Ethanol (Test 2)

Question 1

Sedative-hypnotic

Answer 1

any drug that diminishes awareness, spontaneity and activity, producing drowsiness and eventually sleep.

Question 2

what kind of drug is alcohol classified as?

Answer 2

sedative-hypnotic

Question 3

Characteristic (1) of Depressants

Answer 3

1) Additive w/ other S-H and w/ person’s affect.

Question 4

Characteristic (2) of Depressants

Answer 4

2) Cannot be directly antagonized by stimulants (caffeine is not an alcohol antagonist, neither is cocaine or amphetamine)

Question 5

Characteristic (3) of Depressants

Answer 5

3) Can produce both neural and behavioral disinhibition (usually at low doses: you talk more, you act faster) – you are inhibiting things which are inhibitory.
GABAeric transmission is decreased at first, then when the dose goes up, you agonize GABAergic effects.
Low doses ethanol – small increase of dopamine
High doses ethanol – lowering of dopamine

Question 6

Characteristic (4) of Depressants

Answer 6

4) Sedative hypnotics produce severe withdrawal symptoms (can be fatal) -> no one has ever died from cocaine/heroin withdrawal. People withdrawing from ethanol are often prescribed Valium.

Question 7

Characteristic (5) of Depressants

Answer 7

5) Can lead to psychological dependence

Question 8

Physically dependant

Answer 8

I’m going to go into physical withdrawal

Question 9

Psychologically dependant

Answer 9

no fear of physical withdrawal, but I need to feel the “calming effects” of jack daniels or needing beta-blockers to give a talk.

Question 10

Beta blockers

Answer 10

norepinephrine works at beta receptors, which facilitate arousal. Beta blockers produce calming effects

Question 11

What is the solubility and bioavailability of ethanol?

Answer 11

Ethanol is highly water soluble. However, it is small enough to rapidly pass through cell membranes (though NOT highly lipid soluble)

Ethanol is easily absorbed from any biological tissue or space

Question 12

What effect does the blood-brain barrier have on ethanol?

Answer 12

The blood brain barrier has no effect on ethanol.

Question 13

Where is ethanol mostly absorbed?

Answer 13

It is mostly absorbed at the small intestine; it is slowed by full stomach or exercise; accelerated by carbonation.

Question 14

Pylorospasm

Answer 14

the pyloric sphincter spasms. Ethanol at a high enough concentration might not produce the effects you want because it makes the pyloric sphincter spasm

Question 15

Why do women get drunk faster than men?

Answer 15

Women have less of their body weight as water, meaning that they get drunk faster as ethanol is water-soluble.

Question 16

How can one reduce absorption of ethanol?

Answer 16

Absorption is lower if one eats proteins or fats

Question 17

What is “start-up” in the context of psychopharmacology?

Answer 17

“Start-up” refers to the fact that SSRIs require a period of time where you are taking the drug but not feeling any effects. Sedative-hypnotics do not experience “start-up”

Question 18

How is alcohol metabolized?

Answer 18

95% is metabolized by alcohol dehydrogenase (specific for alcohol) or cytochrome P-450 (a hundred group of enymes) in liver

Question 19

What is an example of cross tolerance? What happens when an alcoholic drinks coffee?

Answer 19

Alcoholics have amped up liver enzymes; thus, they need to ingest more caffeine/nicotine to feel effects.

Question 20

How are enzymes related to gender and alcohol intoxication?

Answer 20

Females have less active enzymes; this contributes to increased female intoxication at a given dose.

Question 21

Antabuse

Answer 21

this drug is an antagonist for acetaldehyde dehydrogenase, so if you’re on it and you drink, you will feel crappy. However, only 20% of people with a history of alcohol abuse will not relapse on it (within 18 months).

Question 22

What is the first metabolite of EtOH dehydrogenase?

Answer 22

First metabolite of EtOH dehydrogenase is acetaldehyde; toxic metabolite that leads to headaches, nausea and other symptoms of hangover.

Question 23

Tolerance to ethanol

Answer 23

usually metabolic tolerance

Question 24

Functional tolerance

Answer 24

not measured in BAC: measured in terms of intoxicated/sober. Has more to do with the nervous system than the liver

Question 25

“ethanol antidote”

Answer 25

a group from UCLA has produced a nanotech “ethanol antidote”: it uses a polymer to encapsulate alcohol dehydrogenase (breaks down ethanol) and catalase (breaks down hydrogen peroxide produced as a metabolite). It reduced BAC in mice.

Question 26

Bedspins

Answer 26

bedspins are caused to differences in ethanol distribution in the vestibular apparatus. EtOH enters the fluid of the endolymph and changes density

Question 27

What should you do if you’re having bedspins?

Answer 27

If you are having bedspins – you should take your leg out and put your foot on the floor. Physically connect to some part of the world – it will override the stuff going on in your vestibular apparatus.

Question 28

Where exactly does ethanol facilitate GABA neurotransmission?

Answer 28

Ethanol facilitates GABA neurotransmission at the alpha 1, b2, or delta subunits

Question 29

What happens in your brain after long term exposure to ethanol in relation to GABA?

Answer 29

Long term expose to ethanol leads to decrease in GABA-A receptor sensitivity (down-regulation) and decreased inhibition of CNS neurons.

Question 30

Does ethanol antagonize any neurotransmission?

Answer 30

Yes. EtOH is also an effective glutamate antagonist at both AMPA (epsps) and NMDA-type (synaptic plasticity/perception/learning + memory) receptors.

Question 31

What are AMPA receptors?

Answer 31

AMPA receptors – really common, direct gating channels, create EPSPs when active.

Question 32

What does ethanol do at low doses which could account for it’s reinforcing properties?

Answer 32

At low doses, ethanol increases rate of dopamine neurons in the VTA, which could account for some of EtOH’s reinforcing properties.

Question 33

Ethanol’s pharmacodynamics:

Answer 33

At lower doses, ethanol is a glutamate antagonist at AMPA and NMDA receptors and is a GABA agonist at the GABA-A receptor complex.
CNS becomes hyper excitable because of alterations at the GABA-A and AMPA/NMDA

Question 34

How does ethanol effect learning and memory?

Answer 34

Ethanol effects learning and memory because it inhibits NMDA receptors which allow Ca into the cell which activate second messenger systems.

Question 35

What ends up killing neurons when taking ethanol?

Answer 35

The upregulation of NMDA can reach a point that’s toxic and can kill neurons.

Question 36

What are the effects of long-term exposure to alcohol?

Answer 36

• Chronic ethanol exposure produces impairment in liver function.
• The liver enzymes for ethanol are toxic on their own
• Fat builds up because the liver doesn’t metabolize fats when it’s busy with ethanol.
• Leads to decreases in attention, memory, problem solving, perseveration.

Question 37

Wernicke-Korsakoff syndrome

Answer 37

Nutritional deficiency of thiamine leading to brain damage, common in people with alcohol abuse because they don’t eat as much.

Question 38

Fetal alcohol syndrome (FAS)

Answer 38

• The #1 cause of retardation and cognitive impairment in the US. Completely preventable.
• There is no “safe” amount of alcohol when pregnant.
• Produces change in cranio-facial features. Square nose, characteristic eye shape, etc.
• Brain doesn’t have as many of the distinctive sulci and gyri.

Question 39

What are NMDA receptors?

Answer 39

A ligand-gated channel that allows positively charged ions (Ca and Na) to enter and cause localized depolarization.
- Of the several subtypes of glutamate receptor, alcohol has its greatest effect on the NMDA receptor

Question 40

What does “up-regulation” mean in regards to NMDA receptors?

Answer 40

In the adult brain, repeated use of alcohol leads to a neuroadaptive increase in the number of NMDA receptors (up-regulation) in response to reduced glutamate activity.