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Depression supersensitive receptors

Some of the depressant behavioral effects of hallucinogens may involve inhibitory postsynaptic 5-HT receptors. For example, depressant effects of hallucinogens on startle and locomotor activity may result from activation of these receptors, since 5-HT itself has similar effects. Studies on supersensitivity are lacking, however, and, again, the absence of selective antagonists prevents definitive conclusions. [Pg.162]

Thus it may be speculated that the 5-HTib/id receptors are supersensitive in depression, thereby leading to a reduced intersynaptic concentration of 5-HT with a consequent increase in the number of postsynaptic 5-HT2 receptor sites. However, only the development of highly selective 5-HTib/id antagonists will enable this hypothesis to be tested. [Pg.152]

Evidence that central muscarinic receptors are supersensitive in depressed patients and that chronic antidepressant treatments normalize the supersensitivity of these receptors. This effect does not depend on any intrinsic anticholinergic activity of the antidepressant (i.e. it is an indirect, adaptive effect). [Pg.161]

Although postsynaptic DA agonists and presynaptic Dj autoreceptor antagonists share a common property of enhancing DA transmission, Dj autoreceptor agonists have been developed specifically to block DA transmission as an alternative approach to antipsychotic therapy (Benkert et al. 1992). A variety of such compounds are available (Seyfried and Boettcher 1990), four of which—talipexole, pramipexole, roxindole, and OPC-4392 —have been evaluated as antipsychotics in schizophrenic patients (Benkert et al. 1992). Only roxindole has been tested in depression, and then only in two uncontrolled pilot studies over 4 weeks of treatment (Benkert et al. 1992 M. Kellner et al. 1994). Response rates similar to those of imipramine were observed, with a fast onset of action in some patients. Roxindole s antidepressant action may lie in its ability to selectively stimulate supersensitive postsynaptic Dj receptors, and thereby enhance DA function, or in its additional properties as an inhibitor of serotonin reuptake and as a 5-HT, receptor agonist (Benkert et al. 1992 Seyfried et al. 1989). [Pg.230]

On balance, these actions could support a decrease rather than an increase in the functional state of CNS NE transmission, because depression can be conceptualized as a state of supersensitive catecholamine receptors secondary to decreased NE availability. This reasoning is consistent with the original hypothesis of diminished NE functioning, with antidepressants returning receptors to a more normal state of sensitivity. Siever and Davis ( 41) further elaborated on this concept by suggesting the possibility of dysregulation in the homeostatic mechanisms of one or more neurotransmitter systems, culminating in an unstable or erratic output. [Pg.115]

Evidence accumulated in 1978 for a catecholamine receptor supersensitivity theory of depression. 8 The therapeutic action of antidepressants may be due to delayed post-synaptic changes in receptor sensitivity, rather than to acute events like uptake. Various drugs, including TCA, mianserin, viloxazine and iprindol, as well as electroconvulsive therapy (ECT), but not selective 5-HT uptake inhibitors, caused central alpha-adrenoceptor subsensitivity in rats as measured by noradrenaline (NA)-associated adenylate cyclase or by receptor binding. In vivo, the effects were associated with chronic but not acute treatment, paralleling the clinical effects. MAOI may cause similar effects on chronic but not acute treatment. , 24-27 Brain NA turnover in rats was decreased by chronic desipramine and other TCA, but unaffected by iprindol and increased by mianserin.3,28... [Pg.1]

Berk, M., Plein, H., and Ferreira, D. 2001. Platelet glutamate receptor supersensitivity in major depressive disorder. Chn. Neuropharmacol. 24 129-132. [Pg.362]


See other pages where Depression supersensitive receptors is mentioned: [Pg.114]    [Pg.133]    [Pg.516]    [Pg.171]    [Pg.175]    [Pg.314]    [Pg.30]    [Pg.162]    [Pg.234]    [Pg.78]    [Pg.162]    [Pg.22]    [Pg.133]    [Pg.14]    [Pg.42]    [Pg.44]    [Pg.358]   
See also in sourсe #XX -- [ Pg.175 ]




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