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Biochemistry Year 2 > Neurotransmitter Classification > Flashcards

Neurotransmitter Classification Flashcards

1
Q

neurotransmitters are classified based on

A
  • chemical nature
  • response they elicit
  • their receptors mechanism of action
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2
Q

how is the activity of a neurotransmitter changed?

A

regulated by changing the rates of synthesis and release at the synapse, and by blocking reuptake and degradation

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3
Q

what is the endocannainoid system

A

a group of endogenous cannabinoid receptors located in the mammalian brain and throughout the central and peripheral nervous systems, consisting of neuromodulatory lipids and their receptors

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4
Q

list criteria necessary to be a nt

A
  • synthesis in the neuron
  • storage within nerve ending
  • release in response to stimulus
  • bonding and recognition at post synaptic cell
  • mechanism for inactivation and termination of activity
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5
Q

name some neuromodulators

A
  • NO
  • adenosine
  • neurosteroids
  • polyamines
  • lipids
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6
Q

how are nt released?

A

(A) In the resting state, vesicles are attached to microtubules.
(B) When an action potential is received, calcium channels open. (C) Vesicles move to the plasma membrane, and (D) bind to a complex of docking protein
(E) Neurotransmitter is released, and
(F) vesicles are recycled

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7
Q

name amine nts

A

Ach, norepinphrine, epinephrine, dopamine, 5-HT

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8
Q

name amino acid nts

A

glutamate GABA

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9
Q

Name purine nts

A

ATP, adenosine

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10
Q

name gase nts

A

NO

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11
Q

name peptide nts

A

endorphons, tachykinins

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12
Q

name lipid nts

A

anandamide, 2-AG (arachidony glycerol)

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13
Q

excitatory nts

A 
Acetylcholine 
Aspartate 
Dopamine 
Histamine 
Norepinephrine 
Epinephrine 
Glutamate 
Serotonin
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14
Q

inhibitory nts

A

GABA
Glycine
Anandamide
2-AG

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15
Q

fast mode nts use

A

ionotropic receptors

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16
Q

modulatory mode nts use

A

GPCR (metabotopic receptors)

17
Q

how is Ach synthesized

A

in cholinergic neurons, by choline acetyltransferase. you need choline and acetyl coA as reactants

18
Q

where is Ach released and why

A

Motoneurons at the level of the neuromuscular junction (muscle contraction)
Pre-ganglionic neurons of the sympathetic nervous system and parasympathetic post-ganglionic neurons (slowing of the heart rate, bronchoconstriction, stimulation of intestinal smooth muscle)
Neurons of the reticular system (wakefulness, sleep-wake transition)
Cholinergic synapses of basal ganglia (learning, memory)

19
Q

what are the 2 cholinergic receptors

A
  • nicotinic (ionotropic):
  • Nm depolarization of NMJ
    -Nn activation of post ganglionic neurons
  • muscarininc receptors (metabotropic)
    -M1: Depolarization of autonomic and CNS neurons
    – M2 Negative inotropic and chronotropic effects on the heart
    – M3 Stimulate sweat, bronchial, salivary and gastric acid secretion; increase NO production from vascular endothelium and vasorelaxation
20
Q

how to remove Ach from synaptic cleft

A
  • ACh released from synaptic vesicles is hydrolyzed to choline and acetate by acetylcholinesterase (AChE), an enzyme that is localized in the synaptic cleft. Choline is a poor binder of the cholinergic receptors, however is taken up by the uptake system on the presynaptic membrane
  • The remainder of ACh (i.e., that has not been hydrolyzed by acetylcholinesterase) is taken back up into the pre-synaptic nerve by specific transporters (reuptake).
21
Q

explain ACHe

A

is an enzyme which hydrolyses Ach, its active site contains 2 subsites. An anionic subsite to bind Ach to the enzyme. The esteratic subsite where the hydrolytic action occurs, releasing acetate and choline

22
Q

list the 3 ionotropic glutamate receptors

A

AMPA
NMDA
KAINATE

23
Q

GABA-a receptors are

A

ionotropic, and ligand gated Chloride channels

24
Q

GABA-b receptors are

A

metabotropic

25
Q

benzodiazepines bind to

A

GABA-a, cause a potentiation of the response to endogenous GABA; these drugs reduce anxiety and also cause muscle relaxation

26
Q

barbiturates bind to

A

GABA-a, stimulate them directly in the absence of GABA; because of this lack of dependence on endogenous ligand, they are more likely to cause toxic side effects in overdose.

27
Q

how is GABA re-uptaken?

A

by plasma membrane transporters (symports):

GABA transporters 1-3 (GAT-1, GAT-2, GAT-3) Betaine-GABA transporter-1 (BGT-1) (GAT1-3 in brain, BGT-1 mostly in kidney but also present in brain)

28
Q

where is glycine found?
what does it do?
what kind of receptor is it?

A
  • inhibotry nerons in spinal cord
  • where it blocks impulses travelling down the cord in motor neurons
  • ionotropic. And is blocked by strychinine. They are ligand gated chloride channels.
29
Q

all catecholamines (dopamine, nor-/epinephrine) are derived from?

A

tyrosine.

They are biogenic amines. They are released through varicosities along the axon not only the end of it.

30
Q

where is epinehrine produced

A

adrenal medulla

31
Q

L-DOPA in melanocytes is the precursor or

A

melanins

32
Q

norepinephrine is the major transmitter in

A

sympathetic nervous system, in post ganglionic neurons. for fight or flight. Also in the brainstem, for overall awareness or attention (locus ceruleus)

33
Q

amphetamines

A

have stimulatory effects since they increase the concentration of catecholamines in the synaptic cleft

34
Q

epinephrin traits

A
  • influences heart, lung
  • redirection of blood to skeletal muscle
  • stimulatory effects on glycogen metabolism in liver
  • is not essential for life
35
Q

dopamine traits

A
  • nerves that interconnect the nuclei of the basal ganglia in the brain and control voluntary movement
  • damage causes parkinsons
  • schizophrenia
  • causes vasodilation and used for treatment of renal failure
  • found in the nigrostriatal tract
36
Q

how are catelcholamines catabolised?

A
  • half life of 1 min
  • Monoamine oxidase (MAO): catecholamines by oxidative deamination to yield the corresponding aldehyde.
    Catechol-O-methyltransferase (COMT) also inactivates catecholamines by methylation using S-adenosylmethionine (SAM) as the one-carbon donor.
    MAO inhibitors and methamphetamine block catecholamine degradation, allowing their accumulation in the presynaptic neuron and subsequent leakage into circulation, providing an antidepressant action.
37
Q

serotonin

A

aka 5-HT

  • Trp hydrolase need cofactor BH4
  • 5-HT is converted to serotonin by DOPA decarboxylase
  • in raphe nuclei, more active when awake
  • involved in feeding, sexual behavior, temperature
38
Q

how is serotonin broken down?

A
  • oxidation by monoamine oxidase

- dehydration: aldehyde deydrogenase

39
Q

NO

A
  • in ANS and enteric NS is made from arginine by BH4 NOS.
  • excessive NO= alzheimers and parkinsons
  • is not stored in vesicles but released immediately

Biochemistry Year 2 (11 decks)

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