week 2- neurotransmitters Flashcards
ID
name the three types of axonic connections
axoaxonal
axodendritic
axosomatic
differentiate classic versus PT NTs
classic- synthesized and packaged at the terminal
peptide- translated and packaged in the cell body
differentiate the impact of chronic adminstration of an agonist versus antagonist
chronic agonist- results in receptor downregulation
chronic antagonist results in receptor upregulation
ID the 11 ways that you can target synaptic transmission
name the enzyme used to convert glutamine to glutamate and where it is converted
glutaminase
astrocytes recycle glutamate from receptors and turn it into glutamine with the help of glutamine synthase, they then shuffle the glutamine to the neuron where it is turned into glutamate
enzyme: glutamine synthase is inside of astrocytes and glutaminase inside of the neuron
ID all of the glutamate receptors and their channel type and their ionic flow
name a + allosteric modulator
and a synthetic antagonist for NMDA
NMDA- Ca –> NA + CA
AMPA- NA –> NA
Kainate- NA–> NA
metabotriphic channel
- allosteric modulator: glycine
- antagonist: PCP and ketamine and Mg
(Mg within the channel of NMDA defines its on/off state)
steps for NT release
ID the enzyme that converts glutamate to GABA
differentiate A versus B
name some agonists
ID some BDZ agonist and antagonists
when are BDZ’s perscribed
glutamic acid decarboxylase
A- ionotrophic B- metabotrophic
alcohol and benzodiazepine, barbituates
BDZ Agonists: Anxiolytic, Amnestic, Sedative/hypnotic
BDZ antagonists: flumazenil ( can be used for reversal)
prescribed: muscle spasms, tremors, acute seizures, and alcohol and drug withdrawal symptoms
what enzyme created acetylcholine
choline acetyltransferase from Acetyl CoA and choline
describe actions that you could block stimulate at the level of the receptor in terms of agonist or antagonistic and their impact on NT release
blocking the autoreceptor- indirect agonist and would increase NT
stimulating the autoreceptor- would result in decreased NT
What type of acetycholine receptors are present in the brainstem and in the basal forebrain and what do they function in
brainstem reticular activing system- Muscularinic in thalmus and cortex to increase arousal and wakefulness by activating thalmocortico circuits
basal forebrain (N. basalis of meynert)- nicotinic and muscularinic in the neocortex and hippocampus to promote attention ( neocortex) and learning and memory (hipp)
what is the molecular mechanism behind Myasthenia gravis and how can you treat this
antibodies against the postsynaptic AcH receptors, can target with acetyccholinesterase inhibitors to increase ach at the cleft
how does a black widow spider bite impact the nervous system
stimulated ACH rlease
what AA do you need for catecholamines synthesis
Differentiate between the dorsal and ventral pathways for dopamine
dosal- •Meso striatal system (subs. nigrato caudate-putamen): D1 and D2 receptors in dorsal striatum; motor control, especially initiation of movement.
ventral-Mesolimbic system (ventral tegmental area to ventral striatum and limbic structures): D1 and D2 receptors in ventral striatum, frontal cortex, amygdala, and other limbic; appetitive or affective motivation (i.e. wanting), reward (but not pleasure per se), attention/arousal
what is the impact on amphetamines and cocaine on the dopaminergic system
amphetamines- releases cathecolamine
cocoaine- inhibits cathecolamine reuptake
haloperadol (schitozphrenia)- antagonist to D2
name the important brain region for NE and its function
Locus coeruleus (Pons) projections to forebrain and spinal cord (a diffuse neuromodulatorysystem): α and β adrenergic receptors throughout CNS: Attention, arousal, wakefulness, stress responses.
how do drugs for depression impact NE system
desipramine- inhibits Ne uptake
what is the brain region involved in serotonin release, its pathway and impact on behavior
region: raphe nuceli in midbrain-medulla
Pathway: Raphe nuclei projections to forebrain and spinal cord (a diffuse neuromodulatorysystem): multiple receptor subtypes:
Role: Modulates activity in all sensory systems (e.g. pain), regulation of emotional states, attention/arousal
decribe the new theory of depression
Depression is a disorder of synaptic plasticity (trophic theory of depression).
It’s time retire the monoamine theory of depression. Though monoamine abnormalities MAYbe involved in depression. Depression is not primarily a problem of low serotonin.
Where are opoid receptors and how do they regulate pain
•Opioid peptide-containing neurons (coexisting with other NTs) are primarily inhibitory distributed throughout pain pathways, limbic structures and the striatum: μ, δ, κ(all metabotropic) receptors
Pain regulation, endocrine control, regulation of motor activity, pleasure. But the impact on pain and pleasure are separate
wanting think dopamine, opoids think pleasure
Opioid peptides thus “close the gate”on ascending pain signals –> adaptive survival response. stress-induced analgesia
where are CB receptors in the brain and what do they do
Cannabinoid-containing neurons (coexisting with other NTs) are distributed throughout the CNS: CB-1 and CB-2 receptors (metabotropic),
retrograde signaling-decreases presynaptic NT release;Stimulates feeding, inhibits emesis, regulates pain.
also closes the gate on ascending pain pathway by diff mechanism
enzymes involved in NE synthesis
enzymes involved in serotonin synthesis
