Drugs And Behavior Final Exam

Front 1

Amphetamine: How it effects neurotransmission

Back 1

1. Blocks re-uptake of DA and NEpi
2. Causes release of DA and NE pi -
3. Mild Inhibition of MAO
4. Tolerance is due to depletion of catelcholamines, primarily by reduced synthesis due to increased autoreceptor activity

Front 2

Amphetamine/cocaine tolerance

Back 2

depletion of neurotransmitter so that additional administration of the drug produces less effects

Front 3

Sensitization to cocaine

Back 3

-Chronic use depletes DA
-In response to depleted DA, neurons compensate by UPREGULATING, receptor numbers and INCREASING SENSITIVITY
-Effect of cocaine is enhanced because of number of receptors

Front 4

Pharmacodynamics of caffeine

Back 4

-Adenosine receptor ANTAGONIST
-Adenosine normally slows down neural activity
-Relief of inhibition increases neuronal activity
-Therefore, blocking adenosine receptors increases neural activity
-Caffeine is AGONIST of transmitter release

Front 5

Mechanisms of action: caffeine

Back 5

-GABA is inihibotory
-GABA receptor ANTAGONIST
-Blocking GABA receptors reduces inhibition in the brain, and leads to overall arousal.

Front 6

Pharmacodynamic tolerance of caffeine

Back 6

Due to UP-REGULATION of ADENOSINE receptors as the brain tries to deal with continued suppression of adenosine activity

Front 7

Pharmacodynamics of Nicotine

Back 7

-Acts as AGONIST at nicotine acetylcholine receptor
-Stimulates the receptor, then blocks it via inactivation

Front 8

Alcohol's effect on receptors

Back 8

-Enhances activity of GAPA receptor: hyperpolarizes neuron by allowing Cl- to enter
-Decreases the activity of some glutamate receptors: inhibits excitatory effects at the NMDA receptor by blocking the ion channel pore decreasing the amount of Na and Ca ion entry
-Net result is to decrease excitability of neurons, and reduce spontaneous firing

Front 9

CNS (physiological effects) of alcohol

Back 9

-Mechanism for apparent stimulation is thought to be inhibition of inhibitory neurotransmission
- Loss of inhibitory control in RAS and cortex which are normally used for mental functions
-Inihibition in RAS and Cortex results in a decrease of self-control
1. Reduces release of inhibitory neurotransmission
2. Reduces firing of inhibitory pathways
3. Decreases excitatory neurotransmission

Front 10

tolerance of alcohol

Back 10

-Mechanism: induction of liver enzymes
-Decreased neurotransmission may lead to upregulation and sensitization of postsynaptic receptors
-Upregulation of NMDA receptors important to with drawal.
-Little tolerance to lethal effects

Front 11

Alcohol: Dependence and Withdrawal

Back 11

-Both physical AND psychological dependence
-Reinforcing properties due to stimulation of 5-HT3 receptor (important step for releasing DA into the NA)

Front 12

Pharmacodynamic tolerance

Back 12

-Drugs that amplify or mimic the actions of a neurotransmitter tends to DECREASE receptor activity.
****Down-regulation:decrease in number of functional receptors
****Desentization: decrease in receptor's ability to elicit changes
-Drugs that act as antagonists of tend to INCREASE receptor activity

Front 13

Cannabis Pharmacodynamics

Back 13

-effects can be both excitatoy and inhibitory

Front 14

Cannabis mechanism of action

Back 14

-Binds to CB1 and CB2 Receptors - localize to hippocampus, cerebral cortex, amygdala
-All canabanoid receptors are METABOTROPIC
-Meteabotropic receptors are linked to G-Proteins
-DECREASE neurotransmission release
-inhibit acetylcholine release in hippo, inhibit NE release

Front 15

Cannabis receptors in the brain

Back 15

Few to no cannabanoid receptors in the VTA, however it does activate central reward pathways, leading to release of DA in NA.
-Therefore marijuana's effect on reward pathway is indirect
-THC decreases GABA inhibition of VTA, therefore DA in NA

Front 16

Cannabis tolerance

Back 16

Primarily due to desensitization/down-regulation of cannabanoid receptors (because cannabanoid receptors are agonists)

Front 17

LSD effects at cellular level

Back 17

-Serotonin receptor AGONIST
-Agonist of 5HT-2 receptors (post-synaptic)
-Actively altered in RAS: No longer filters sensory info.

Front 18

PCP cellular effects

Back 18

-Acts as channel blocker for a subtype of glutamate receptor
-Ionotropic NMDA receptor: Precents CA+ and Na+ from flowing into neuron
-Prevents DA re-uptake

Front 19

MDMA (ecstasy) cellular effects

Back 19

-Destroy monoamine (DA, NE, and Seratonin) neurons
-Decrease in brain's serantonin transporter

Front 20

Heroin effects

Back 20

- Opiates bind to endogenous opioid receptors to produce INIHIBITION
-Increases DA in the NA
-Heroin converted to morphine in the brain which acts at the mu and delta receptors expressed on inihibitory GABA neurons.
-The binding of mu and delta at GABA causes REDUCTION in amount of GABA released. This inhibition leads to increases of DA in NA

Front 21

Heroin tolerance

Back 21

desensitization/down-regulation

Front 22

Tricyclic Anti-depressants vs SSRI

Back 22

TCAs: block re-uptake of NE and 5-ht, thereby increasing synaptic levels
SSRI: SELECTIVELY blocks 5-ht re-uptake rather than both

Front 23

Monoamine theory of depression

Back 23

Monoamines are low in depressed people.
If this is the case, what would you expect to see in the brains of patients: UPREGULATION of 5ht and NE receptors

Front 24

Kluver-Buchy Syndrome (anxiety)

Back 24

Reduction of fear after BILATERAL AMYGDALA DAMAGE

Front 25

HPA (Anxiety)

Back 25

-Very important in stress
-Boosts cortisol and activates it

Front 26

Factors implicated in medication of Anxiety disorders

Back 26

Central: NE, 5HT, GABA
Peripheral: Release of ACTH, adrenal cortisol, and NE
Increased NE firing in Locus Ceruleus
Increased sensitivity in amygdala
HPA activation

Front 27

Barbituates - Pharmacodynamics

Back 27

-Barbituates enhance GABA receptor activity
-Noncompetitve Agonist
-Results in opening of Cl- Channel
-Results in hyperpolarization of neuron, less excitable

Front 28

Benzos

Back 28

Decreases excitatory neuronal activity in cortex, RAS, limbic system
Difference: seems to decrease hypothalamus activity
Enhance activity of endongenous GABA
INDIRECT GABA AGONISTS

Front 29

Difference between Benzos and Barbituates

Back 29

Barbs - Absorbed rapidly, low TI, REM sleep
Benzos - Absorbed slowly, longer duration of action, higher TI, less effects on REM sleep

Front 30

Anti-psychotic treatment

Back 30

Primary dopamine receptor ANTAGONISTS