By Earl Usdin, Menek Goldstein, Arnold Friedhoff, Anastasios Georgotas (eds.)
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Additional resources for Frontiers in Neuropsychiatric Research
F. (1977). Norepinephrinestimulated cyclic AMP accumulation in brain slices i n vitro after serotonin depletion or chronic administration of selective amine reuptake inhibitors. Arch. , 229: 42-51 Schweitzer, J. , Schwartz, R. and Friedhoff, A. J. (1979). Intact presynaptic terminals required for beta-adrenergic receptor regulation by desipramine. , 33: 377-379 Sellinger, M. , Mendels, J. and Frazer, A. (1980). The effect of psychoactive drugs on B-adrenergic receptor binding sites in rat brain .
C. J. (1975). Catecholamine-induced sub-sensitivity of adenylate cyclase associated with loss of B-adrenergic receptor binding sites. Proc. Natl. Acad. Sci. , Schwartz. P. and Costa, E. (1981). Dopaminergic modulation of vasoactive intestinal peptide in anterior pituitary. Proc. Natl. Acad. Sci. , Briley, M. Z. (1981). Regional distribution of [3H]-imipramine in rat brain . M. J. (1981). Immunoreactive substance P and serotonin present in the same dense-core vesicles. A. Z. (1979). Specific tricyclic antidepressant binding sites in rat brain.
If the interpretation of the experi men t s described above is correct, it is difficult to believe that a deficiency of noradrenergic transmission is a cause for those symptoms of depressive illnesses that are ameliorated by imipramine. In fact this drug causes an attenuation of the signal amplification elicited by NE on the adenylate cyclase activity coupled to S-adrenergic recognition sites. Therefore, a long-term treatment with imipramine aggravates rather than relieves the symptoms of NE deficiency .