CNS Neurotransmitters Flashcards
glutamate: inhibitory or exitatory?
GABA: inhibitory or excitatory?
enzyme that converts glutamate to GABA
glutamate- excitatory
GABA- inhibitory
glutamic acid decarboxylase (GAD)
neuropeptide that functions as pain perception
substance P
EPSP vs IPSP; which one is hyperpolarizing? which is depolarizing?
EPSP- excitatory postsynaptic potential (glutamate); depolarizing
IPSP- inhibitory post synaptic potential (GABA); hyperpolarizing
are EPSPs or IPSPs fast or slow?
both can be fast or slow
acetylcholinergic receptors- nicotinic vs muscarinic: where are each found? are IPSPs/EPSPs slow or fast?
nicotinic: in PNS on NM junction; fast EPSP
muscarinic: in CNS in brain & autonomy. ganglia; fast IPSP, slow EPSP
location of glutamate neurons and the locations of their terminals
cns interneurons- local and long tract connections
primary sensory neurons- second-order neurons in CNS
pyramidal cells of cerebral cortex- basal ganglia, thalamus, spinal cord, other cortical areas
location of GABA neurons and their terminals
CNS interneurons- local connections
cerebellar cortex (purkinje cells)- deep cerebellar nuclei
caudate nucleus, putamen- globus pallidus, substantia nigra
globus pallidus, substantia nigra- thalamus, subthalamic nuclei
thalamic reticular nucleus- other thalamic nuclei
believed to be the source of learning
glutamate NMDA receptor
the NMDA receptors requires these 2 things
glutamate/NMDA
AND
depolarization (voltage-gated)
the depolarization of the Glutamate NMDA receptor frees…
Mg2+ that blocks the channel at rest, allowing influx of Ca2+, which augments transmission at the synapse
regulation of the strength of connection between two synapses
synaptic plasticity
describe pathology and causes of glutamate toxicity
excessive Ca2+ intake triggers neuronal injury/death; stems from excessive glutamate release, or poor glutamate reuptake; stroke anoxia can release toxic amts of glutamate
GABA hyperpolarizes the cell by influx od
Cl-
GABAa- ligand gated
GABAb- GPCR
benzos and barbituates bind to these receptors
GHB, alcohol, baclofen bind to these types of receptors
GABAa
GABAb
disease models of GABA excess or inhibition
huntingtons- destruction of GABA nerons
tetanus and strychnine- inhibit presynaptic GABA release
stiff-person syndrome- antibodies to GAD prevent GABA production, causing autoimmune or paraneoplastic syndrome
excess- seizures
treat seizures (too much glutamate) with more GABA via these drugs..
benzos- increase GABA efficiency
valproate- inhibit GABA-deactivating enzymes
topiramate- inhibit GABA reuptake
side effects: sedation, cognitive slowing
non-therapeutic GABA
anxiolysis, hypnosis, amnesia; date rate drugs (GHB, benzos)
nuclei of origin of dopamine
substantia nigra, ventral tegmental area, hypothalamus
nigrostriatal tract function of dopamine
fluid, smooth muscle action
mesolimbic tract function of dopamine
fear and reward responses
mesocortical tract function of dopamine
motivation and response
tubero-infundibular tract function of dopamine
secretion of hormones, notably prolactin
pathology of Parkinson’s disease
death of PARS COMPACTA within the SUBSTANTIA NIGRA
drugs that block dopamine reuptake, and cause exocytosis of dopamine, leading to excess dopamine
cocaine, methamphetamine- can cause paranoia, hallucinations, delusions, disorganized thoughts
why give L-DOPA to Parkinson’s patients?
increases dopamine by skipping the rate-limiting step (tyrosine hydroxylase)
drugs for depression and ADHD
buproprion/methylphenidate to prevent dopamine reuptake
many psychotics operate via..
D2 receptor antagonism- blocking the inhibition of adenylate cyclase, so cAMP is formed and PKA activated
nuclei of origin of serotonin; serotonin tracts
raphe nucleus (pons/midbrain)
brain: cortex, cerebellum, hypothalamus; spinal column, PNS
receptor subtypes for serotonin
5HT-1 and 2: mood, appetite, energy, sexual function
5HT-3: localized in area postrema/nausea
therapeutics for major depressive disorder
SSRIs, TCA and MAOIs
DOC for anxiety disorders
benzos
drug for nausea; its mechanism of action
ondansentron - 5HT-3 receptor antagonist
serotonin toxicity induced by excessive serotonin causes these symptoms
headache, delirium
autonomic: hyperthermia, hypertension
somatic: tremor, hyperreflexia, clonus
drugs and compounds that can be abused and cause serotonin syndrome
LSD, MDMA
tyramine “cheese effect”: MAOs decrease, tyramine increases, hypertension ensues
nuclei of origin of norepinephrine; tracts
locus ceruleus
broad projections throughout frontal cortex, limbic, spinal
norepinephrine receptors function to induce sympathetics or parasympathetics?
sympathetics
panic attacks may be caused by deficiency in
norepinephrine reuptake
antidepressants increase the availability of
norepinephrine
a selective norepinephrine and dopamine reuptake inhibitor drug
buproprion (wellbutrin)
selective serotonin/norepinephrine reuptake inhibitor drugs
venlafaxine (Effexor)
duloxetine (Cymbalta)
acetylcholine nuclei of origin
nucleus basalis of Mynert
pedunculopontine nucleus
acetylcholine tracts
pedunculopontine projects to thalamus, basal ganglia
nucleus basalis of mynert (NBM) projects to cortex
NMB/acetylcholine is associated with
memory, learning, deficits with Alzheimer’s, LIMBIC SYSTEM, HOMEOSTASIS
effect of acetylcholine in CNS and PNS
PNS: parasympathetic stimulation
CNS: inhibitory OR excitatory
acetylcholine toxicity symptoms, and what causes them
SLUDGE-M (pupil constriction)
organophosphates, sarin gas
disease involving degeneration of ACh-producing neurons at nicotinic receptors
Alzheimer’s
anti-muscarinic toxicity symptoms and causes
hot as a hare, blind as a bat, dry as a bone, mad as a hatter
anti-nausea meds, anti-depressants, anti-psychotics, antihistamines, atropine
stiff person syndrome associated with this transmitter
GABA
