Glucocorticoid enhancement of serotonergic facilitation of cat spinal monosynaptic motor neuron excitation

Edward D. Hall

doi:10.1016/0014-4886(80)90112-0

Glucocorticoid enhancement of serotonergic facilitation of cat spinal monosynaptic motor neuron excitation

Edward D. Hall

Neuroscience

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

Intensive pretreatment with triamcinoline diacetate (8 mg/kg, i.m. once daily for 7 days) was found in the acute spinal (decerebrate) cat to potentiate the increase in monosynaptic spinal reflex transmission caused by coadministration of the serotonin precursor, d, l-5-hydroxytryptophan, and amitriptyline, a selective serotonin reuptake inhibitor. In addition, the ability of methysergide, a selective serotonin receptor antagonist, to reverse the monosynaptic excitatory actions of d, l-5-hydroxytryptophan plus amitriptyline was significantly reduced. This apparent glucocorticoid enhancement of the actions of a serotonergic spinal system that is facilitatory to motor neuron excitation may have relevance to the therapy of degenerative motor neuron disorders.

Original language	English
Pages (from-to)	589-594
Number of pages	6
Journal	Experimental Neurology
Volume	68
Issue number	3
DOIs	https://doi.org/10.1016/0014-4886(80)90112-0
State	Published - Jun 1980

Bibliographical note

Funding Information:
Abbreviations: 5-HTP-D,r-5hydroxytryptophan. ’ The author gratefully acknowledges the dedicated technical assistance of Mrs. Brigitte Hirst’and a gift of triamcinolone diacetate (Aristocort) from Lederle Laboratories of Pearl River, New York. The support for this project was provided by a grant from the Amyotrophic Lateral Sclerosis Society of America.

ASJC Scopus subject areas

Neurology
Developmental Neuroscience

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title = "Glucocorticoid enhancement of serotonergic facilitation of cat spinal monosynaptic motor neuron excitation",

abstract = "Intensive pretreatment with triamcinoline diacetate (8 mg/kg, i.m. once daily for 7 days) was found in the acute spinal (decerebrate) cat to potentiate the increase in monosynaptic spinal reflex transmission caused by coadministration of the serotonin precursor, d, l-5-hydroxytryptophan, and amitriptyline, a selective serotonin reuptake inhibitor. In addition, the ability of methysergide, a selective serotonin receptor antagonist, to reverse the monosynaptic excitatory actions of d, l-5-hydroxytryptophan plus amitriptyline was significantly reduced. This apparent glucocorticoid enhancement of the actions of a serotonergic spinal system that is facilitatory to motor neuron excitation may have relevance to the therapy of degenerative motor neuron disorders.",

author = "Hall, {Edward D.}",

note = "Funding Information: Abbreviations: 5-HTP-D,r-5hydroxytryptophan. {\textquoteright} The author gratefully acknowledges the dedicated technical assistance of Mrs. Brigitte Hirst{\textquoteright}and a gift of triamcinolone diacetate (Aristocort) from Lederle Laboratories of Pearl River, New York. The support for this project was provided by a grant from the Amyotrophic Lateral Sclerosis Society of America.",

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PY - 1980/6

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N2 - Intensive pretreatment with triamcinoline diacetate (8 mg/kg, i.m. once daily for 7 days) was found in the acute spinal (decerebrate) cat to potentiate the increase in monosynaptic spinal reflex transmission caused by coadministration of the serotonin precursor, d, l-5-hydroxytryptophan, and amitriptyline, a selective serotonin reuptake inhibitor. In addition, the ability of methysergide, a selective serotonin receptor antagonist, to reverse the monosynaptic excitatory actions of d, l-5-hydroxytryptophan plus amitriptyline was significantly reduced. This apparent glucocorticoid enhancement of the actions of a serotonergic spinal system that is facilitatory to motor neuron excitation may have relevance to the therapy of degenerative motor neuron disorders.

AB - Intensive pretreatment with triamcinoline diacetate (8 mg/kg, i.m. once daily for 7 days) was found in the acute spinal (decerebrate) cat to potentiate the increase in monosynaptic spinal reflex transmission caused by coadministration of the serotonin precursor, d, l-5-hydroxytryptophan, and amitriptyline, a selective serotonin reuptake inhibitor. In addition, the ability of methysergide, a selective serotonin receptor antagonist, to reverse the monosynaptic excitatory actions of d, l-5-hydroxytryptophan plus amitriptyline was significantly reduced. This apparent glucocorticoid enhancement of the actions of a serotonergic spinal system that is facilitatory to motor neuron excitation may have relevance to the therapy of degenerative motor neuron disorders.

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Glucocorticoid enhancement of serotonergic facilitation of cat spinal monosynaptic motor neuron excitation

Abstract

Bibliographical note

ASJC Scopus subject areas

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