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While most research pertaining to glutamate disruption and cognitive dysfunction in schizophrenia has focused on the NMDA receptor [9,10,11], recent attention has turned to manipulations that target glutamate synthesis, release or reuptake

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14 - 21 Consequently, as we emphasized, 4 since the original organoprotective/healing intention of stress coping response 22 confronts with unsuccessful realization by the Selye’s “first mediator” in stress response, 25 that integrative mediator that integrates the adaptive bodily response to stress, remains obscured in the highly sophisticated latter Selye’s stress concept presentation