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Serotonergic receptor

Correlation between clinical effectiveness and receptor affinities, however, can be seen with other receptors in addition to the dopamine D2 receptor. These include other dopaminergic receptors, as well as noradrenergic and serotonergic receptors. For example, most antipsychotics also have high affinity for a -adrenoceptors and 5-HT2 receptors (225). Some antipsychotics have been shown to be selective for the adrenoceptor versus the a -adrenoceptor, for example, spiperone [749-02-0] (226) and risperidone (61) (221]... [Pg.236]

Agrawal AK, Anand M, Zaidi NE, et al. 1983. Involvement of serotonergic receptors in endosulfan neurotoxicity. Biochem Pharmacol 32 3591-3593. [Pg.273]

HT1D receptors—3-hydroxytrypfamine receptors (a subclass of serotonergic receptors)... [Pg.284]

Lesions of serotonergic neurons in laboratory animals have been reported by some, but not all, investigators to disrupt locomotor rhythms or to result in the loss of the daily rhythm of corticosterone. There is evidence that, in the hamster, the median raphe nucleus projects to the SCN whereas the dorsal raphe nucleus innervates the IGL furthermore, the serotonergic innervation to the SCN and not the IGL is necessary for the photic entrainment of locomotor activity [22]. It appears then, that the SCN circadian pacemaker or clock is modulated by stimulation of serotonergic receptors in the SCN and that serotonergic projections to the SCN may modulate the phase of the SCN in intact animals. [Pg.239]

The 5-HT syndrome can also be produced by a number of treatments whose primary actions are not expressed at serotonergic receptors. For example, in MAOI-pretreated rats, the intraventricular administration of dopamine or systemic treatment with the dopamine precursor /-dihydroxyphenylalanine (/-DOPA) in combination with an MAOI results in the 5-HT syndrome... [Pg.36]

Jacobs, B. L., Rasmussen, K., and Heym, J. (1982) Evidence that some of the behavioral effects of LSD are mediated by a direct action at postsynaptic serotonergic receptors. Soc. Neurosci. Abstr., 8 390. [Pg.107]

Bourgoin, S., Artaud, F., Enjalbert, A., Hery, F., Glowinski, J., and Hamon, M. (1977) Acute changes in central serotonin metabolism induced by the blockade or stimulation of serotonergic receptors during ontogenesis in the rat. J. Pharmacol. Exp. Ther., 202 519-531. [Pg.119]

The most commonly used therapies for anxiety and depression are selective serotonin reuptake inhibitors (SSRIs) and the more recently developed serotonin noradrenaline reuptake inhibitors (SNRIs). SSRIs, which constitute 60% of the worldwide antidepressant and antianxiety market, are frequently associated with sexual dysfunction, appetite disturbances and sleep disorders. Because SSRIs and SNRIs increase 5-HT levels in the brain, they can indirectly stimulate all 14 serotonergic receptor subtypes [2,3], some of which are believed to lead to adverse side effects associated with these drugs. Common drugs for short-term relief of GAD are benzodiazepines. These sedating agents are controlled substances with addictive properties and can be lethal when used in combination with alcohol. The use of benzodiazepines is associated with addiction, dependency and cognitive impairment. [Pg.458]

Sponge -Astrosclera willeyana Manzacidins A-D - a-ad renoreceptor blockers and serotonergic receptor antagonists 264, 265... [Pg.57]

Figure 7. A serotonergic synapse including a depiction of the acute tryptophan depletion method discussed in the text. All large neutral amino acids (SLNAAs) share a common blood-brain barrier transporter. The serotonergic precursor, tryptophan, essentially competes with the other LNAAs for transport. Thus tryptophan is uniquely susceptible to acute dietary manipulation. Numerous serotonergic receptor types exist, including presynaptic S-HTm and (somatodendritic) 5-HTia autoreceptors and postsynaptic 5-HTia, 5-HTid, 5-HT2a 5-HT2c 5-HT3 and 5-HT4 receptors. Additional modulation of serotonin activity can occur via the action of selective serotonin re-uptake inhibitors (SSRls) including fluoxetine, fluvoxamine, and citalopram. Figure 7. A serotonergic synapse including a depiction of the acute tryptophan depletion method discussed in the text. All large neutral amino acids (SLNAAs) share a common blood-brain barrier transporter. The serotonergic precursor, tryptophan, essentially competes with the other LNAAs for transport. Thus tryptophan is uniquely susceptible to acute dietary manipulation. Numerous serotonergic receptor types exist, including presynaptic S-HTm and (somatodendritic) 5-HTia autoreceptors and postsynaptic 5-HTia, 5-HTid, 5-HT2a 5-HT2c 5-HT3 and 5-HT4 receptors. Additional modulation of serotonin activity can occur via the action of selective serotonin re-uptake inhibitors (SSRls) including fluoxetine, fluvoxamine, and citalopram.
Metabotropic G-protein linked receptors are also modulated by general anesthetics. In particular, the current produced through activation of muscarinic receptors (Ml) for acetylcholine and the serotonergic receptor 5HT2 is inhibited by halothane, isoflurane and enflurane (Lin et al., 1993 Minami et al., 1994 Durieux, 1995). Ketamine inhibits muscarinic receptors although there is no stereospecificity of inhibition (Durieux Nietgen, 1997). The S-isomer of ketamine is more potent as an anesthetic than the R-isomer (Benthuysen et al., 1989). It is thus unlikely that the Ml muscarinic receptor plays a role in... [Pg.157]

Beyond their action upon SERT and NET, venlafaxine (1), milnacipran (2) and duloxetine (3) are remarkably selective molecules. All three of them have displayed very low in vitro affinity Ki > 3(X)0 nM) for ai- and a2-adrenergic, histamine Hj, muscarinic, and DA D2 receptors, consistent with favorable side-effect profiles. Venlafaxine (1) and duloxetine (3) also have low affinity for a number of serotonergic receptors, and do not inhibit monoamine oxidase A or B. An expanded in vitro receptor profile of >50 receptors and binding sites... [Pg.202]

Agents from this class of antidepressants are selective blockers of the re-uptake of serotonin at presynaptic neurones and have little if any effects on muscarinic, histaminergic, adrenergic or serotonergic receptors. They are as effective as the tricyclic antidepressants in the management of depressive disorders, but have less cardiovascular effects. They have less anticholinergic activity and because of their lower risk of cardiotoxicity in overdose they... [Pg.353]

Which Serotonergic Receptor Subsystem Is Implicated in Obsessive-Compulsive Disorder ... [Pg.476]

Lapierre YD, Browne M, Horn E, et al Treatment of major affective disorder with fluvoxamine. J Clin Psychiatry 48 65-68, 1987 Lapierre YD, Ravindran AV, Bakish D Dysthymia and serotonin. Int Clin Psychopharmacol 8 (suppl 2) 87-90, 1993 Lapin 1, Oxenkrug G Intensification of the central serotonergic process as a possible determinant of thymoleptic effect. Lancet 1 132-136, 1969 Larkin JG, McKee PJ, Blacklaw J, et al Nimodipine in refractory epilepsy a placebo-controlled, add-on study. Epilepsy Res 9 71-77, 1991 Larsson LI, Rehfeld JF Localization and molecular heterogeneity of cholecystokinin in the central and peripheral nervous system. Brain Res 165 201-218, 1979 Laruelle M, Abi-Dargham A, Casanova M, et al Selective abnormality of prefrontal serotonergic receptors in schizophrenia a post mortem study. Arch Gen Psychiatry 50 810-818, 1993... [Pg.680]

Newman ME, Drummer D, Lerer B Single and combined effects of desimipramine and lithium on serotonergic receptor number and second messenger function in rat brain. J Pharmacol Exp Ther 252 826-831, 1990 Newman ME, Lerer B, Lichtenberg P, et al Platelet adenylate cyclase activity in depression and after clomipramine and lithium treatment. Psychopharmacology 109 231-234, 1992... [Pg.709]


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