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  Indian J Med Microbiol
 

Figure 2: (a) Increase serotonin neurotransmitter at the somatodendritic region and the terminal presynaptic region, which is as a result of an SSRI or SNRI or NASSA or TCA pharmacodynamics effect activates the combinations of the somatodendritic serotonergic 5-HT1A/5-HT7 autoreceptors and the terminal presynaptic serotonergic 5-HT1B/1D autoreceptors thereby leading to a decrease in the firing rate at the somatodendritic region and a decrease in serotonin neurotransmitter release from the terminal presynaptic region, respectively, thus reducing the antidepressant and the anxiolytic clinical responses (sensitization or pre-desensitization phenomenon/effects). (b) The addition of a drug like a selective 5-HT7 autoreceptor antagonist with 5-HT1A autoreceptor partial agonism (such as an atypical antipsychotic); or alternatively a selective 5-HT1A autoreceptor partial agonist (such as buspirone or tandospirone); or alternatively a selective 5-HT1A and 5-HT1B/1D autoreceptors antagonist (such as pindolol) can hasten the antidepressant and the anxiolytic clinical responses to an SSRI or SNRI or NASSA or TCA treatment by bypassing the serotonergic autoreceptors desensitization phenomenon/effects.

Figure 2: (a) Increase serotonin neurotransmitter at the somatodendritic region and the terminal presynaptic region, which is as a result of an SSRI or SNRI or NASSA or TCA pharmacodynamics effect activates the combinations of the somatodendritic serotonergic 5-HT<sub>1A</sub>/5-HT<sub>7</sub> autoreceptors and the terminal presynaptic serotonergic 5-HT<sub>1B/1D</sub> autoreceptors thereby leading to a decrease in the firing rate at the somatodendritic region and a decrease in serotonin neurotransmitter release from the terminal presynaptic region, respectively, thus reducing the antidepressant and the anxiolytic clinical responses (sensitization or pre-desensitization phenomenon/effects). (b) The addition of a drug like a selective 5-HT<sub>7</sub> autoreceptor antagonist with 5-HT<sub>1A</sub> autoreceptor partial agonism (such as an atypical antipsychotic); or alternatively a selective 5-HT<sub>1A</sub> autoreceptor partial agonist (such as buspirone or tandospirone); or alternatively a selective 5-HT<sub>1A</sub> and 5-HT<sub>1B/1D</sub> autoreceptors antagonist (such as pindolol) can hasten the antidepressant and the anxiolytic clinical responses to an SSRI or SNRI or NASSA or TCA treatment by bypassing the serotonergic autoreceptors desensitization phenomenon/effects.