Flow of information through receptor subtypes at norepinephrine and serotonin synapses following chronic TCA drug administration. A cascade of events leads to altered receptor-mediated physiology of the norepinephrine (NE) and serotonin (5-HT) synapses of the brain following long-term TCA drug administration. The adaptive changes in synaptic physiology are triggered by selective inhibition of the NE and/or 5-HT neuronal reuptake systems. Responses at p- and a2-adrenoceptors are depressed, whereas responses at 5-HT1A receptors are enhanced. Responses at a1-adrenoceptors and 5-HT1B receptors remain unchanged. Accordingly, the postsynaptic flow of information at NE and 5-HT synapses will be reduced through p-adrenoceptors but enhanced through 5-HT1A receptors. Although the responsiveness of a1-adrenoceptors remains unchanged, it is likely that transmission through these postsynaptic sites will be enhanced. In this regard, desensitization of a2-adrenoceptors will provide greater concentrations of synaptic NE to activate normosensitive postsynaptic a1-adrenoceptors.
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