A nicotinic receptor antagonist enhances the hypothermic response to a muscarinic agonist

  title={A nicotinic receptor antagonist enhances the hypothermic response to a muscarinic agonist},
  author={S. Dilsaver and M. Majchrzak and R. Snider and R. Davidson},
  journal={Progress in Neuro-Psychopharmacology and Biological Psychiatry},
1. Chronic treatment with amitriptyline produces supersensitivity to the hypothermic effects of the muscarinic agonist oxotremorine. 2. Chronic treatment with amitriptyline also produces supersensitivity to the hypothermic effects of nicotine. 3. Oxotremorine and other naturally occurring muscarinic agonists are also nicotinic agonists. 4. Chronic treatment with amitriptyline produces time-dependent and reversible supersensitivity to the hypothermic effects of nicotine. 5. The authors assessed… 
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Involvement of nicotinergic mechanisms in thyrotropin-releasing hormone-induced neurologic recovery after concussive head injury in the mouse.
The results imply that TRH-induced improvement of recovery after concussion is not associated with increased activity of monoaminergic neurons in the brain, and suggests that the inhibitory effect of TRH upon unconsciousness after concussion in mice is mainly produced by activation of central cholinergic systems via nicotinic receptors.
Nicotine pretreatment diminished physostigmine-induced tremor in rats
The data analysis shows that acute or chronic nicotine administration can alleviate the physostigmine-induced tremor, and that the acute and chronic nicotine pretreatments alter physostIGmine spectrum profile.
Participació dels receptors muscarínics presinàptics (mAChRs) en l'eliminació de les connexions sinàptiques redundants durant el desenvolupament neuromuscular
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Cholinergic properties of desipramine and amoxapine: Assessment using a thermoregulation paradigm
  • S. Dilsaver, R. Davidson
  • Psychology, Medicine
    Progress in Neuro-Psychopharmacology and Biological Psychiatry
  • 1987
Mechanisms whereby drugs can produce cholinergic system supersensitivity, and the use of thermoregulation paradigms in assessing the properties of therapeutic agents is discussed.
Amitriptyline supersensitizes a central cholinergic mechanism
Evidence is presented that the chronic administration of amitriptyline can produce supersensitivity of a central muscarinic cholinergic mechanism, consistent with the facts that all tricyclic antidepressants are antimuscarinic agents and that classical antimuscarsinic compounds, such as scopolamine, up-regulate and supersensitize mus carinic cholinergic systems.
Regulation of catecholamine release. The muscarinic inhibitory mechanism
Publisher Summary This chapter discusses the muscarinic inhibitory mechanism for regulation of catecholamine release. The elucidation of a muscarinic mechanism which inhibits the release of
Amitriptyline: Long-term treatment elevates α-adrenergic and muscarinic receptor binding in mouse brain
It is suggested that the increase in alpha-adrenergic as well as in muscarinic binding is a consequence of a chronic blockade of these two types of receptors by amitriptyline in vivo.
Blockade by psychotropic drugs of the muscarinic acetylcholine receptor in cultured nerve cells.
The ability of antimuscarinics, tricyclic antidepressants, and antipsychotics to block the muscarinic acetylcholine receptor was determined using an assay for this receptor in cultured nerve cells using radioactively labeled guanosine 5'-triphosphate.
Nicotinic Effects of Antidepressants
Tricyclic antidepressants (TCAs) bind to muscarinic cholinergic receptors (mAChRs) and produce biochemical and physiological evidence of the blockade of muscarinic mechanisms.1 Supersensitization of
Cholinergic activity regulates muscarinic receptors in central nervous system cultures.
  • R. Siman, W. Klein
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1979
The receptor blocker atropine causes an increase in receptor levels in central nervous system cultures but has no effect on receptors in cultures of adrenergic neuroblastoma cells, the increase likely reflects blockade of endogenous regulation.
Regulation of Muscarinic Acetylcholine Receptor Concentration in Cloned Neuroblastoma Cells
Kinetically, the increase in receptors following withdrawal of agonists is slower than the decrease caused by addition of agonist, suggesting that bursts of receptor activation could lower receptor levels.
Long-term regulation of muscarinic acetylcholine receptors on cultured nerve cells.
Results indicate that different cellular mechanisms are involved in the short-term and long-term desensitization of muscarinic receptors, suggesting that this process may involve a conformational change in theMuscarinic receptor.
The Nature of Muscarinic Receptor Binding
During the last decade, the availability of muscarinic cholinergic drugs of high specific activity has enabled a direct characterization of the way in which acetylcholine and other drugs interact