week 2- neurotransmitters

Question 1

ID

Answer 1

Question 2

name the three types of axonic connections

Answer 2

axoaxonal

axodendritic

axosomatic

Question 3

differentiate classic versus PT NTs

Answer 3

classic- synthesized and packaged at the terminal

peptide- translated and packaged in the cell body

Question 4

differentiate the impact of chronic adminstration of an agonist versus antagonist

Answer 4

chronic agonist- results in receptor downregulation

chronic antagonist results in receptor upregulation

Question 5

ID the 11 ways that you can target synaptic transmission

Answer 5

Question 6

name the enzyme used to convert glutamine to glutamate and where it is converted

Answer 6

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

Question 7

ID all of the glutamate receptors and their channel type and their ionic flow

name a + allosteric modulator

and a synthetic antagonist for NMDA

Answer 7

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)

Question 8

steps for NT release

Answer 8

Question 9

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

Answer 9

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

Question 10

what enzyme created acetylcholine

Answer 10

choline acetyltransferase from Acetyl CoA and choline

Question 11

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

Answer 11

blocking the autoreceptor- indirect agonist and would increase NT

stimulating the autoreceptor- would result in decreased NT

Question 12

What type of acetycholine receptors are present in the brainstem and in the basal forebrain and what do they function in

Answer 12

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)

Question 14

what is the molecular mechanism behind Myasthenia gravis and how can you treat this

Answer 14

antibodies against the postsynaptic AcH receptors, can target with acetyccholinesterase inhibitors to increase ach at the cleft

Question 15

how does a black widow spider bite impact the nervous system

Answer 15

stimulated ACH rlease

Question 16

what AA do you need for catecholamines synthesis

Answer 16

Question 17

Differentiate between the dorsal and ventral pathways for dopamine

Answer 17

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

Question 18

what is the impact on amphetamines and cocaine on the dopaminergic system

Answer 18

amphetamines- releases cathecolamine

cocoaine- inhibits cathecolamine reuptake

haloperadol (schitozphrenia)- antagonist to D2

Question 19

name the important brain region for NE and its function

Answer 19

Locus coeruleus (Pons) projections to forebrain and spinal cord (a diffuse neuromodulatorysystem): α and β adrenergic receptors throughout CNS: Attention, arousal, wakefulness, stress responses.

Question 21

how do drugs for depression impact NE system

Answer 21

desipramine- inhibits Ne uptake

Question 22

what is the brain region involved in serotonin release, its pathway and impact on behavior

Answer 22

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

Question 23

decribe the new theory of depression

Answer 23

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.

Question 24

Where are opoid receptors and how do they regulate pain

Answer 24

•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

Question 25

where are CB receptors in the brain and what do they do

Answer 25

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

Question 26

enzymes involved in NE synthesis

Answer 26

Question 27

enzymes involved in serotonin synthesis

Answer 27