College 3 Drugs and hormones Flashcards
Antagonist
Substance that blocks/decreases the function of neurotransmission
Dopaminergic antagonist
Supresses the dopamine (& norepinephrine) reuptake
antipsychotics
Adenosinergic antagonist
Endogenous adenosine induses drowsiness
Caffeine is a antagonist
works in the oposite direction and peps you up instead of getting drowsi
Glutamatergic antagonist
Works on the glutamate system, glutamate is excitatory so a glutamatergic antagonist works calming or even sedative
Ketamine, aneasthesia
Also used to treat parkinsons desease symptoms
Agonist
Substance that enhances the function of neurotransmission
Dopaminergic agonist
Blocks dopamine and norepinephrine reuptake, which therefor stays available in the synaptic cleft
Cocaine and meth are dopaminergic agonists, so are methulphenidate (Ritalin) and L-dopa
more focus and arousal –> makes it highly addictive, less feeling of coherence and stability
L-dopa is used to treat parkinsons –> it has effect on motor problems
Cannabinergic agonist
Reduce anxiety and enhances forgetting
THC is an example of a cannabinergic agonist
Serotinergic agonist
They alter sensory perception and cognitive processes, can also produce hallucinations
Examples are LSD and MDMA
Also have adrenergic effects –> higher hearrate, etc.
Opiodergic agonists
Opiod: endo/exogenous copound binds opiod receptors and give a morphine like effect
endorphine: pain killer
reduce stress and pain
addictive
GABAergic agonist
At a low dose they reduce anxiety, disinhibit behavior and reduces brain activation
at medium dose they sedate
at a high dose they anesthesize, coma and eventually death
Alcohol and benzodiazepines (valium, ssri’s (antidepressants))
Cholinergic agonist
At low doses it is a stimulant on memory, selective attention, and emotional processing functions.
example: nicotine
Antipsychotics
1st and 2nd generation
1st generation - block the D2 dopamine receptor - produce symptoms like parkinsons 2nd generation - Weakly block the D2 dopamine receptor - block reotonin receptor - increased motivation and reduced agitation - possible side effect is weight gain
Endogenous
Excisting in the brain
Exogenous
From outside the body
Anti depressants
1st and 2nd generation
1st genration
- Block enzyme MAO from degrading serotonine and dopamine
- tricyclic –> block serotonine uptake
2nd generation (SSRI’s)
- Block uptake of serotonine
- more selective in action on serotonine synapses
Endocrine glands
Release the apropriate hormones into the blood stream to act on target organs and tissue
Glucocorticoids
Fast
- fight or flights preparation
Slow
- mobilizes the body to confront a stressor
- repair stress related damages (mostly damaged by cortisol)
Hormone
Chemical substance
Controls and regulates the activity of certain cells or organs
Function of hormones
Homeostatic hormones
- maintain a state (balance) of internal metabolic balance and regulation of physiological systems (hunger, blood sugar, temperature)
Gonodal (sex) hormones
- reproductive functions
Glucocorticoids
- Secrated (produced) in times of stress
Incentive sensitization theory
Wanting and liking
Wanting
Craving
sensitizises cues with repeated drug use
Related to dopamine system
Liking
opiod activation
marks certain activities or states as pleasurable
as tolerance grows, pleasure decreases
nucleus accumbens
Nucleus Accumbens
the neural interface between motivation and action, playing a key role on feeding, sexual, reward, stress-related, drug self-administration behaviors, etc.
Pituitary gland
Secretes (produce) and release hormones to influence endocrine glands (hormones into bloodstream)
Tolerance
Habituation
Response to stimulus weakens with repeated presentations
Metabolic: increase in enzymes to break down
Cellular: activaties of brain cells adjust
Learned: learn to cope with being intoxicated
Sensitization
Increases responsiveness to equal doses
Feutal Alcoho Syndrom FAS
GABA is involved in developing the fetus –> when alcohol is used during pregnancy GABA can not do its job in developing the fetus
Synaptic processes that can be affected by drugs
- Synthesis of the neurotransmitter in the cell body, axon, or terminal
- Storage of the neurotransmitter in granules or in vesicles
- Release of the transmitter from presynaptic terminal
- Receptor interaction in the postsynaptic membrane
- Inactivation of excess neurotransmitter at the synapse
- Reuptake into the presynaptic terminal
- Degradation of excess neurotransmitter
- Synthesis of the neurotransmitter in the cell body, axon, or terminal
- Storage of the neurotransmitter in granules or in vesicles
- Release of the transmitter from presynaptic terminal
- Receptor interaction in the postsynaptic membrane
- Inactivation of excess neurotransmitter at the synapse
- Reuptake into the presynaptic terminal
- Degradation of excess neurotransmitter