chemical communication - neurotransmitters

sparks vs soup debate

the debate between ‘sparks’ (who thought that synaptic communication was electrical) and ‘soups’ (who thought it was chemical) lasted until the 1950s

neurotransmitters

• synthesized in presynaptic neurons and stored in axon terminals

• are released when action potentials arrive at axon terminals

• cause some change in the postsynaptic neurons that, when blocked, prevent the two cells from communicating

how can botulinum toxin prevent neurotransmitters from doing their job?

it is incorporated into synaptic vesicles, preventing them from docking with the inside of the postsynaptic membrane which prevents neurotransmitter release

potency

the amount of drug needed to produce an effect, such as relief of pain

ionotropic receptors

ion channels that open when neurotransmitters bind to them, causing IPSPs or EPSPs directly

monobotropic receptors

activate molecules called G-proteins on the interior of the neuron / these 2nd messengers can themselves open ion channels and/or trigger a cascade of intracellular events that leads to things like protein synthesis

what are the two mechanisms that can inactivate neurotransmitters once they have been released?

• enzymatic degradation

• reuptake

enzymatic degradation

enzymes (protiens) in the synaptic cleft break down the NT

reuptake

transporter molecules on the presynaptic cell and glia grab the NT and pull it out of the synaptic cleft

pharmacokinetics

subsection of pharmacology that deals with the absorption, distribution, metabolism, and excretion of drugs (how drugs move through the body)

pharmacodynamics

subsection of pharmacology that deals with how drugs exert their effects at their site of action (how the body responds to drugs)

what is a ligand?

molecule that binds to a receptor site

endogenous ligands

molecules produced by the body that exert their effects through receptor binding, such as NTs

exogenous ligands

molecules produced outside the body that bind to receptor sites (e.g. drugs, such as nicotine). these can be: agonists / antagonists

agonists

binds and mimics the endogenous ligand

antagonists

binds and blocks the action of the exogenous ligand (or of an agonist)

dose-response curve

graph of the relationship between the amount of a drug administered (dose) and the effects that it causes (response)

what does it mean for one drug to have a larger therapeutic index (TI) compared to another?

the larger the TI, the safer the drug is / a drug with a narrow TI has generally a steep concentration response relationship for efficacy, toxicity or both so that there is a narrowly defined range between risk and benefit

the three effects of repeated drug exposure

• sensitization

• tolerance

• dependence

sensitization

drug effects get bigger with repeated exposure, shifting the dose-response curve to the left

tolerance

drug effects get smaller with repeated exposure, shifting the dose-response curve to the right

dependence

the body becomes accustomed to functioning in the presence of the drug and reacts with withdrawal symptoms if the drug leaves the system. withdrawal is usually the opposite of the drug’s acute effects