Brain and Behavior Flashcards - Day 3

Question 1

Immediate (primary) vesicles

Answer 1

1000 vesicles at the presynaptic membrane; Primary vesicles interact with the neuronal cell membrane in order to facilitate their release

Question 2

Mobilization (secondary) storage vesicles

Answer 2

10,000 vesicles that can replace primary store in a few seconds

Question 3

Reserve (tertiary) storage vesicles

Answer 3

100,000 vesicles in the axon

Question 4

NMJ protein complex

Answer 4

the AChR is associated with several other proteins, including MuSK – often, defects in one of these other proteins can create a “bystander effect,” mimicking problems w/the AChR itself

Question 5

Compound Muscle Action Potential

Answer 5

If lower motor neurons innervating a muscle are depolarized and there is normal NMJ transmission, then all muscle fibers will generate action potentials. The sum of these action potentials is called the CMAP.

Question 6

Lambert Eaton Myasthenic Syndrome

Answer 6

Mechanism: auto-antibodies directed against presynaptic Ca2= channels results in decreased Ca2+ influx with depolarization and decreased release of ACh vesicles; Symptoms: fluctuating symmetric proximal limb weakness, worse in legs; may, but does not always, improve with exercise (more Ca2+ released w/repetitive depolarization)

Question 7

Botulism: mechanism

Answer 7

Mechanism: botulinum toxins are proteinases that interfere with the fusion of vesicle & presynaptic membrane

Question 8

Organophosphorous gases: mechanism

Answer 8

Irreversibly binds to AChE; repetitively activates the receptor b/c ACh remains unmetabolized in the synaptic cleft; raises the cell’s membrane potential – new resting potential is +45 mV; Na+ channels enter inactive state, causing paralysis of muscles (including diaphragm)

Question 9

Myasthenia Gravis: mechanism

Answer 9

auto-antibodies directed against AChR (and, less commonly, MuSK); antibodies result in inflammation and destruction of motor end plate, reduced number of AChR; this results in a decreased EPP, which may not be greater than -50 mV, and an AP may not be generated

Question 10

MG: symptoms

Answer 10

fluctuating skeletal muscle weakness and fatigue in the affected muscles; ptosis, double vision, chewing/swallowing, proximal limb weakness are common symptoms (15% pt have only ocular symptoms)

Question 11

LEMS: symptoms

Answer 11

fluctuating symmetric proximal limb weakness, worse in legs; may, but does not always, improve with exercise (more Ca2+ released w/repetitive depolarization)

Question 12

LEMS: epidemiology

Answer 12

1) young women predisposed to autoimmune dx – 30%, 2) pt with squamous cell lung cancer – 70% [neuro symptoms evident years before cancer is diagnosed]

Question 13

Succinylcholine: MOA

Answer 13

activates AChR and maintains channel open for a longer duration; raises the membrane’s potential initially, causing contraction of muscle via opening of Na+ channels; however, Na+ channels enter an inactive state and paralysis follows

Question 14

Pancuronium: MOA

Answer 14

Selective competitive antagonist to ACh for the receptor

Question 15

Ionotropic messaging

Answer 15

ligand-gated ion channel receptors; fast; made up of multiple subunits (allows for diversity)

Question 16

Metabotropic messaging

Answer 16

G protein-coupled receptors; slower; can modulate input; can activate a variety of post-synaptic events; more sustained

Question 17

Inhibitory NTs

Answer 17

Glycine, GABA

Question 18

Main inhibitory NT in the brain

Answer 18

GABA

Question 19

Main excitatory NT in the CNS

Answer 19

Glutamate

Question 20

Excitatory NTs

Answer 20

Glutamate, ACh, Serotonin, Histamine, Catecholamines (Epinephrine, NE, Dopamine)

Question 21

Primary Glutamate receptor

Answer 21

NMDA; ionotropic; Permeable to Ca2+; Glycine co-agonist; Mg plug removed upon depolarization; currents slower & more sustained (long-term changes, minimal desensitization)

Question 22

GABA A receptor

Answer 22

Ionotropic; Fast synaptic transmission in brain; post-synaptic, gates Cl-; made of α, β, γ subunits; problems: epilepsy, anxiety, addiction

Question 23

GABA B receptor

Answer 23

Metabotropic; Slow, long-lasting inhibitory currents; pre- and post-synaptic; modulate K+ and Ca2+; drugs that work here include GHB, ecstasy

Question 24

ACh receptor types

Answer 24

nicotonic (ionotropic), muscarinic (metabotropic)

Question 25

ACh nicotonic receptors

Answer 25

Ionotropic; Gates cations; made up of 5 subunits (muscle v. neuron type, most neuron have α, β subunits); highly expressed in CNS in early life & then decline with age; mutations can cause epilepsy; decreased numbers in Parkinson’s, Alzheimer’s

Question 26

ACh muscarinic receptors

Answer 26

Metabotropic; Pre- and post-synaptic; found in CNS, PNS, end organs; decreased in Alzheimer’s; antagonists treat Parkinson’s Dx, make people feel euphoric

Question 27

Norepinephrine & epinephrine - receptors

Answer 27

a, B adrenergic (metabotropic)