Abstract
This chapter concerns the animal model of endogenous depression produced by clorimipramine (CLI) treatment of neonatal rats. Three hypotheses about this model are discussed: (1) the CLI treated rats are a valid animal model of human endogenous depression; (2) the neonatal CLI treatment produces the adult rat “depression” by neonatal REM sleep deprivation (RSD), rather than by altering neonatal aminergic neurotransmission; and (3) the neural substrate of adult “depressed” behaviors is an altered neuronal firing pattern, rather than an altered aminergic neurotransmission. At the end of the chapter I propose a theory about how neonatal RSD produces alterations in neuronal firing patterns that form a physiological substrate for depressed behaviors.
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