Neuroanatomy Flashcards
Parts of pituitary development
Anterior-stomodeum
Posterior-neuroectoderm
Schizencephaly
Ependymal lining continuous with cerebral hemispheres
Rexed laminae level for substantia gelantinosa
II
Rexed laminae level for nucleus of Clarke
VII
Nuclei in midbrain
Oculomotor
Edinger-Westphal
Trochlear
Mesencephalic
Nuclei in pons
Abducens Superior salivary Motor Trigeminal motor facial spinal trigeminal principle sensory of V
Nuclei in the medulla
Hypoglossal Dorsal motor of vagus Inf salivatory nucleus ambiguous solitary vestibular cochlear spinal trigeminal
Neurotransmitter used in raphe nuclei
Serotonin (5HT)
Result of damage to pontomesencephalic reticular formation
coma (loss of consciousness)
Result of damage to medullary reticular formation
insomnia
Reticular formation nucleus active during wake?
During sleep?
locus ceruleus
raphe nuclei
Function of pineal gland
circadian rhythm, melatonin production
Function of habenula
olfactory stimuli
Circumventricular organs: (6)
Pineal gland median eminence Subfornical organ area postrema subcommissural organ organum vasculosum
Area for speech/writing creation
Brocca’s
Area for speech/writing understanding
Wernicke’s
Function of nucleus accumbens
DA, pleasure center
Amygdala output pathway
Through stria terminalis
Function of globus pallidus
coordination center
Geniculate body functions:
Medial-auditory
Lateral-visual
Hippocampus circuit
hippocampus->fornix->mamillary bodies->anterior nucleus of thalamus->cingulate cortex->entorhinal cortex->hippocampus
Function of ant thalamus nucleus
Mamillary bodies-> A -> cingular cortex (memory)
Function of dorsomedial thalamus nucleus
frontal hypothalamus-> DM -> prefrontal
Function of ventral ant thalamus nucleus
basal nuclei-> VA -> premotor area (motion initiation)
Function of ventral lat thalamus nucleus
cerebellum-> VL -> motor cortex
Function of VPL of thalamus
body -> VPL -> sensory cortex
Function of VPM of thalamus
head -> VPM -> sensory cortex
Function of pulvinar of thalamus
back and forth from visual cortex
Function of lateral post thalamic nucleus
visual cx -> LP -> parietal cx
Most common NT in brain
glutamate, it’s everywhere!
Storage of NT in vesicles
NT/H+ antiport, vesicles are acidic
Receptor activity for D1, D5
increase cAMP
Receptor activity for D2-4
decrease cAMP
Receptor activity for 5HT 1 and 5
decrease cAMP
Receptor activity for 5HT 2
increase IP3/DAG
Receptor activity for 5HT 3
Na+ channel
Receptor activity for 5HT 4,6 and 7
increase cAMP
Receptor activity for alpha 1
increase IP3/DAG
Receptor activity for alpha 2
decrease cAMP
Receptor activity for betas
increase cAMP
Receptor activity for H1
increase IP3/DAG
Receptor activity for H2
increase cAMP
Receptor activity for H3,4
decrease cAMP
Receptor activity for N1,2
Na+ channel
Receptor activity for M1,3,5
increase IP3/DAG
Receptor activity for M2,4
decrease cAMP
Mechanism of MPTP
Metabolized by MAO to MPP+
Crosses BBB
Selectively taken up by DA cells
Is toxic to mitochondria
Histological sign of Parkinson’s
Lewy bodies (alpha-synuclein among other things inside)
Sign of idiopathic Parkinson’s
asymmetric
Targets of DA cells: (5)
striatum limbic cortex amygdala nucleus accumbens prefrontal cortex
DA pathways and diseases associated with each
nigrostriatal ->Parkinson’s, decreased DA
mesolimbic -> Schizophrenia, increased DA
mesocortical-> occurs in both
Other pathways using DA: (4)
Inner/outer plexiform layers of retina
Periglomerular cells of olfactory bulb
tuberhypophysial/incertohypothalamic
medullary periventricular group
Action of carbidopa
Prevent breakdown of L-dopa outside the BBB
Action of recerpine
blocks DA uptake into vesicles, decreases DA released
Parkinson’s like symptoms
Transport of DA into cell
Na+/DA symporter on cell membrane
Metabolism of DA:
DA -> DOPAL via MAO-B
DOPAL -> DOPAC via aldehyde DH
DOPAC -> HVA via COMT
Speed of reaction
DOPAL-> DOPAC very quick
DOPAL is aldehyde, so MAO and ADH are on cell membrane adjacent
DA degradation blockers: (4)
deprenyl, selegiline (MAOI)
tolcapane, entacapone (COMTI)
DA receptor agonist:
bromocriptine
DA receptor antagonist:
chlorpromazine
loxapine
haloperidol
Side effect of L-dopa
hallucinations -> like schizophrenia
Action of cocaine:
blocks DA reuptake
Action of amphetamines:
increases DA release
Environmental toxins causing Parkinson’s
Paraquat and manganese
Physical findings with schizophrenia
Enlarged ventricles
altered orientation of hippocampal pyramidal cells
Substances that can pass BBB:
caffeine
alcohol
nicotine
cocaine
Reason for BCAA in sports drinks:
compete with Trp in BBB amino acid transporters, preventing Trp into brain
(which would cause tiredness/sleepiness)
Phenylketonuria
phenylalanine hydroxylase deficiency
phe prevents other large AA’s from entering brain due to higher concentration
Cause of ketone production in liver:
decreased Glc -> decrased oxaloacetate
decreased OA -> FA synthesis
increased FA synthesis -> increased acetyl-CoA
Excess acetyl-CoA -> ketone bodies
Production of glutamate in brain:
alpha-ketoglutarate (from TCA) to glutamate
Molecules made from glutamate in the brain:
GABA
glutathione
Function of glutamine in brain:
NH4+ removal
transport of AA’s between brain cells
Metachromatic leukodystrophy
accumulation of sulphatides
Gaucher disease
beta-glucosidase defect
glucocereroside accumulation
Tay-Sachs disease
hexoaminidase defect
ganglioside GM2 accumulation
Fabry disease
alpha-galactosidase A defect
ceramide trihexoside accumulation
X-linked
Krabbe disease
beta-galactosidase defect
galactocerebroside accumulation
Niemann-Pick disease (A,B)
sphingomyelinase defect
sphingomyelin accumulation
Niemann-Pick disease (C,D)
cholesterol accumulation
Sx of Gaucher disease
Hepatosplenomegaly
crumpled tissue paper appearance in Gaucher cells
Sx of Tay-Sachs
cherry red spot on macula
blindness/mental retardation
Sx of Fabry disease
kidney failure
Sx of Krabbe disease
absence of myelin
Types of Gaucher
I- nonneuropathic, treatable
II- acute neuropathic, death around 2 y/o
III- subacute neuropathic, juvenile
Sx of B12/Folate deficiency
megablastic anemia
Discerning B12 or Folate deficiency
B12 would have methylmalonyl-CoA build up and neuropathic deficiencies
Neurotoxicity of ammonia:
Gln leaving brain causes decrease glutamate
decreases glutamate for NT production
Gln causes cerebral edema
Gln causes mitochondrial permeability
Hereditary hyperammonia types:
I- carbomyl phosphate synthetase I, accumulation of NH4+
II- ornithine transcarbamoylase, accumulation of ornithine/carbomyl phosphate (X-linked)
What forms the lens placode?
surface ectoderm
Layers of cornea:
epithelium Bowman's membrane (cannot regenerate) corneal stroma Descemet's membrane corneal endothelium
Layers of iris:
posterior pigmented epithelium anterior pigmented epithelium myoepithelial cells smooth muscle stromal melanocytes
What surrounds the retina?
Choroid
Specifically Bruch’s membrane (hyaline)
Ten layers of retina:
retinal pigmented epithelium photoreceptors of rods/cones outering limiting membrane outer nuclear membrane (rods/cones) outer plexiform layer inner nuclear layer (bodies of bipolar cells) inner plexiform layer ganglion cell layer layer of optic n. fibers inner limiting membrane
Photosensitive molecule for rods:
rhodopsin
Photosensitive molecule for cones:
iodopsin
What layer produces cells in the lens?
subcapsular epithelium
What maintains composition of cornea?
Bicarbonate pumps, maintaining H2O levels
4 tx types of glaucoma:
prostanglandin analogs/cholinergic agonists-> increase outflow
beta-blockers/carbonic anhydrase inhibitors ->decrease secretion
Growth of the lens:
from inside out
Mechanism of cataracts:
increase in H2O causes crystallines to fall out of solution
Tx for wet macular degeneration:
VEGF inhibitor injections
laser tx
Rapidly adapting receptors:
Meissner’s corpuscle-> tactile impulse (under epidermis)
hair follicle receptor-> tactile impulse
Paccinian corpuscle-> vibration (in subcutaneous)
Slowly adapting receptors:
Merkel’s disc-> pressure in epidermis
Ruffini’s ending -> pressure
Synapses of anterior spinocerebellar tract:
lamina V, VII
lateral cerebella vermis
Synapses of posterior spinocerebellar tract:
lamina V, VII
medial cerebella vermis
Synapses of rostral spinocerebellar tract:
lamina VII
lateral cerebellar vermis
Synapses of cuenocerebellar tract:
lateral cuneate nucleus
medial cerebellar vermis
Synapses of trigeminocerebellar tract:
sup: mesencephalic (pseudounipolar) and cerebellum
inf: spinal trigeminal nucleus and cerebellum
Synapses of spinothalamic tract:
lamina I, V or II
VPL
cortex
Synapses of spinoreticular tract:
lamina II,III interneurons reticular formation intralaminar/post nuclei of thalamusSyn cortex
Synapses of spinocervicothalamic tract:
lamina III, IV
lateral cervical nucleus
VPL
cortex
Synapsese of anterior trigeminothalamic tract:
spinal trigeminal nucleus
VPM
cortex
Wallenberg syndrome:
lesion of posterior inferior cerebellar artery
area where ALS and ant trigeminothalamic tracts cross
Sx: ipsilateral loss over face
contralateral pain, temp, crude touch on body
Brown-Sequard syndrome:
lesion of 1/2 spinal cord
ipsilateral tactile sensation lost-> post column
contralateral temp/pain lost -> ALS
ipsilateral motor loss
Syringomyelia:
bilateral loss of pain/temp around and slightly below level
Pain inhibition of spinal cord:
lamina II/III -> release enkephalin
Post column can also release it
Increases elements in CSF:
Na+
Mg2+
Cl-
Innervation of the cranial vault:
Anterior- CN V
Middle- CN V
Posterior- CN X and C1-C3
Uncal herniation result:
CN III compression
corticospinal and reticular formation compression
Pathways crossing via anterior commissure:
Anterior spinocerebellar
Spinothalamic
Spinoreticular
Pathways crossing via medial lemniscus:
posterior columns
spinocervicothalamic
Pathway crossing via reticular formation:
anterior trigeminothalamic
Tissue origin of statoacoustic ganglion:
neural crest and surface ectoderm
Role of spiral ligament:
tether cochlear duct to surrounding cartilage
Pharyngeal arch origins of ear bones:
malleus, incus -> I
stapes -> II
What produces wax in the ear?
ceruminous glands
Cells types in spiral ganglion:
bipolar
myelinated
Function of stria vascularis:
produce endolymph
located medially to spiral ligament
Sound propogation pathway:
tympanic membrane malleus, incus, stapes oval window scala vestibuli/tympani basilar membrane organ of corti hair cell movement-> nerve impulse
Organization of sound analysis in cochlea
basilar membrane lengthens up the spiral
allows higher frequency detected at bottom
lower frequency detected nearer the top
Called tonotopy
Damage above and below cochlear nucleus:
Above: bilateral deficiencies
Below: ipsilateral deficiencies
Synapses in auditory pathway:
Cochlear nucleus superior olivary complex inferior colliculus MGB temporal cortex
Organization of lateral lemniscus:
high frequencies anterior
low frequencies posterior
Area passing through from MGB to temporal cortex
sublenticular limb of internal capsule
Organization of auditory cortex:
high frequencies caudal
lower frequencies rostral
Middle ear muslces:
tensor tympani
stapedius-> decreases 10dB
Focal length for humans:
17mm (57 diopters)
How do you shorten focal length? When would you need to do this?
add convex lens
needed with hyperopia (farsightenedness)
How do you lengthen focal length? When would you need to do this?
add concave lens
needed with myopia (nearsightenedness)
Refraction of the eye contribution:
mostly cornea
1/3 from lens
Action of accommodation:
contract ciliary m. decrease tension on suspensory ligaments increase refraction decrease focal length used for near vision
Presbyopia:
Loss of accommodation with age
Function of retinal pigmented layer:
absorb excess light
store vitamin A
degrade old photoreceptor discs
Cycle of rhodopsin:
cis to trans retinal, dissociates from opsin retinal to retinol taken up in pigmented epithelium converted back to cis retinal taken up into photoreceptor cells
Retina phototransduction:
light causes rhodopsin to active Gs Gs turns on PDE which degrades cGMP Na+ channels close (cGMP keeps them open) cell hyperpolarizes NT release stops
Types of color blindness:
Deuteranopia-> loss of green
Protanopia -> loss of red
NT used in retina:
glutamate
Function of horizontal cells:
lateral inhibition
helps with patterns/acuity/contrast
Threshold for salty:
10mM (NaCl)
Threshold for sweet:
20mM (sucrose)
Threshold for bitter:
0.008mM (quinine) or 0.0001 (strychine)
Threshold for sour:
2mM (citric acid)
Types of taste buds:
circumvallate (50%)
foliate
fungiform
Tests for supertasters:
PROP and PTC
have 2x more buds (10,000)
Signal transduction for salty taste:
Na+ channels
Signal transduction for acid/sour taste:
H+ sensitive channels
Signal transduction for bitter:
Gs-> IP3-> Ca2+ channels
Signal transduction for sweet:
dimerized Gs
Signal transduction for AA’s:
dimerized Gs -> IP3-> Ca2+ channel
Activation with multiple tastes:
Taste cells have multiple receptors
Strongest stimulant will be activated
Pathway for taste:
taste cell sensory neuron solitary tract VPM insula Stays ipsilateral
Parts of olfactory membrane:
bipolar receptor neuron
basal cells (make more receptors)
Bowman’s glands (mucous production)
Receptors on olfactory cells:
only 1 receptor type
multiple odorants can activate the 1 receptor type
Signal transduction for odorants:
Gs ->
cAMP ->
Ca2+/Na+ cotransporter
Olfactory bulb cells/function: (5)
glomerular-sort smells mitral-project to cortex tufted-refines glomerular synapse periglomerular-refine glomerular synapse granule-inhibitory from CNS/tufted cells
Special visceral afferents:
taste and olfaction
Special somatic afferents:
balance/hearing and vision
Special somatic efferents:
CN VIII hair cells
Nuclei/function of CN V:
mesencephalic-proprioception
principle sensory-touch/pressure
spinal trigeminal-pain/temp
Muscles innv. by CN V
m. of mastication tensor tympani tensor veli palatini mylohyoid ant belly of digastric
Input to the spinal trigeminal nucleus:
CN V
CN VII
CN IX
CN X
Muscles innv. by CN VII:
facial m.
stapedius
stylohyoid
post belly of digastric
Role of solitary nucleus:
taste
GVE of CN IX/nucleus:
parotid gland through inf salivatory nucleus
GVE of CN VII/nucleus
submandibular glands through sup salivatory nucleus
Muscle innv by CN IX:
stylopharyngeus via nucleus ambiguous
Function of dorsal vagal nucleus:
parasympathetics to viscera
Medial medullary syndrome:
CN XII lesioned -> ipsilateral tongue deviation
medial lemniscus ->loss of discriminative touch/vibration and proprioception
Caused by occlusion of anterior spinal artery
Lateral medullary syndrome:
ALS lesioned -> contralateral pain/temp, crude touch
nucleus ambiguus-> no cough/gag reflex
Caused by posterior inferior cerebellar artery or vertebral a. infarct
Medial pontine syndrome:
CN VI ->ipsilateral eye abduction lost
contralateral touch/vib and proprioception lost
Caused by occlusion of paramedian branch of basilar artery
Lateral pontine syndrome:
CN VII motor -> facial weakness
salivatory nucleus -> dry eyes/mouth/nose
contralateral pain/temp and crude touch lost
Caused by anterior inferior cerebellar a.
When in glutamate released in the retina?
When there is no light stimulation (in the dark)
Purpose of Off/On Centers in retina:
creates contrast/edges in retina
Mechanism of rods/cones in dark:
Na+/Ca2+ channels opened by cAMP
cell is depolarized and releasing glutamate
Mechansim of rods/cones in light:
cAMP degrade by PDE
Na+/Ca2+ channels close
cell hyperpolarizes and glutamate not released
What do On-center cells do?
See light in a dark field
What do Off-center cells do?
See dark in a light field
Action of horizontal cells:
excitatory on surrounding rods/cones via GABA
Result of aneurysm of opthalmic artery:
loss of vision in one eye
Result of pituitary tumor:
tunnel vision
nasal retina axons impinged (posteromedial OX)
Result of aneurysm of anterior cerebral artery lateral to OX:
loss of vision on ipsilateral side with 1/2 of contralateral side loss
M and P in LGB:
M-from rods, large axons
P-from cones, small axons
Result of infarct of anterior choroidal artery:
loss of contralateral lateral field of vision
Retinotopy of LGB:
ipsilateral side- 2,3 and 5
contralateral side- 1,4 and 6
M and P layers:
M- 1,2 (black and white)
P- 3-6 (color)
Pathway for pupillary reflex:
CN II
pretectal area
EWN
CN III
Pathway for eye tracking:
CN II
SC
pulvinar/LP nuclei of thalamus
parietal/frontal cortex
Meyer’s Loop:
inf pathway
from ventrolateral LGB
carries upper field of vision
Baum’s Loop:
sup pathway
from dorsomedial LGB
carries lower field of vision
Lesion of Meyer’s Loop:
superior homonymous quadrantanopia
Lesion of Baum’s Loop:
inferior homonymous quadrantanopia
Location for central (macular) vision in cortex:
posterior occipital lobe
Location for peripheral vision in cortex:
anterior occipital lobe
What is stria of Gennari:
extra band of white matter in visual cortex
Result of infarct of posterior cerebral artery:
macular sparing/circular tunnel vision
middle cerebral artery sometimes supplies post occipital lobe
Ocular dominance structure:
for stereovision (3D static) cells responding to different angles of light
Result of damage to areas 18, 20 or 21 in occipital lobe:
agnosia (cannot recognize things)
Visual impact on circadian rhythm:
suprachiasmatic nucleus via the retinohypothalamic tract
4 maps of superior colliculus:
visual space
body surface
auditory space
motor map
Meniere’s disease:
excess fluid/pressure in inner ear
causes hearing/balance defects
Function of cristae ampullaris:
detect angular/rotational motion
Kinocilium mechanism:
cilia pushed toward kinocilium->depolarization
cilia away from kinocilium ->hyperpolarization
Opens or closes Na+ channels
Spontaneous firing of vestibular cells:
100 spikes/s
allows deviation in either direction
Movement detection of utricle macula:
rotation
Movement detection of saccule macula:
nodding motion
Positioning of 3 semicircular canals:
horizontal
Anteriorly rotated 45 degrees
Posteriorly rotated 45 degrees
All at 90 degrees of each other
Activation of horizontal cristae ampullaris turning the head left:
Fluid stays in same place
Left cristae ampullaris pulls toward kinocilium ->depolarization
Right cristae ampullaris pulls away-> hyperpolarization
Outputs of vestibular nuclei: (4)
lateral vestibulospinal (balance)
medial longitudinal fasciculus (eyes)
VL/VP of thalamus to cortex
cerebellum
Synapses of vestibulospinal tracts:
interneurons of lamina VII and VIII
Nystagmus:
named from direction of fast movement
Caloric test:
Cold water->opposite side nystagmus
Warm water-> same side nystagmus
Cause of vertical nystagmus
Central lesion
Threshold of feeling:
about 130dB
dB at which vibrations can be felt
Impedance matching:
air/fluid waves converted efficiency
best between 300-3000Hz
Electrochemical gradient between endolymph and hair cells:
150mV, allows for higher sensitivity to frequencies
Hair cell stimulation:
basilar membrane displacement K+ from endolymph enters cell Ca+2 enters via voltage gated channels glutamate released Ca2+ dependent K+ channels repolarize cell
Coding of frequencies below 200Hz:
by cochlear nuclei
Sound localization nucleus:
superior olivary complex
Interaural timing disparities:
for large sound waves
interpret difference in time it takes to hit each ear
No interference from head
Interaural intensity disparities:
for small sound waves
interpret difference in intensity between each ear
Interference from head decreases intensity
Weber Test for hearing:
tuning fork on head
ear that sounds louder has air conduction loss
Rinne test for hearing:
tuning fork on mastoid process
once vibration stops, move in front of ear
should be able to hear
if not -> air conduction loss
Result of vestibular schwannoma:
Affects on CN VII and VIII
Loss of posterior column:
loss of discriminative touch, vibration, motion sense, and position sense
Often caused by neurosyphilis
Damage to ipsilateral thalamus:
Contralateral somatosensory loss
Result of normal pressure hydrocephalus:
urinary incontinence
memory defects
trouble walking
Small central cord lesion:
pain/temp bilaterally lost at level
Large central cord lesion:
total sensory loss below, sparing genitals
Cause of post cord syndrome:
Neurosyphilis
