Exam 2 (Pt. 1)

Question 1

Glutamate - Commonality

Answer 1

Ubiquitous neurotransmitter; involved in every behavior

Question 2

Glutamate - Receptor/Effect

Answer 2

Excitatory neurotransmitter – causes EPSPs

Question 3

GABA - Commonality

Answer 3

Ubiquitous neurotransmitter - involved in every behavior

Question 4

GABA - Effect

Answer 4

Question 5

GABA - Type

Answer 5

• GABA_a - Ionotropic (chloride ion influx)
• GABA_b - Metabotropic

Question 6

GABA - Drug Use

Answer 6

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

Question 7

Serotonin (5-HT) - Role

Answer 7

Roles in sleep and arousal, aggression, and mood

Question 8

Serotonin (5-HT) - Effect

Answer 8

Primarily acts on metabotropic receptors

Question 9

Serotonin (5-HT) - Drug Use

Answer 9

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

Question 10

Serotonin (5-HT) - Cell Bodies

Answer 10

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.

Question 11

Dopamine (DA) - Receptor

Answer 11

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

Question 12

Dopamine (DA) - Localization

Answer 12

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.

Question 13

Synthesis of Epinephrine, Norepinephrine, and Dopamine

Answer 13

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

Question 14

Norepinephrine (NE) - Role

Answer 14

Primarily involved in stress and arousal

Question 15

Norepinephrine (NE) - Production

Answer 15

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

Question 16

Norepinephrine (NE) - Disorders

Answer 16

Contributes to anxiety disorders and PTSD

Question 17

Acetylcholine (ACh) - Role

Answer 17

Role in learning & memory, cognition, and arousal.

Question 18

Acetylcholine (ACh) - Cell Bodies

Answer 18

Cell bodies in the nucleus basalis and brainstem nuclei

Question 19

Acetylcholine (ACh) - Disorders

Answer 19

ACh neurons degenerate in Alzheimer’s disease

Question 20

Acetylcholine (ACh) - Receptor

Answer 20

• Musarinic - which are GPCRs
• Nicotinic - which are ionotropic receptors

Question 21

Synthesis of Acetylcholine

Answer 21

Question 22

Degredation of Acetylcholine

Answer 22

Question 23

Myasthenia Gravis - Disorders

Answer 23

Syndrome of fatigue and exhaustion of the muscle system.

Question 24

Myasthenia Gravis - Effect

Answer 24

• Impaired acetylcholine neurotransmission
• Destruction of post-synaptic acetylcholine receptors

Question 25

Myasthenia Gravis - Type of Disease

Answer 25

Autoimmune Disease

Question 26

Ptosis

Answer 26

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.

Question 27

Neuromuscular Junction of Normals v. Myasthenia Gravis - Normal Release

Answer 27

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

Question 28

Neuromuscular Junction of Normals v. Myasthenia Gravis - Normal Movement

Answer 28

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

Question 29

Neuromuscular Junction of Normals v. Myasthenia Gravis - Normal Termination

Answer 29

Acetylcholinesterase in the cleft rapidly terminates transmission by hydrolyzing ACh.

Question 30

Neuromuscular Junction of Normals v. Myasthenia Gravis - Myasthenia Junction

Answer 30

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

Question 31

Treatment of Myasthenia Gravis - Treatment

Answer 31

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

Question 32

Treatment of Myasthenia Gravis - Image A

Answer 32

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

Question 33

Treatment of Myasthenia Gravis - Image B

Answer 33

In myasthenia patient there is a rapid decrease in amplitude.

Question 34

Treatment of Myasthenia Gravis - Image C

Answer 34

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

Question 35

Neuropeptides - Localization

Answer 35

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