Abstract
Evidence related to the mediation of amphetamine anorexia is discussed in terms of adrenergic, “release-of-restraint,” and “irritative” conditions. Although the primary sire of the drug's action appears to be the adrenergic classical “feeding center,” further changes in the action following subcortical lesions of the CNS are less clearly understood. Proposed frameworks for the organization of such further changes are suggested in terms of “release-of-restraint” and “irritative” conditions. Finally, the need for investigating the role of cortical sites and cortical-hypothalamic interaction in the mediation of amphetamine anorexia is indicated.
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6 articles.
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