drugs and the brain

agonist

activates receptor

antagonist

blocks or prevents receptor activation

competitive

bind directly to site 

noncompetitive 

binds somewhere else 

Pharmacokinetics

what body does to drugs

Pharmacodynamics

what drugs do to the body

ADME in Pharmacokinetics

administration, distribution, metabolism, excretion

Ingestion bioavailability

low bc passes through stomach and liver

injection bioavailability

very high, goes straight into blood

inhalation bioavailability

high and fast due to blood supply of lungs

absorption bioavailability

mid, depends

major organs responsible for metabolism and excretion

liver + kidneys

Binding affinity

chemical attraction between a ligand and receptor

Efficacy

ability of a bound ligand to activate the recepto

DRC tell us about potency

 how much of the drug is needed to produce a certain effect

a drug is more potent if it produces the effect at a

lower dose

DRC tells us about drug’s safety

therapeutic window; the range between an effective dose and a harmful dose, showing how safe the drug is

Therapeutic index

separation between useful doses and dangerous doses 

increase in tolerance is a dose response curve shift to the

right

Metabolic tolerance/Pharmacokinetic 

body gets better at breaking down the drug

Functional tolerance/Phramacodynamic tolerance

 target cells or receptors become less sensitive to the drug

Down-regulation in response to an agonist = 

fewer receptors

up regulation in response to an antagonist =

more receptors

effects of drugs on NT production

increase/decrease synthesis, storage, transport

effects of drugs on NT release

increase/decrease release via channels or auto receptors

Drug effect on neurotransmitter clearance

reuptake/breakdown

Drug effect on receptors

activate, block, or change sensitivity

reward pathway

VTA

opioids treatment

delta, kappa, mu

Methadone

agonist against opioid receptors

Buprenorphine

partial agonist 

opioid use

painkiller, “rush” feeling

THC

relaxation + mood or stimulation + paranoia

Possible correlation between cannabis use and

schizophrenia

Nicotine 

Direct agonist @ nicotinic acetylcholine receptors 

THC synaptic mechanism 

CB1 and CB2

Cocaine synaptic mech

indirect agonist → blocks reuptake into presynaptic terminal on dopamine neurons

Amphetamines

blocks dopamine reuptake; reverses transporters

Alcohol synaptic mech

noncompetitive agonist @ GABAA, antagonist @ NMDA

Psychedelics

agonists at the 5-HT2A serotonin receptor

The Dopamine Hypothesis

schizophrenia caused by an excess of dopamine

The Glutamate Hypothesis

schizophrenia caused by under-activation of glutamate receptors