presynaptic & postsynaptic effects

Presynaptic effects

Changes that affect neurotransmitter production, release, or clearance before/at the presynaptic terminal

Block neurotransmitter synthesis

Decreases the amount of neurotransmitter produced and available for release

Block 5-HT synthesis

Prevents or decreases production of serotonin (5-HT)

Colchicine

Interferes with axonal transport, disrupting movement of materials to the axon terminal

Axonal transport disruption

Prevents needed materials from being efficiently transported along the axon

Reserpine

Blocks packaging of neurotransmitters into synaptic vesicles

Blocking vesicle packaging

Decreases the amount of neurotransmitter stored and available for release

Tetrodotoxin (TTX) & Novocain

Blocks voltage-gated Na⁺ channels, preventing normal action potential transmission

Voltage-gated Na⁺ channel blockade

Prevents normal action potential propagation to the axon terminal, reducing neurotransmitter release

Ca²⁺ and neurotransmitter release

Ca²⁺ entering the presynaptic terminal triggers synaptic vesicle fusion and neurotransmitter release

Ca²⁺ channel blockade

Decreases Ca²⁺ entry, reducing vesicle fusion and neurotransmitter release

Amphetamine

Stimulates neurotransmitter release from the presynaptic terminal

Botox (botulinum toxin)

Blocks the release of acetylcholine (ACh)

Neurotransmitter clearance

Removal of neurotransmitter from the synapse through reuptake or enzymatic degradation

Reuptake

Transport of neurotransmitter out of the synaptic cleft, often back into the presynaptic neuron

Reuptake inhibition

Causes neurotransmitter to remain in the synaptic cleft longer and increases its concentration there

Cocaine

Inhibits neurotransmitter reuptake, leaving more neurotransmitter in the synapse

SSRIs

Selective serotonin reuptake inhibitors that block serotonin reuptake, increasing 5-HT in the synapse

Prozac (fluoxetine)

An SSRI that inhibits serotonin reuptake

Neurotransmitter degradation

Enzymatic breakdown of neurotransmitter that helps terminate its action

Inhibition of degradative enzymes

Prevents neurotransmitter breakdown, allowing it to remain active longer

Acetylcholinesterase (AChE)

Enzyme that breaks down acetylcholine

Monoamine oxidase (MAO)

Enzyme involved in the breakdown of monoamine neurotransmitters

AChE inhibition

Reduces acetylcholine breakdown, allowing ACh to remain available longer

MAO inhibition

Reduces monoamine breakdown, allowing these neurotransmitters to remain available longer

Postsynaptic effects

Changes involving receptors or intracellular processes in the receiving cell

Receptor blockade

Prevents a neurotransmitter from activating its postsynaptic receptor

Receptor activation

Activates a postsynaptic receptor and produces or mimics a neurotransmitter response

Antagonist

Substance that blocks or reduces activation of a receptor

Agonist

Substance that activates a receptor and mimics or enhances neurotransmitter action

Haloperidol

Antipsychotic drug that blocks dopamine receptors

Curare

Blocks acetylcholine receptors

Nicotine

Activates nicotinic acetylcholine receptors

LSD

Activates serotonin receptors, including 5-HT₂A receptors

Morphine

Activates opioid receptors

Change in postsynaptic receptor number

Alters a cell's sensitivity to a neurotransmitter by increasing or decreasing available receptors

Alcohol and GABA

Alcohol enhances GABAergic signaling by increasing the number of postsynaptic receptors

Second messengers

Intracellular signaling molecules that transmit a signal after receptor activation

Alteration of second messengers

Changes intracellular signaling downstream of neurotransmitter receptor activation

cAMP

A second messenger involved in intracellular signaling pathways

Morphine and cAMP

Morphine can alter intracellular signaling; ex. decrease cAMP signaling

Lithium and cAMP

Lithium can alter second-messenger signaling, including decreasing cAMP

Colchicine

interferes with axonal transport

Reserpine

blocks neurotransmitter packaging into vesicles

TTX

blocks voltage-gated Na⁺ channels

Novocain

blocks voltage-gated Na⁺ channels

Ca²⁺ channel blocker

decreases neurotransmitter release

Amphetamine

stimulates neurotransmitter release

Botox

blocks ACh release

Cocaine

inhibits neurotransmitter reuptake

SSRIs/Prozac

inhibit serotonin reuptake

AChE/MAO inhibitors

decrease neurotransmitter degradation

Haloperidol

blocks dopamine receptors

Curare

blocks ACh receptors

Nicotine

activates nicotinic ACh receptors

LSD

activates 5-HT₂A serotonin receptors