous sinus, and at the level of the optic chiasm, the ICA bifurcates into the anterior cerebral (ACA) and middle cerebral (MCA) arteries

Front 183

ACA

Back 183

supplies most of the medial aspect of the frontal and parietal lobes and overlaps slightly onto the lateral side

Front 184

MCA

Back 184

branch of the internal carotid, travels in the lateral fissure → cortical surface and supplies most of the lateral surface of the cerebral hemispheres

Front 185

Posterior communicating artery

Back 185

Pcomm, proceeds posteriorly (towards the back of the brain) and eventually joins with the arteries of the vertebral basilar system

Front 186

Vertebral arteries:

Back 186

arise from the subclavian arteries → ascend through the transverse processes of the rostral 6 cervical vertebrae, enter the cranial vault via the foramen magnum, the two vertebral arteries run rostrally along the ventral side of the medulla and fuse at the pontomedullary junction to form the single midline basilar artery

Front 187

Anterior spinal artery

Back 187

branches of the vertebral arteries, artery from each side fuse at the midline and descend along the ventral SC

Front 188

Posterior spinal artery

Back 188

branches of the vertebral arteries,2 posterolateral arteries descending along the spinal cord (dorsally)

Front 189

Posterior inferior cerebellar artery

Back 189

PICA, branch of the basilar arteries, supply blood to the inferomedial aspect of the cerebellum, has a very characteristic hair pin loop

Front 190

Anterior inferior cerebellar artery

Back 190

branch of the basilar arteries, supplies inferolateral aspect of the cerebellum

Front 191

Superior cerebellar artery

Back 191

SCA, supplies superior aspect of the cerebellum and inferior colliculus

Front 192

Posterior cerebral artery

Back 192

PCA, supplying inferior central hemisphere (temporal and occipital lobes) and superior colliculus

Front 193

Brain uptake index

Back 193

BUI, relative uptake of a molecule as compared to the uptake of DOD (water); Is arbitrarily set as 100%; Nicotine is 131%, alcohol 104%, aspirin 1.8%, etc

Front 194

Mannitol

Back 194

poorly permeable through the BBB, use to dehydrate the brain by osmosis → ↓ swelling

Front 195

Antibodies to transferrin receptors

Back 195

may sneak drugs through the BBB, TR’s are abundant in the BBB so if agents are coupled to it or an antibody → complexes can be taken up

Front 196

Billirubin encephalopathy

Back 196

end result of injury to the CNS by bilirubin (which is more toxic to newborns than adults), only the free bilirubin is taken up, bilirubin influx is ↑ and efflux is ↓ in newborns; Bilirubins binding to gangliosides may interfere w/ glycolysis → impaired neuronal conduction

Front 197

Basal nuclei

Back 197

gray matter masses located within the white matter of the cental hemispheres, includes the caudate nucleus, putamen, globus pallidus, claustrum and amygdaloid body

Front 198

Striatum

Back 198

consists of the putamen and the caudate, receive the major input to the BN from the motor cortex

Front 199

Globus palidus

Back 199

consists of the externa (GPe) and the interna (GPi)

Front 200

Subthalamic nucleus

Back 200

part of the diencephalon and is located ventral t the thalamus and lateral to the hypothalamus, functions with the GPe to modulate BN output

Front 201

Substantia nigra

Back 201

component of the midbrain and extends from the level of the diencephalon to the upper pons and occupies a position between the crus cerebri ventrally and the tegmentum dorsally; It is divided into a dorsal strip (pars compacta, SNpc) containing pigmented neurons and a ventral strip (pars reticulate, SNpr) which has non-pigmented neurons

Front 202

Direct pathway (BN and motor activity)

Back 202

helps to initiate wanted movement by reducing the BN output

Front 203

Indirect pathway (BN and motor activity)

Back 203

inhibits unwanted movement

Front 204

Dopamine

Back 204

is released at the terminals of the nigrostriatal projections in the striatum; Binds to cell surface receptors → interacts with G-proteins

Front 205

D-1 receptors

Back 205

Dopamine receptor, found on neurons involved in the direct pathway → coupled to stimulatory G-proteins that ↑ cAMP → excitatory effect on the direct pathway

Front 206

D-2 receptors

Back 206

Dopamine receptors found on neurons involved in the indirect pathway → inhibit cAMP production through a different G-protein → inhibition

Front 207

Glutamate

Back 207

excitatory AA released by cortical neurons that project to the stiatum, thalamocotical axons of the VA/VL nuclei and axons of the STN

Front 208

GABA

Back 208

inhibitory NT released by striatal neurons that end in the GPe, GPe axons that end in the STN and the axons that convey BN output to the VA/VL nuclei of the thalamus

Front 209

Hyperkinetic disorders

Back 209

abnormal involuntary movements

Front 210

Athetosis

Back 210

slow and twisting movements of the limb, face and trunk

Front 211

Dystonia

Back 211

sustained abnormal posturing of the trunk and extremities

Front 212

Chorea

Back 212

brief rapid jerks involving parts of the limbs as in Huntington’s disease

Front 213

Hemiballismus

Back 213

gross rapid flinging movements of an entire limb, often due to lesions of the STN

Front 214

Hypokinetic events

Back 214

reduction in mobility (ex: Parkinson’s; Reduction in the amount (hypokinesia to akenesia), rate and amplitude of voluntary movements (bradykinesia); Movements are slow and stiff and are either started or stopped with great difficulty

Front 215

PD

Back 215

idiopathic variety of hypokinetic disorders; There is a significant loss of dopaminergic neurons in the SNpc which can be seen in a PET scan; This leads to a ↓ in the activity of the direct pathway → ↓ facilitation of the cortex by the thalamus → ↓ sustenance of desired movement; Also → ↑ in the activity of the indirect pathway → ↑ BN output → ↑ inhibition of VA/VL nuclei and ↓ in facilitation of the cortex → excessive suppression of both unwanted and desired movements and an inability to switch to new motor programs

Front 216

pontine trigeminal nucleus

Back 216

central processes of trigeminal ganglion cells (neuron 1) enter the mid-pons and synapse here, located in the mid-pons just lateral to the motor nucleus of V

Front 217

trigeminothalamic tract

Back 217

contains axons from the pontine and spinal nuclei of V on their way to the VPM,

Front 218

location of the spinal nucleus of V

Back 218

extends from the mid-pons down to the upper cervical regions

Front 219

location of the mesencaphalic nucleus and what fibers are here

Back 219

located in the upper pons/ lower midbrain, is the 1st neuron!!! (no DRG) propioception fibers from the jaw are the peripheral processes for these, from here they go to the cortex as well as to both motor nucli of V to affect the strength of bite

Front 220

trigeminospinal tract

Back 220

extends from mid-pons down to lower medulla (is lateral), contains the descending pain and temperature fibers, also fibers from 7, 9, 10

Front 221

solitary nucleus

Back 221

extends throughout the medulla, taste fibers from 7, 9, 10 synapse on the superior part of this nucleus

Front 222

Synaptic delay

Back 222

time between depolarization of the presynaptic cell and the initiation of the postsynaptic response (due to time required to release and bind the NT)

Front 223

Neuromuscular junction

Back 223

region where a motor neuron and a muscle cell come close together and where the NT ACh is released; The muscle cell membrane is highly folded in this area → ↑ SA exposed to ACh

Front 224

Motor end plate

Back 224

region where the nerve cell and the muscle cell membranes overlap

Front 225

End plate potential

Back 225

depolarization that occurs at the motor end plate, is NOT an AP, is transient; Only has a few Na channels → does not participate in the AP

Front 226

Acetylcholinesterase

Back 226

present on the post-junctional membrane, rapidly hydrolyze ACh, keep the EPP transient

Front 227

Anticholinesterases

Back 227

inhibitors of acetylcholinesterases, prolong the EPP but can lead to desensitization

Front 228

Hemicholiniums

Back 228

inhibit the uptake of choline by the presynaptic motor neuron; Prolonged stimulation of the presynaptic nerve in the presence of these → depletion of ACh → inhibition of synaptic transmission

Front 229

Myasthenia gravis

Back 229

the density of AChR at the NM junction is < normal; Is characterized by extreme muscle weakness and rapid onset of fatigue; Most patients have circulating Ab’s against AChR (autoimmune, they may bind and cause internalization of the receptors); Leads to smaller EPP’s when ACh is released and it may be so small that it cannot elicit an AP

Front 230

α-bungarotoxin

Back 230

inhibits the nicotinic AChR of skeletal muscle by preventing the opening of ion channels, leads to paralysis

Front 231

Curare

Back 231

blocks the binding of ACh to the receptor, leads to paralysis

Front 232

Catecholamines

Back 232

epinephrine, norepinephrine, dopamine; receptors are linked to cAMP 2nd messangers and G proteins (NOT ion channels)

Front 233

Excitatory AA’s

Back 233

glutamate, aspartate

Front 234

Inhibitory AA’s

Back 234

GABA (can have ion or G-protein coupled receptors), glycine

Front 235

axon hillock

Back 235

EPSP is conducted electrotonically to this area which contains a high # of Na channels and can generate an AP if enough are opened

Front 236

EPSP

Back 236

transient depolarization of the postsynaptic neuron caused by the binding of an excitatory NT → ↑ Na+ and K+ conductance

Front 237

IPSP

Back 237

transient hyperpolarization of the postsynaptic neuron caused by the binding of an inhibitory NT → ↑ K+ and Cl- conductance

Front 238

Spatial summation

Back 238

integration of many synaptic inputs arriving simultaneously from DIFFERENT presynaptic cells

Front 239

Temporal summation

Back 239

series of inputs from a single synapse occurring in rapid succession

Front 240

choline acetyltransferase

Back 240

synthesizes the equation: Choline + Acetyl CoA → ACh + CoA

Front 241

Nicotinic receptors

Back 241

chemically gated Na+ ion-channels; These are “fast action” excitatory receptors prominent in muscle fibers; Nicotine is an agonist and curare is an antagonist; Have 2α, 1β, 1γ and 1δ subunit; Gated channels are normally pentameric

Front 242

Muscarinic receptor

Back 242

slower actions and longer lasting changes are created by these receptors; They are associated with G-proteins; The receptors control the level of 2nd messengers and can be excitatory or inhibitory; Muscarine is an agonist, atrophine is an antagonist; 5 subtypes are recognized which are the products of 5 different but homologous genes; Have a wide distribution: heart muscles, interneurons in ganglia, neurons in gut plexus, SM, gland cells, CNS pathways

Front 243

botulinum toxin

Back 243

destroys the neuro-exocytosis apparatus required for the release of ACh into the cleft → flaccidity, cure requires the sprouting of new nerve terminals

Front 244

Tetanus toxin

Back 244

blocks the release of inhibitory NT’s (by disrupting the synaptic vesicle release apparatus) like glycine and GABA → ↑ firing of α-motor neuron → rigidity