Exam 2 (Pt. 1) Flashcards

1
Q

Glutamate - Commonality

A

Ubiquitous neurotransmitter; involved in every behavior

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2
Q

Glutamate - Receptor/Effect

A

Excitatory neurotransmitter – causes EPSPs

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3
Q

GABA - Commonality

A

Ubiquitous neurotransmitter - involved in every behavior

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4
Q

GABA - Effect

A
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5
Q

GABA - Type

A
  • GABAa - Ionotropic (chloride ion influx)
  • GABAb - Metabotropic
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6
Q

GABA - Drug Use

A

Drugs that promote GABA activity have been used to treat anxiety and sleep disorders.

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7
Q

Serotonin (5-HT) - Role

A

Roles in sleep and arousal, aggression, and mood

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8
Q

Serotonin (5-HT) - Effect

A

Primarily acts on metabotropic receptors

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9
Q

Serotonin (5-HT) - Drug Use

A

Drugs that promote serotonin acitvity are the most widely used anti-depressants

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10
Q

Serotonin (5-HT) - Cell Bodies

A

The serotonin cell bodies are localized in the Raphe Nuclei, which extends from the midbrain to the hindbrain:

  • Only a few hundred serotonin neurons in the brain
  • These serotonin neurons project to most of the brain.
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11
Q

Dopamine (DA) - Receptor

A
  • Dopamine receptors are all metabotropic
  • Primarily 2 Types:
    • D1-like
    • D2-like
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12
Q

Dopamine (DA) - Localization

A

Dopamine neurons are localized to three brain areas

  • Ventral Tegmental Area (VTA)
  • Substantia Nigra
  • Arcuate Nucleus

Each of these areas has its own projections and roles in behavior.

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13
Q

Synthesis of Epinephrine, Norepinephrine, and Dopamine

A

Important to simply know what comes from what: Tyrosine ==> Dopa ==> dopamine (DA) ==> norepinephrine.

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14
Q

Norepinephrine (NE) - Role

A

Primarily involved in stress and arousal

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15
Q

Norepinephrine (NE) - Production

A

NE is made in the locus coeruleus and other structures: projections to forebrain hindbrain, and limbic areas.

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16
Q

Norepinephrine (NE) - Disorders

A

Contributes to anxiety disorders and PTSD

17
Q

Acetylcholine (ACh) - Role

A

Role in learning & memory, cognition, and arousal.

18
Q

Acetylcholine (ACh) - Cell Bodies

A

Cell bodies in the nucleus basalis and brainstem nuclei

19
Q

Acetylcholine (ACh) - Disorders

A

ACh neurons degenerate in Alzheimer’s disease

20
Q

Acetylcholine (ACh) - Receptor

A
  • Musarinic - which are GPCRs
  • Nicotinic - which are ionotropic receptors
21
Q

Synthesis of Acetylcholine

A
22
Q

Degredation of Acetylcholine

A
23
Q

Myasthenia Gravis - Disorders

A

Syndrome of fatigue and exhaustion of the muscle system.

24
Q

Myasthenia Gravis - Effect

A
  • Impaired acetylcholine neurotransmission
  • Destruction of post-synaptic acetylcholine receptors
25
Q

Myasthenia Gravis - Type of Disease

A

Autoimmune Disease

26
Q

Ptosis

A

Myasthenia gravis typically affects the cranial muscles

A Severe dropping of the eyelids, or ptosis, is characteristic of myasthenia gravis. This patient also could not move his eyes to look to either side.

One minute after an intravenous injection of 10 mg of edrophonium, an inhibitor of cholinesterase, both eyes are open and can be moved freely.

27
Q

Neuromuscular Junction of Normals v. Myasthenia Gravis - Normal Release

A

At neuromuscular junctions, vesicles release ACh at specialized release sites in the nerve terminal.

28
Q

Neuromuscular Junction of Normals v. Myasthenia Gravis - Normal Movement

A

Acetylcholine crosses the synaptic space to reach receptors that are concentrated at the peaks of junctional folds.

29
Q

Neuromuscular Junction of Normals v. Myasthenia Gravis - Normal Termination

A

Acetylcholinesterase in the cleft rapidly terminates transmission by hydrolyzing ACh.

30
Q

Neuromuscular Junction of Normals v. Myasthenia Gravis - Myasthenia Junction

A

The myasthenic junction has reduced numbers of ACh receptors, simplified synaptic folds, a widened synaptic space, but a normal nerve terminal.

31
Q

Treatment of Myasthenia Gravis - Treatment

A

Neostigmine increases the duration of action of ACh and thus can compensate for the reduced ACh activity in myasthenia.

32
Q

Treatment of Myasthenia Gravis - Image A

A

In normal person the amplitude of action potentials evoked by a train of four stimuli at 16.6 ms intervals remains constant.

33
Q

Treatment of Myasthenia Gravis - Image B

A

In myasthenia patient there is a rapid decrease in amplitude.

34
Q

Treatment of Myasthenia Gravis - Image C

A

After injection of 2 mg neostigmine into the brachial artery of the myasthenic patient, the decrease in amplitude was partially reversed.

35
Q

Neuropeptides - Localization

A
  • Neuropeptides tend to be more discrete in location and function.
  • For example, opioid peptides are well-known for their role in pain and reward.