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Pharmacology and Medical Chemistry I > Exam 2 (Lecture 12/13) > Flashcards

Exam 2 (Lecture 12/13) Flashcards

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1
Q

Sympathetic

A

Fight or flight

Thoracolumbar

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2
Q

Parasympathetic

A

Rest and Digest

Craniosacral

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3
Q

Neuron

A

fundamental units of the nervous system for transforming and relaying the electrical signals

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4
Q

Astrocyte

A

provides biochemical support of endothelial cells that form the blood–brain barrier (BBB),
supplies nutrients to the nervous tissue

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5
Q

Oligodendrocyte

A

provides he axon of long-range projection neurons insulation by a myelin sheath

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6
Q

Vasculature

A

supplies oxygen and nutrients, the brain would quickly suffer damage from any stoppage
in blood supply

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7
Q

Myelin Sheath

A

insulates the projections of neurons and increases conductivities.

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8
Q

Schwann Cells found in

A

PNS

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9
Q

Oligodendrocytes found in

A

CNS

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10
Q

Blood Brain Barrier

A

functions as a border that prevents solutes in the circulating blood from non-selectively to avoid toxic substance coming in.

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11
Q

Soma

A

cell body; perikaryon

contains nucleus and most of cytoplasm
features of active secretory cell (large nucleus, lots of endoplasmic reticulum, prominent Golgi)

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12
Q

Dendrites

A

information “receiving” elements

fine processes extending from soma in tree-like arrangement;

can be many along with soma comprises receptive field of neuron

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13
Q

Axon

A

information “transmitting” element

a thin process extending from axon hillock (initial segment of axon as it leaves soma) along which action potential is conducted

one per neuron: can be long or short, single or branched, myelinated or not myelinated

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14
Q

Axon Terminal

A

(terminal boutons; presynaptic terminals)
swelling of axon at its terminal end, enriched with vesicles containing neurotransmitter

forms “synaptic contact” with receptive region of
a second neuron (i.e. a postsynaptic neuron)

swellings filled with vesicles can also occur along length of axon giving rise to a beaded appearance (these swellings are called varicosities); may form synapses

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15
Q

Basic Elements of chemical neurotransmission

A
  1. Arrival of action potential at axon terminal
  2. Depolarization of axon terminal membrane
  3. Influx of Ca++ into terminal via voltage-gated Ca++ channels
  4. Fusion of vesicles with terminal membrane
  5. Extrusion of vesicle contents into synapse: exocytosis
  6. Binding of transmitter to postsynaptic receptors
  7. Opening of chemically-gated ion channel
  8. Change in membrane potential
    EPSP if Na+ Channels open (depolarization)
    IPSP if K+ or Cl- channels open (hyperpolarization)
  9. Termination of transmitter action by re-uptake into presynaptic terminal, or by enzymatic degradation, or both
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16
Q

Criteria for Neurotransmitter

A
  1. Substance must be present in presynaptic neuron and its terminals (precursors and synthetic enzymes should also be present)
  2. Substance must be released from presynaptic terminals with neuronal activity
  3. Effects of the applied substance on a target neuron (postsynaptic cell) must be same as effects of stimulating the presynaptic neuron
    - antagonist of the substance should also block both
  4. Mechanism for the transmitter candidate’s inactivation must be present in the synapse
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17
Q

SNARE Cycle

A
  1. Synaptobrevin interacts with two plasma membrane target proteins, the transmembrane protein syntaxin and the peripheral membrane protein SNAP-25.
  2. The three proteins form a tight complex bringing the vesicle and presynaptic membranes in close apposition (see part B). Munc18 binds to the SNARE complex.
  3. Calcium influx triggers rapid fusion of the vesicle and plasma membranes; the SNARE complex now resides in the plasma membrane.
  4. Two proteins, NSF and SNAP (unrelated to SNAP-25), bind to the SNARE complex and cause it to dissociate in an ATP-dependent reaction.
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18
Q

Neurotransmitter structures

A 
Amines
Purines
Monoamines
Amino Acids
Endocannabinoids
Peptides
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19
Q

Linked to cationic channels (excitatory)

A

Glutamate

Aspartate

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20
Q

Linked to anionic channels (inhibitory)

A

GABA

Glycine

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21
Q

Glycine

A

• Receptor antagonist: strychnine
• Mechanism of action: similar to GABA (i.e.
increases Cl- conductance)
• Major inhibitory transmitter in spinal cord

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22
Q

γ-Aminobutryic acid (GABA) cycle

A
  • Reuptake (GAT1)
  • Transport into glial cells (GAT3)
  • Conversion to glutamine (GS)
  • Transport into GABAergic neuron (SAT)
  • Package into vesicles (VGAT)
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23
Q

Glutamic acid (glutamate) cycle

A
  • Reuptake (GLT)
  • Transport into glial cells (GLT/GLAST)
  • Conversion to glutamine (GS)
  • Transport into GABAergic neuron (SAT)
  • Package into vesicles (VGLUT)
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24
Q

Glutamate synthesis

A

a dietary amino acid, also synthesized in neurons from precursor glutamine

25
Q

Glutamate receptor subtypes

A

NMDA, AMPA, Kainate = ligand-gated

mGLuR 1-8 = metabotropic

26
Q

Glutamate receptor angonists

A 
monosodium glutamate (MSG, food additive, flavor enhancer)
Kainic acid (potent neurotoxin, excites neurons to death)
27
Q

Glutamate mechanism of action

A

increases in membrane cation (Na+ and Ca++) permeability thereby depolarizing neuronal membrane

28
Q

LTP

A

Long Term potentiation

Increase AMPA
Synaptic strengthening

Post synaptic end senses Glutamate, increases receptors to adjust, they stay for a period

29
Q

LTD

A

Long term depression

Synaptic weakening
decreasing AMPA
receptors get internalized, fewer at surface

30
Q

Acetylcholine (ACh) synthesis

A

Choline + Acetyl Coenzyme A = Acetylcholine + Coenzyme A via Choline acetyltransferase

31
Q

ACh inactivation

A

Acetyle Choline = Choline + Acetate via acetylcholinesterase

32
Q

2 Classes Cholinesterase enzymes

A

acetylcholinesterase “true” - neural tissue, in synaptic cleft

Butyrlcholinesterase “pseudo” - plasma, liver

33
Q

ACh receptors

A

Nicotinic = ligand-gated ion channel, agonist is nicotine

Muscarinic = g-protein coupled M1-M5 subtypes, agonist is muscarine

34
Q

ACh cycle

A
  • Degradation (AChE)
  • Transport into presynaptic site (CHT)
  • Conversion to ACh (ChAT)
  • Package into vesicles (VAChT)
35
Q

Catecholamine synthesis

A

Tyrosine -> Dopa via Tyrosine Hydroxylase (TH)
Dopa -> Dopamine via AADC (or DOPA decarboxylase)
Dopamine -> Norepinephrine vis DBH
Norepinephrine -> Epinephrine via PNMT

36
Q

Catecholamine inactivation

A
  1. Re-uptake = Rapid (blocked by cocaine and tricyclic antidepressants
  2. Enzymatic Degradation = slower 2 enzymes
    MAO and COMT
37
Q

MAO

A

Monoamine oxidase

blocked by drugs known as MAO inhibitors
primarily intraneuronal, cytoplasm of nerve terminal

38
Q

COMT

A

Catechol-o-methyltransferase

Extraneuronal metabolism

39
Q

Catecholamine Cycle

A

Reuptake (DAT/NET)

Package into vesicles (VMAT2)

40
Q

dopamine receptors

A

All G-protein coupled, D1-D5

41
Q

Norepinephrine receptors

A

two families, designated α and β, all G- protein coupled

42
Q

Serotonin (5-HT) synthesis

A

Tryptophan -> 5-hydroxytryptophan via TPH

5-hydroxytryptophan - > Serotonin via AADC

43
Q

Serotonin cycle

A

Reuptake (SERT)

Package into vesicles (VMAT2)

44
Q

Serotonin receptors

A

5HT3 - ligand-gated ion

All others are G-protein

45
Q

Histamine Synthesis

A

Histidine -> Histamine via Histidine Decarboxylase

46
Q

Histamine Metabolism

A

histamine N-methyltransferase

47
Q

Glutamate apoptosis (Excitotoxicity

A

All signaling activated by calcium, leading to cell death

48
Q

Ultra Short neurons

A

retina and olfactory bulb neurons

49
Q

Intermediate length neurons

A

Hypothalamus to pituitary (mediate endocrine functions)

50
Q

dopaminergic pathways

A

A9, motor functions, substantia nigra pars compact to striatum

A10, mediate pleasure and reward, Ventral Tegmental area to limbic areas of brain

51
Q

Norepinephrine pathways

A

A1,A2,A5,A7

52
Q

Serotonergic pathway

A

begins Raphe nuclei

53
Q

H1 receptor

A

antihistamine target

54
Q

H2 receptor

A

Gastric acid secretion target

55
Q

Peptide transmitters

A

mRNA -> rough ER to make -> Golgi to pack -> move to synapse via large dense-core vesicles -> no reuptake, catabolic peptidases turn into inactive metabolite once released in synapse.

Need more control/ high frequency for release not CA like other neurotransmitters.

56
Q

GABA A/C

A

ionotropic receptor - fast

57
Q

GABA B

A

G protein receptor

58
Q

Cholinergic Pathways

A

Originate in Nucleus Basalis of Meynert

59
Q

Where do Norepinephrine neurons originate?

A

Locus Ceruleus

Pharmacology and Medical Chemistry I (30 decks)

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