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Neurobiology > Test 4 - Drugs > Flashcards

Test 4 - Drugs Flashcards

1
Q

What are some examples of barbiturates?

A

alcohol and amobarbital

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2
Q

What are the physiological effects of barbiturates

A
  1. produce sedation, sleep
  2. produce general anesthesia (high levels- coma/death)
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3
Q

What are some examples of Benzodiazepines?

A

Valium, Xanax, Ativan, Klonopin

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4
Q

What physiological effects do benzos have?

A
  1. minor tranquilizers
  2. coping (temporary use)
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5
Q

What is the similarity between benzos and barbiturates?

A

both bind to GABAa receptors

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6
Q

What are the 2 types of GABAa receptors anti-anxiety/sedatives bind to:

A
  1. sedative-hypnotic site (barbs)
  2. anti-anxiety site (benzos)
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7
Q

Describe the mode of action of barbiturates

A

bind to sedative-hypnotic site which leads to a chlorine influx and hyperpolarization which shuts down cell to cell communication

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8
Q

Describe the mode of action of benzos

A

bind to anti-anxiety site which increases the binding effects of GABA (which increases the length of GABA binding and enhances GABA amounts)

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9
Q

On what is the benzos mode of action dependent?

A

GABA concentration - if lacking in GABA won’t have much if any effect

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10
Q

What physiological effects do antipsychotics have on a person?

A

major tranquilizers (reduction in motor activity, used for schizophrenia and bipolar)

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11
Q

How do antipsychotics work in the brain?

A

they block D2 dopamine receptors (atypical like clozapine acts on serotonin as well as dopamine)

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12
Q

What are the 3 classes of antidepressants?

A
  1. monoamine oxidase inhibitors (MAOIs)
  2. tricyclic antidepressants
  3. second-generation antidepressants
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13
Q

How do MAOIs work?

A

block the enyzme MAO from degrading neurotransmitters (specifically serotonin, but also dopamine, NER) - this is similar to AChase digestion of ACh - block degradation to enhance the efficacy of available NTs

(stop the breakdown of NT)

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14
Q

How do Tricyclic antidepressants work?

A

block reuptake of neurotransmitters (e.g. serotonin) by blocking reuptake transporter proteins

(stop the reuptake of NT)

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15
Q

How do second-generation antidepressants act?

A

like tricyclic - block reuptake of neurotransmitters - but have a more selective action - SSRIs for serotonin (Prozac & Zoloft) and SNRIS for serotonin and NER (Cymbalta)

(stop the reuptake of NT)

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16
Q

What is the physiological function of a mood stabilizer?

A
  1. treat bipolar disorder
  2. dampens one pole-other poles less likely to recur (makes swings less extreme)
17
Q

How do mood stabilizers work?

A
  1. not well understood
  2. lithium - may affect serotonin release
  3. sodium valproate - stimulates GABA activity by action on sodium channels
18
Q

Discuss sodium valproate.

A

Sodium valproate is a mood stabilizer that stimulates GABA active by directly depolarizing sodium channels - it can also modulate miR-132 expression similar to glutamate (HDAC inhibitor - inhibits removal of acetyl groups - which leads to side effect since non-specific)

19
Q

From what you know in the sensory chapter, how do opioid analgesics work?

A

opiates bind opioid receptors concentrates in laminae I or II of dorsal horn - this stops neurotransmitter and endorphins release (serotonin and NER respectively)

20
Q

Are all opioid analgesics illegal drugs?

A

No - Codeine is used as a cough medicine and in some pain killers. Morphine is also used in hospitals and after surgery as a powerful pain reliever

21
Q

Cocaine is a psychomotor stimulant. How does it “stimulate” the brain?

A

blocks dopamine reuptake which leaves more dopamine in the synaptic cleft

(they are dopamine agonists and release dopamine into the synapse which blocks the reuptakes of dopamine since bound to its receptor)

22
Q

How is the amphetamine effect different from that of cocaine?

A

dopamine agonists (release dopamine into synapse but also block the reuptake of dopamine by binding to its receptors)

23
Q

What is an example of a legally readily available/non-prescription stimulus?

A

caffeine

24
Q

How does caffeine affect the brain?

A

it inhibits the enzyme that normally breads down the second messenger cAMP - this leads to an increase in cAMP and an increase in glucose production within cells, which makes more energy available and allows for higher rates of cellular activity (camp -> pka -> pc -> glycogen phosphorylase -> breakdown glycogen)

25
Q

Overall, what do psychedelic/hallucinogenic drugs do to a person’s physiology/sensory acuity?

A
  1. alter sensory perception
  2. alter cognitive abilities
  3. can induce hallucinations
26
Q

Positive outcomes of THC with brain regions

A
  1. antinausea - brain stem
  2. increased appetite - hypothalamus
  3. euphoria - nucleus accumbens (dopamine output)
  4. altered pain sensitivity - spinal cord
27
Q

Negative outcomes of THC with brain regions

A
  1. panic/paranoia - amygdala
  2. slowed reaction time - basal ganglia
  3. impaired memory - hippocampus
  4. impaired coordination - cerebellum
  5. altered thinking, judgment, and sensation - neocortex
28
Q

Negative reinforcement of addiction cycle theory

A

starts with drug craving (dysregulated reward pathways) -> loss of control/poor decision-making -> drug administration/drug-seeking -> drug euphoria -> withdrawal -> back to drug craving

29
Q

Positive reinforcement of addiction theory

A

starts with drug euphoria (activated reward pathways) -> withdrawal -> drug craving -> loss of control -> drug administration -> and back to euphoria

30
Q

What is something that throws people back into addiction cycle?

A

drug-related cues (limbic activiation) from stressors

31
Q

Explain the role of the VTA and NAc in addiction

A

VTA & the NAc both produce dopamine and send to the prefrontal cortex and amygdala. When dopamine reaches the PFC, it sends glutamate to the VTA & NAc which increases the dopamine output and reinforces the cycle.

32
Q

Explain why an addicted person’s behaviors all turn towards drug seeking.

A

Drug-seeking behavior almost becomes involuntary movement, because of the involvement of glutamate signaling which changes epigenetic marks

33
Q

Why is it easier to overdose on benzos and not alcohol?

A

Benzodiazapines and barbiturates (which alcohol is classified within) both act on ionotropic GABA-A Receptors, but they each have their own binding site on these receptors. Alcohol binds to the sedative-hypnotic site and Benzos to the anti-anxiety site. Once bound, alcohol has a direct affect on the chlorine influx into the cell and leads to hyperpolarization which shuts down cell communication. On the other hand, benzos enhance the binding effects of GABA and are dependent on an individuals natural GABA levels, which makes it harder to overdose on benzos than alcohol.

Neurobiology (15 decks)

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