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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 selective serotonin reuptake inhibitor or serotonin–norepinephrine reuptake inhibitor or noradrenergic α2-receptor antagonist with specific serotonergic receptors-2 and -3 antagonism or tricyclic antidepressant 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 such as 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 selective serotonin reuptake inhibitor or serotonin–norepinephrine reuptake inhibitor or noradrenergic α2-receptor antagonist with specific serotonergic receptors-2 and -3 antagonism or tricyclic antidepressant by bypassing the serotonergic autoreceptors desensitization phenomenon/effects. Finally, the pro-serotonergic neurotransmission enhancing activity of an atypical antipsychotic in the absence or presence of selective serotonin reuptake inhibitor or serotonin–norepinephrine reuptake inhibitor or noradrenergic α2-receptor antagonist with specific serotonergic receptors-2 and -3 antagonism or tricyclic antidepressant is completely antagonized and diverted away from the somatodendritic serotonergic 5-HT1A and 5-HT7 autoreceptors, and postsynaptic serotonergic 5-HT1A, 5-HT2A, 5-HT2C, 5-HT6, and 5-HT7 receptors toward the other terminal presynaptic- and postsynaptic-serotonergic subtype receptors in the central nervous system

Figure 2: (a) Increase serotonin neurotransmitter at the somatodendritic region and the terminal presynaptic region, which is as a result of selective serotonin reuptake inhibitor or serotonin–norepinephrine reuptake inhibitor or noradrenergic α<sub>2</Sub>-receptor antagonist with specific serotonergic receptors-2 and  -3 antagonism or tricyclic antidepressant 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 such as 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 selective serotonin reuptake inhibitor or serotonin–norepinephrine reuptake inhibitor or noradrenergic α<sub>2</Sub>-receptor antagonist with specific serotonergic receptors-2 and  -3 antagonism or tricyclic antidepressant by bypassing the serotonergic autoreceptors desensitization phenomenon/effects. Finally, the pro-serotonergic neurotransmission enhancing activity of an atypical antipsychotic in the absence or presence of selective serotonin reuptake inhibitor or serotonin–norepinephrine reuptake inhibitor or noradrenergic α<sub>2</Sub>-receptor antagonist with specific serotonergic receptors-2 and  -3 antagonism or tricyclic antidepressant is completely antagonized and diverted away from the somatodendritic serotonergic 5-HT<Sub>1A</Sub> and 5-HT<Sub>7</Sub> autoreceptors, and postsynaptic serotonergic 5-HT<sub>1A</Sub>, 5-HT<sub>2A</Sub>, 5-HT<sub>2C</Sub>, 5-HT<sub>6</Sub>, and 5-HT<sub>7</Sub> receptors toward the other terminal presynaptic-  and postsynaptic-serotonergic subtype receptors in the central nervous system