The finding that some opioid-mediated forms of stress-induced analgesia are antagonized by hypophysectomy and dexamethasone has led to the suggestion that beta-endorphin, released from the pituitary, may mediate these analgesic reactions. "Long-term analgesia" (an opioid-mediated form of stress-induced analgesia), which is blocked by dexamethasone and hypophysectomy, was also blocked by adrenalectomy and reinstated with corticosterone therapy. Corticosterone is proposed to play a permissive role in long-term analgesia and to be a critical hormone mediating this phenomenon.

There is compelling evidence that behavioral events after neurochemical function and that altered neurochemical function can change behavior. Such processes have been related both to neurotransmitters and to neuromodulators, together termed neuroregulators. Available research tools and theoretical constructs have begun to permit studies of certain types of behavior, primarily those related to emotional states and drives. This work is changing long-held concepts about severe mental disorders and the treatment of them.

Five products of the dynorphin gene-cY-neo-endorphin, P-neo-endorphin, dynorphin A, dynorphin A-(1-8), and dynorphin B-were measured in various regions of rat brain and in rat spinal cord and pituitary. Specific antisera were used, supplemented by gel permeation analysis and high performance liquid chromatography, confirming the presence of dynorphin-32, dynorphin A, and dynorphin B in rat brain. In whole brain, a-neo-endorphin, dynorphin A-(1-8), and dynorphin B are present in much greater amounts than P-neo-endorphin or dynorphin A. Although a general parallelism was found in the distribution of the five peptides, there were also noteworthy exceptions, suggesting that differential processing may occur.

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