Hostname: page-component-76fb5796d-x4r87 Total loading time: 0 Render date: 2024-04-26T00:42:04.129Z Has data issue: false hasContentIssue false
  • English
  • Français

A Pilot Study of the Mechanism of Action of Desipramine

Published online by Cambridge University Press:  29 January 2018

S. A. Checkley ,
A. P. Slade ,
E. Shur  and
S. Dawling
S. A. Checkley
Affiliation:
Institute of Psychiatry, De Crespigny Park, London SE5 8AF; Maudsley Hospital, London SE5 6AZ
A. P. Slade
Affiliation:
Institute of Psychiatry, De Crespigny Park, London SE5 8AF
E. Shur
Affiliation:
Institute of Psychiatry, De Crespigny Park, London SE5 8AF
S. Dawling
Affiliation:
Poisons Unit, Guys Hospital, London SE1
Get access Rights & Permissions [Opens in a new window]

Summary

To test the hypothesis that desipramine alters α adrenoceptor function in depressed patients, the effects of clonidine upon growth hormone sedation and blood pressure have been measured in depressed patients before and after treatment with desipramine. After three weeks of treatment the hypotensive and sedative effects of clonidine were inhibited in all patients even though plasma desipramine concentrations at this time varied from 42 to 560 μg/l. Growth hormone responses to clonidine were enhanced in five of the six patients but this effect was not statistically significant. These findings are consistent with the hypothesis that in these patients desipramine altered α adrenoceptor function: other explanations are discussed.

Type
Research Article
Information
The British Journal of Psychiatry , Volume 138 , Issue 3 , March 1981 , pp. 248 - 251
Copyright
Copyright © Royal College of Psychiatrists, 1981 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Bergstrom, D. A. & Kellar, K. F. (1979) Adrenergic and serotonergic receptor binding in rat brain after chronic desmethylimipramine treatment. Journal of Pharmacology and Experimental Therapeutics, 209, 256–261.Google Scholar
Braithwaite, R. (1979) Measurement of antidepressant drugs. Proceedings of the Analytical Division of the Chemical Society, 16, 69–72.Google Scholar
Checkley, S. A. & Crammer, J. L. (1977) Hormone responses to methylamphetamine in depressive illness. British Journal of Psychiatry, 131, 582–586.Google Scholar
Checkley, S. A. (1979) Corticosteroid and growth hormone responses to methylamphetamine in depressive illness. Psychological Medicine, 9, 107–115.Google Scholar
Checkley, S. A. (1980) Neuroendocrine tests of monoamine function in Man: a review of basic theory and its application to the study of depressive illness. Psychological Medicine, 10, 35–53.Google Scholar
Checkley, S. A. Slade, A. P. & Shur, E. (1981) Growth hormone and other responses to clonidine in patients with endogenous depression. British Journal of Psychiatry, 138, 51–55.Google Scholar
Chiodo, L. A. & Antelman, S. M. (1980) Tricyclic antidepressants induce subsensitivity of presynaptic dopamine autoreceptors. European Journal of Pharmacology, 64, 203–204.Google Scholar
Crews, F. T. & Smith, C. B. (1978) Pre-synaptic alpha-receptor subsensitivity after long-term anti-depressant treatment. Science, 202, 322–324.Google Scholar
De Montigny, C. & Aghajanian, G. K. (1978) Tricyclic antidepressants: long-term treatment increases responsivity of rat forebrain neurons to serotonin. Science, 202, 1303–1305.Google Scholar
Finch, L. Harvey, C. A. Hicks, P. E. & Owen, D. A. A. (1978) Clonidine induced hypotension: further evidence of a central interaction with histamine H2 receptor antagonists in the rat. Neuropharmacology, 17, 307–313.Google Scholar
Green, J. P. & Maayani, S. (1977) Tricyclic antidepressants block histamine H2 receptors in the brain. Nature, 269, 163–165.CrossRefGoogle Scholar
Iversen, L. L. (1965) The uptake and storage of noradrenaline in sympathetic nerves. Cambridge University Press.Google Scholar
Kanof, P. D. & Greengard, P. (1978) Brain histamine receptors as targets for antidepressant drugs. Nature, 272, 329–333.Google Scholar
Karppanen, H. Paakari, I. Paakari, P. Huotari, R. & Orua, A-L (1976) Possible involvement of central histamine H2 receptors in the hypotensive effect of clonidine. Nature, 259, 587–588.Google Scholar
Maggi, A. U'Prichard, D. C & Enna, S. J. (1980) Differential effects of antidepressant treatment of brain monoaminergic receptors. European Journal of Pharmacology, 61, 91–98.CrossRefGoogle ScholarPubMed
Maj, J. Baran, L. Sowinska, H. & Zielinski, M. (1975) The influence of cholinolytics on clonidine action. Polish Journal of Pharmacology and Pharmacy, 27, 17–26.Google Scholar
McMillen, D. A. Warnack, W. W. German, D. C. & Shore, P. A. (1980) Effects of chronic desipramine treatment on rat brain noradrenergic responses to α-adrenergic drugs. European Journal of Pharmacology, 61, 239–246.Google Scholar
Menkes, D. B. Aghajanian, G. K. & McCall, R. B. (1980) Chronic antidepressant treatment enhances α-adrenergic and serotonergic responses in the facial nucleus. Life Sciences, 27, 45–55.CrossRefGoogle ScholarPubMed
Olpe, R.-R & Schellenberg, A. (1980) Reduced sensitivity of neurons to noradrenaline after chronic treatment with antidepressant drugs. European Journal of Pharmacology, 63, 7–13.Google Scholar
Peroutka, S. J. & Snyder, S. H. (1980) Long-term antidepressant treatment decreases spiroperidollabelled serotonin receptors. Science, 210, 88–90.Google Scholar
Sarai, K. Frazer, A. Brunswick, D. & Mendels, J. (1978) Desmethylimipramine-induced decrease in beta-adrenergic receptor binding in rat cerebral cortex. Biochemical Pharmacology, 27, 2179–2181.CrossRefGoogle ScholarPubMed
Sellinger-Barnette, M. M. Mendels, J. & Frazer, A. (1980) The effect of psychoactive drugs on beta-adrenergic receptor binding sites in rat brain. Neuropharmacology, 19, 447–454.Google Scholar
Senna, G. Argiolas, A. Klimek, U. Fadda, F. & Gessa, G. L. (1979) Chronic treatment with antidepressants prevents the inhibitory effects of small doses of apomorphine on dopamine synthesis and motor activity. Life Sciences, 25, 415–424.Google Scholar
Slade, A. P. & Checkley, S. A. (1980) A neuroendocrine study of the mechanism of action of ECT. British Journal of Psychiatry, 137, 217–221.Google Scholar
Snyder, S. H. & Yamamura, H. I. (1977) Antidepressants and the muscarinic acetylcholine receptor. Archives of General Psychiatry, 34, 236–239.Google Scholar
Spitzer, R. L. Endicott, J. & Robbins, E. (1977) Research diagnostic criteria (RDC) for a selected group of functional disorders. 3rd edition. New York State Psychiatric Institute: New York, 1977.Google Scholar
Svensson, T. H. & Usdin, T. (1978) Feedback inhibition of brain noradrenaline neurones by tricyclic antidepressants: α receptor mediation. Science, 202, 1089–1091.Google Scholar
Wolfe, B. B. Harden, T. K. Sporn, J. R. & Molinoff, P. B. (1978) Presynaptic modulation of beta adrenergic receptors in rat cerebral cortex after treatment with antidepressants. Journal of Pharmacology and Experimental Therapeutics, 207, 446–457.Google ScholarPubMed
Vogt, M. (1977) Histamine H2 receptors in the brain and sleep produced by clonidine. British Journal of Pharmacology, 61, 441–443.Google Scholar
Vetulani, J. Stawarz, R. J. Dingell, J. U. & Sulser, F. (1976) A possible common mechanism of action of antidepressant treatments. Naunyn-Schmiedeberg's Archives of Parmacology, 293, 109–114.Google Scholar
Submit a response

eLetters

No eLetters have been published for this article.