Ch. 16.9- Antidepressants

Monoamine theory of depression

under activity of serotonin and norepinephrine synapses - generates depression

• up regulation of serotonin/norepinephrine receptors in autopsies studies of people with depression

• most effective drugs target monoamines

monoamine oxidase inhibitors (MAOIs)

deactivates monoamine oxidase; an enzyme that breaks down serotonin, dopamine and norepinephrine - important for neural communication to clear the synapse for new communication. preventing this will leave more neurotransmitters allowing more binding

replaced by selective serotonin reuptake inhibitors (SSRIs)

Tricyclic antidepressants

block reuptake of serotonin/norepinephrine - blocking these makes neurotransmitters more available and allowing easier binding

replaced by selective serotonin reuptake inhibitors (SSRIs)

mechanisms of action

antidepressant drugs take weeks to months before producing a clinical effect - immediate increase in serotonin but no affect for awhile

• down regulation of 5HT1A receptors aligns with the clinical affect

Down regulation

Pré-synaptic neuron: A process where neurons decrease receptor number or sensitivity in response to prolonged stimulation.

Post-synaptic neuron: may reduce neurotransmitter release by detecting excess levels through autoreceptors.

Mechanisms of action (BDNF)

SSRIs stimulate release of BDNF which promotes neurogenesis in the hippocampus

hippocampus helps regulate HPA axis and reward circuitry, involved in contextualizing fear memories, and supports new learning and memories - helps also regulating feelings of reward. benefits circuitry and more behavioural adaptable ways