Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/125

Click to flip

125 Cards in this Set

  • Front
  • Back
glutamate synthesis rate-limiting step
glutaminase
glutamate uptake/location of uptake
Na+ dependent transporter specific for glutamate

located: glia, neurons
glutamate receptors
kainate, NMDA, AMPA, metabotropic
glutamate autoreceptors
kainate
glutamate CNS effects
learning

excitotoxicity

epilepsy

motor control
glutamate CNS: learning
hippocampal NMDA receptors activated when 2+ neurons are simultaneously firing
glutamate CNS: excitotoxicity
trauma, stroke - excessive glutamate release

NMDA/kainate stimulation - increase intracellular Ca++/cell swelling, death
glutamate CNS: epilepsy
excess excitation/depolarization in foci
glutamate CNS: motor control
long projection from motor cortex to striatum
glutamate: kainate
autoreceptor
(inc) Na+
(dec) K+
excitatory
glutamate: NMDA
(inc) Ca++
(inc) Na+
(dec) K+
excitatory
glutamate: AMPA
(inc) Na+
(dec) K+
excitatory
glutamate: metabotropic
(dec) cAMP - Gi
(inc) IP3 - Gq
(inc) DAG - Gq
???
glutamate (glutamatergic) pathways
cortex to striatum
many short internuerons in all parts of brain
glutamate metabolism
glutamine synthase in glia
GABA synthesis rate-limiting step
glutamic acid decarboxylase
GABA uptake
Na+ dependent transport specific for GABA, taurine, glycine

different transporters located on glia, neurons
GABA metabolism
GABA-transaminase after glial uptake
GABA receptors
GABA-A, GABA-B
GABA CNS effects
anxiety

sedation

epilepsy

motor function
GABA: GABA-A
(inc) Cl-
inhibitory

subtypes: alpha(6), gamma(3), beta(4), delta, epsilon, rho
GABA: GABA-B
(dec) Ca++ - Go
(dec) K+
(dec) cAMP - Gi
inhibitory

receptor heterodimers may selectively activate Gi/Go
GABA CNS effects: anxiety
increased GABA function decreases locus cerulues output

GABAergic inhibition of amygdala, hippocampus
GABA CNS effects: sedation
overall increase in GABA function inhibits neuronal firing
GABA CNS effects: epilepsy
inhibits neuronal hyperactivity in foci, SN inhibits colliculi
GABA CNS effects: motor function
5 of 6 cerebellar neurons are GABAergic

caudate/putamen inhibits globus pallidus and SN via GABA
GABA CNS effects: Huntingtons chorea
degeneration of striatal GABA neurons
GABAergic pathways
striatum to substantia nigra
substantia nigra to colliculi
short interneurons in all parts of brain
norepinephrine synthesis rate-limiting step
tyrosine hydroxylase
norepinephrine uptake
Na+ dependent neuronal transmitter somewhat specific for NE
norepinephrine metabolism
neuronal MAO-A: 66%
glial MAO-B: 34%
norepinephrine receptors
alpha 1
alpha 2
beta
norepinephrine CNS effects
arousal
mood
BP regulation
memory
pain inhibition
norepinephrine: alpha 1
(inc) IP3 - Gq
(inc) Ca++
???
norepinephrine: alpha 2
(dec) cAMP - Gi
(dec) Ca++ - Go
inhibitory
norepinephrine: beta
(inc) cAMP - Gs
inhibitory
norepinephrine autoreceptors
alpha 2
norepinephrine CNS effects: arousal
reticular activating system to cortex, hypothalamus
norepinephrine CNS effects: mood
???
norepinephrine CNS effects: BP regulation
alpha 2 receptors in brain stem

nucleus tractus solitarius increases the baroreceptor reflex
norepinephrine CNS effects: memory
RAS to hippocampus, cortex
norepinephrine CNS effects: pain inhibition
RAS descending pathways to spinal cord
noradrenergic pathways
locus ceruleus to hippocampus, cortex, hypothalamus, BP control centers in brain stem
serotonin synthesis rate-limiting step
dietary tryptophan levels
serotonin uptake
Na+ dependent neuronal transporter specific for serotonin
serotonin metabolism
neuronal MAO-A: 99%
serotonin receptors
5-HT1 family
5-HT2 family
5-HT3
5-HT4,6,7
serotonin CNS effects
sleep, arousal
inhibitory sensory transmission
pain inhibition
anxiety/depression, aggression
psychosis
emesis
migraine
serotonin: 5-HT1 family
A,B,D,E,F
(dec) cAMP - Gi
(dec) K+
inhibitory
serotonin: 5-HT2 family
A,B,C
(inc) IP3 - Gq
(inc) DAG - Gq
excitatory
serotonin: 5-HT3
ligand-gated ionophore
(inc) Na+
(dec) K+
excitatory
serotonin: 5-HT4,6,7
(inc) cAMP - Gs
???
serotonin: 5-HT5
(dec) cAMP - Gi
???
serotonin CNS effects: sleep, arousal
rostral RAS to cortex, hypothalamus
serotonin CNS effects: inhibit sensory transmission
rostral RAS to thalamus, cortex
serotonin CNS effects: pain inhibition
caudal RAS to lamina II spinal cord
serotonin CNS effects: anxiety/depression, aggression
5-HT1A in hippocampus, amygdala
serotonin CNS effects: psychosis
5-HT2 receptors in prefrontal cortex and NAc
serotonin CNS effects: emesis
5-HT3 receptors in area postrema
serotonin CNS effects: migraine
5-HT1D receptors on cranial blood vessels
serotonin autoreceptors
5-HT1B,D
serotonergic pathways
rostral raphe nuclei to anterior brain regions

caudal raphe nuclei to spinal cord, brain stem
dopamine synthesis rate-limiting step
tyrosine hydroxylase
dopamine uptake
Na+ dependent neuronal transporter specific for DA
dopamine metabolism
neuronal MAO-A
glial MAO-B: 30-50%
extracellular COMT
dopamine receptors
D1-like
D2-like
dopamine CNS effects
euphoria, addiction
motor systems
schizophrenia
prolactin inhibition
emesis
dopamine autoreceptors
D2/3
dopamine: D1-like
(inc) cAMP - Gs
inhibitory
dopamine: D-2 like
(dec) K+
(dec) cAMP - Gi
(dec) Ca+ - Go
dopamine CNS effects: euphoria, addiction
VTA to nucleus accumbens, frontal cortex
dopamine CNS effects: motor systems
substantia nigra to striatum
dopamine CNS effects: Parkinson's disease
deficit in DA - hypokinesia
dopamine CNS effects: Huntington's chorea
excess DA - involuntary movements
dopamine CNS effects: schizophrenia
imbalance of D2, D3, D4 subtypes
dopamine CNS effects: prolactin release inhibition
hypothalamus to anterior hypophysis
dopamine CNS effects: emesis
D2 receptors in area postrema
dopaminergic pathways
substantia nigra to caudate/putamen
ventral tegmental area to nucleus accumbens
hypothalamus to pituitary gland
Parkinson's disease
too little DA
too much ACh
too much GABA

hypokinesia
rigidity
tremor
Huntington's chorea
too much DA
too little ACh
too little GABA

hyperkinesias
chorea
acetylcholine synthesis rate-limiting step
choline uptake
actetylcholine uptake
Na+ dependent neuronal transporter specific for choline
acetylcholine metabolism
extracellular acetylcholinesterase
acetylcholine receptors
muscarinic: M1, M2, M3, M4
nicotinic: alpha, beta, gamma, delta, epsilon
acetylcholine CNS effects
learning
motor control
acetylcholine autoreceptors
M2
acetylcholine: M1
(inc) DAG - Gq
(inc) IP3 - Gq
excitatory
acetylecholine: M2
(dec) cAMP - Gi
(dec) K+
inhibitory
acetylcholine: M3
(inc) IP3 - Gq
(inc) DAG - Gq
excitatory
acetylcholine: nicotinic
(inc) Na+
(dec) K+
(inc) Ca++
excitatory
acetylcholine CNS effects: learning
basal nucleus to cortex
septal nuclei to hippocampus
acetylcholine CNS effects: motor control
short interneurons in striatum

loss of DA inhibition causes excess ACh, excess ACh causes resting tremor
cholinergic pathways
short interneurons in caudate/putamen

basal nucleus to frontal cortex, parietal cortex, thalamus

septal nucleus to hippocampus

pons to thalamus, hypothalamus

***lose ACh nuerons in Alzheimer's disease
opiod peptide synthesis
cell specific mRNA translated into precursor proteins
precursor proteins transported, stored in vesicles
precursor proteins enzymatically cleaved into products
cleavage is cell-specific
opiod peptide synthesis
none
opiod metabolism
rapidly degraded by extracellular peptidases
opiod receptors
mu, kappa, delta

(dec) cAMP
(dec) Ca++
(dec) K+
ALL inhibitory
opiod CNS effects
analgesia
respiratory depression
euphoria/dysphoria
miosis
sedation
muscular rigidity
nausea
endocrine
opiod CNS effects: analgesia
mu, kappa and delta receptors in spinal cord, PAG, thalamus, cortex, limbic system
opiod CNS effects: respiratory depression
mu receptors in medulla
opiod CNS effects: eupohoria/dysphoria
mu, kappa, delta receptors in VTA, NAc
opiod CNS effects: miosis
mu, kappa receptors in Edinger-Westphal nucleus
opiod CNS effects: sedation
mu, kappa receptors, inhibition of locus ceruleus
opiod CNS effects: muscular rigidity
mu, kappa, delta receptors in nigrostriatal tract
opiod CNS effects: nausea
mu receptors in chemoreceptor trigger zone
opiod CNS effects: endocrine
mu receptors in hypothalamus inhibit gonadotrophin
temporal cortex
primary auditory processing area
occipital cortex
primary visual processing area
hypothalamus
endocrine center
parietal cortex
primary sensory (tactile) processing area

stimulates caudate nucleus
frontal cortex
primary motor processing area

executive function
substantia nigra
inhibits caudate nuclei
putamen
"brakes" of the basal ganglia

basal ganglia afferent region
raphe nuclei
inhibitory center of RAS
globus pallidus
basal ganglia efferent region
locus ceruleus
stimulating center of RAS
dynorphin
small interneurons are present in ventral spinal cord
met-enkephalin
small interneurons are present in dorsal spinal cord
beta-endorphin
cell bodies project from arcuate nucleus to periaqueductal gray
acetylcholine
cell bodies project from septum to hippocampus

rate-limiting step is Na+ dependent transporter
norepinephrine
cell bodies project from locus ceruleus to cortex

shares almost same synthetic pathway as dopamine
dopamine
overactivity is implicated in Huntington's chorea

overactivity is implicated in drug addiction

cell bodies project from ventral tegmental area to nucleus accumbens
GABA
underactivity impliated in epilepsy

shares almost same synthetic pathway as glutamate

cell bodies project from caudate nucleus to substantia nigra
serotonin
cell bodies project from from raphe nucleus to spinal cord

rate-limiting step is dietary levels of precursor molecule
glutamate
overactivity implicated in epilepsy

cell bodies project from cortex to caudate and putamen