Neuroanatomy Flashcards
Basal ganglia
Corpus striatum (caudate, putamen)
Pallidum
Substantia nigra
Subthalamic nucleus
Caudate
OCD
Tics
Huntington
Putamen
Methanol
Globus pallidus
CO monoxide
Wilson’s
Subthalamic nucleus
Ballistic movements
Ideational apraxia
Acts in isolation but not in sequence
Alzheimer’s
Ideomotor apraxia
Can do something spontaneously but not on command (learned sequence)
Wernicke, callosal
MOST COMMON
Facial recognition
Left inferior temporal cortex
Olfactory processing
Right frontal lobe
Prosody
Body language
Right hemisphere
Semantic language
Temporal
Level of consciousness
Ascending reticular activating system
Attention
Right frontal lobe HYPOMETABOLISM
Brain structures involved in memory
Medial temporal lobe
Certain diencephalic nuclei
Basal forebrain
Which areas damaged in thiamine deficiency?
Mammillary bodies
Left hemisphere
Analytical
Lesion in left hemisphere = depression (because only right emotional hemisphere active)
Right hemisphere
Emotional
Lesion in right hemisphere = anosognosia (because only left analytical hemisphere active)
Temporal lobe epilepsy
HYPOsexuality Emotional intensity Perseverative approach to interactions (VISCOSITY) Aggression between seizures Seizures evoke fear
Left prefrontal cortex
Activation = elevated mood (GELASTIC SEIZURE = ictal laughter)
Lesion = depression
Right prefrontal cortex
Activation = depression
Lesion = laughter, euphoria, witzelsucht (jokes + pun)
Serotonin
Cell bodies in midline raphe nuclei of the brainstem
< 2% in CNS, 80% in GI (doesn’t cross BBB)
Made from TRYPTOPHAN
Rate-limiting enzyme = tryptophan hydroxyls
Carbs increase tryptophan
Proteins decrease tryptophan
Low serotonin = aggression
No serotonin activity during REM sleep
Dopamine
Caudate
Made from TYROSINE
Tyrosine –> L-dopa –> Dopamine –> Norepinephrine
Norepinephrine
Locus ceruleus (pons) Lateral tegmental nuclei
Made from TYROSINE
Tyrosine –> L-dopa –> Dopamine –> Norepinephrine
END PRODUCT INHIBITION is rate limiting step
Degraded by MAO = PRESYNAPTIC
Degraded by COMT = POSTSYNAPTIC
To epinephrine = PNMT
Not firing during REM sleep
Histamine
Posterior HYPOTHALAMUS = TUBEROMAMMILLARY NUCLEUS
Decarboxylation of histidine
Not firing during REM sleep
Acetylcholine
Basal forebrain complex + mesopontine complex
RATE LIMITED BY UPTAKE OF CHOLINE FROM BLOOD
REM PROMOTING
MAO-A
Deaminates serotonin and NE
MAO-B
Deaminates dopamine and histamine
Dopamine metabolite
HOMOVANILLIC ACID (HVA)
Norepinephrine metabolite
MHPG (3-methoxy-4-hydroxyphenylglycol)
Acetylcholinesterase
Localized to cholinergic neurons
Butyrylcholinesterase
Primarily in liver, plasma and glia
3 known monoamine transporters?
- SERT (serotonin)
- DAT (dopamine)
- NET (norepinephrine)
Mo histamine or acetylcholine
Cocaine blocks what?
DAT (dopamine transporter)
Buspirone
5HT1a partial agonist
Alpha 1
activating INCREASES serotonin activity
Alpha 2
activating DECREASES serotonin activity
5HT3
Agonist = antiemetic
Pramipexole
D3 agonist
Melatonin
Acts on suprachiasmatic nuclei of HYPOTHALAMUS
Also produced in retina + intestine
Glutamate
Postsynaptic effects mediated by 2 families of receptors:
- Glutamate-gated cation channels (NMDA, AMPA, KA)
- Metabotropic glutamate receptors (G protein coupled, alpha, dopamine receptors)
Excitotoxicity in Alzheimer’s disease
B-amyloid DEPOLARIZES neurons = loss of magnesium block = increased NMDA receptor sensitivity for glutamate
MEMANTINE = WEAK INHIBITOR OF NMDA RECEPTOR targets this glutamate excess in AD
GABA
Synthesized from glutamate by removal of a single carboxyl group by DECARBOXYLASE
GABA-a receptor
FAST
Cl- influx causing hyper polarization (INHIBITION)
GABA-b receptor
SLOW
Potently activated by baclofen
Glycine
INHIBITORY
Schizophrenia
GABAergic deficit (decreased decarboxylase activity) Upregulated GABA-a receptors Hypofunction of NMDA receptors
DECREASED CSF AND BLOOD LEVELS OF D-SERINE
Alcohol dependency
Downregulation of GABA-a receptor
UPREGULATION OF NMDA RECEPTORS
Withdrawal = hyper excitable state as a result
Supersensitive NMDA receptors due to thiamine deficiency contribute to excitotoxicity (Wernicke-Korsakoff)
Anterior pituitary
ACTH
TSH
LH
Posterior pituitary
ADH
Oxytocin
Papez circuit
Hippocampus Fornix Mamillary bodies Anterior nucleus of hypothalamus Cingulate gyrus
NOT AMYGDALA
For learning and storing memories
Which psych illness does not suppress dexamethasone on test?
MDD!
MDD
Decreased TSH response in TRH test
PTSD
LOW cortisol
HIGH norepinephrine and epinephrine
Increased suppression dexamethasone test
Low beta-endorphins
RIGHT HEMISPHERE LOCALIZATION
OCD
Decreased basal ganglia
Increased anterior cingulate cortex
Increased thalamus
Amygdala asymmetry
Anomalies orbitofrontal cortex
Wilson’s
Lenticular nuclei
(Putamen > Pallidus)
Cerebellum
Cerebral cortex
Akinetic mutism
FRONTAL LOBE
ANTERIOR CINGULATE CORTEX
Anomia
ANGULAR GYRUS
DOMINANT PARIETAL LOBE
Anosognosis
NON-DOMINANT PARIETAL LOBE
Understanding emotions in speech of others
NON-DOMINANT TEMPORAL LOBE
Cortical
Aphasia
Apraxia
Agnosia
Seizures
Subcortical
Executive deficits
Memory retrieval deficits
Slowing
Astereognosia
Can’t recognize objects by touch
Prosopagnosia
Don’t recognize familiar faces
FUSIFORM GYRUS (NON-DOMINANT TEMPORAL/OCCIPITAL LOBE)
Atopognosia
Denial of a part of the body
Aprosody
Can’t recognize emotional qualities of speech
NON-DOMINANT FRONTAL LOBE
Conduction aphasia
ARCUATE FASCICULUS
Altered repetition
Comprehension and speech intact
Extrapyramidal system
Connects cerebral cortex, basal ganglia, vestibular system, thalamus, cerebellum, reticular formation, spinal
DOES NOT INCLUDE LOCUS CERULEUS
Red nucleus = involved in motor
Ventromedial nucleus (hypothalamus)
SATIETY
Lesion = increased appetite, rage
Lateral nucleus (hypothalamus)
HUNGER
Lesion = decreased appetite
