Drugs & Synaptic Transmission Flashcards
(20 cards)
What is a synapse?
The gap between a neuron and it’s effector (i.e. neuron, muscle, organ, etc)
-Chemical transmission
Synaptic Transmission (8 steps)
- ) Action potential propagates to axon terminal and causes voltage-gated Ca+ channels to open
- ) Ca+ influx into the presynaptic cell.
- ) Ca+ binds to neurotransmitter vesicles
- ) Vesicles bind to cell membrane
- ) Neurotransmitter is released into synapse
- ) Neurotransmitter binds to receptors on postsynaptic membrane
- ) Bindings leads to a “change” in the postsynaptic cell
- ) Neurotransmitter releases from receptor and:
- is broken down in the synapse (enzymatic deactivation)
- is taken back up into the presynaptic membrane (reuptake)
- diffuses away
- glial cells assist in neurotransmitter clearance
What are the primary effects of a n.t?
To either excite (depolarize) or inhibit (hyperpolarize) the postsynaptic neuron
Ionotropic Effects
Directly opens channel:
- ) N.t. binds
- ) Channel opens
- ) Ions flow across membrane
-May result in an excitatory or inhibitory response
Metabotropic Effects
N.t. attaches to a receptor to open ion channels:
- ) N.t. binds
- ) G-protein is activated
- ) Activates second messenger
- ) Changes DNA
- ) Ion channels open
Acetylcholine
Causes muscles to contract; involved in motor output, learning, general arousal
Agonist
Mimics effects of a n.t.
-Ex: Alcohol acts as GABA
Antagonist
Blocks effects of a n.t.
Anxiety: feelings of apprehension, nervousness, worry
Neurotransmitter changes: ↓GABA, ↑ glutamate, ↓serotonin (and to a lesser extent, dopamine), ↑ norepinephrine
Treatment: medications that block reuptake of serotonin (SSRIs such as Lexapro) or drugs that mimic actions of GABA (Valium or Xanax)
Depression: “a mental state characterized by a pessimistic sense of inadequacy and a despondent lack of activity”
Neurotransmitter changes: decreases in especially serotonin, but also norepinephrine and dopamine (or some combination), ↓ acetylcholine
Treatment: tricylic antidepressants (i.e. amitriptyline); reuptake inhibitors (SSRIs, NRIs, SNRIs, NDRIs)
Bipolar Disorder: characterized by “periods of elevated or irritable mood (mania), alternating with periods of depression”
Neurotransmitter changes: ↓serotonin (especially during times of depression/aggression/suicide attempts), ↑ norepinephrine and dopamine during manic phase, ↓ norepi and dopamine during depression
Treatment: mood stabilizers (i.e. Lithium); antidepressants (controversy)
SSRIs
Selective serotonin reuptake inhibitors (SSRIs) (i.e. Zoloft, Paxil)
NRIs
Selective noradrenaline reuptake inhibitors (NRIs) (i.e. Strattera)
SNRIs
Serotonin and norepinephrine reuptake inhibitors (SNRIs) (i.e. Cymbalta, Effexor)
NDRIs
Norepinephrine and dopamine reuptake inhibitors (NDRIs) (i.e. Wellbutrin)
What do the most commonly abused drugs stimulate the release of?
Dopamine in the nucleus accumbens
Classifications of Recreational Drugs
Stimulants: increase excitement, alertness, motor activity, and elevate mood
Depressants: drugs that slow the activity of the CNS
Hallucinogens: drugs that can produce alterations in perception (i.e. hallucinations)
Stimulants: Amphetamines, Cocaine, MDMA (Ecstasy), Nicotine
Amphetamines:
-Increases release of monamines, especially dopamine
-Enhancing dopamine release, blocks reuptake of dopamine
Cocaine:
-Blocks reuptake of monoamines, especially DOPA
Ecstasy:
-Increases release of DOPA and serotonin
- Overstimulates serotonin releasing neurons, leads to cell death
Nicotine:
- Stimulates acetylcholine receptors, leads to increased release of DOPA
Depressants: Alcohol, Opiates
Alcohol: -Binds to GABA receptors, increases DOPA, decreases glutamate Opiates: - Increased dopamine release -Increase GABA in many brain areas
Hallucinogens: Marijuana, LSD, Ketamine
Marijuana:
- Decrease glutamate in certain areas and GABA in others
- Increased DOPA release same way as opiates
- May also increase serotonin
