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The effects of capsaicin, the major pungent component of hot peppers, were assessed on neuropeptide levels and on sensory function in neonatal and adult rats and in adult guinea pigs. Systemic doses of capsaicin in rats treated while neonates or while adults produced marked depletion of substance P (SP) in dorsal roots plus ganglia (DRG) and in dorsal spinal cord without altering tail-flick latencies in the treated animals. Guinea pigs had several-fold higher levels of SP than did rats in DRG and dorsal cord. In adult guinea pigs, systemic doses of capsaicin as low as 2.5 mg/kg depleted SP in DRG while a 10 mg/kg dose depleted the peptide maximally in DRG (85% decrease) and in the dorsal cord (35% decrease). High doses of capsaicin in guinea pigs had no consistent effects on levels of radioimmunoassayable cholecystokinin (CCK), vasoactive intestinal polypeptide, or somatostatin although a transient decrease in CCK levels was observed four days after dosing in DRG and in ventral cord. A single 5 mg/kg dose of capsaicin rendered animals completely insensitive to chemical irritation of the cornea without affecting sensitivity to noxious heat. Higher doses of capsaicin produced a marked insensitivity to nociceptive and non-nociceptive heat as well as to chemical irritation without affecting other sensory modalities. The SP depletion and sensory deficits produced by a single 50 mg/kg dose of capsaicin were still evident ten weeks later. The pattern of selectivity of the sensory deficits produced by capsaicin differed from that produced by morphine which was active against all forms of nociceptive stimuli. High doses of capsaicin also induced skin lesions and corneal opacities in guinea pigs. The syndrome of sensory effects produced by capsaicin in guinea pigs closely resembles the pattern of sensory deficits in familial dysautonomia, an autosomal recessive disorder in which there is a disappearance of SP from the substantia gelatinosa of the spinal cord. The results indicate that in the guinea pig capsaicin is potent at producing a unique, long-lasting syndrome of peripheral sensory deficits that may result from an action of the compound on SP-containing primary afferent neurons. Capsaicin is a valuable pharmacological tool for investigation of the neurochemistry and neurophysiology of primary afferent neurons and animals treated with the agent may be useful laboratory models of some forms of peripheral neuropathy.

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Thesis (Ph. D.)--West Virginia University, 2003. / Title from document title page. Document formatted into pages; contains xiii, 82, [148] p. : ill. (some col.). Includes abstract. Includes bibliographical references.

Thesis (M.Sc.)--Memorial University of Newfoundland, Memorial University of Newfoundland, 1998. / Typescript. Bibliography: leaves 118-132.

Bibliography: leaves 141-182. / xi, 182, [36] leaves, [12] leaves of plates : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / The aim of this thesis is to analyse the molecular events associated with CD8+ T lymphocyte activity in HSV infected sensory ganglia. The role of CD8+ T cells in cytokine responses to ganglionic HSV infection is investigated, with particular reference to the Th1/Th2 paradigm and a known anti-viral mediator, IFN-[gamma]. A non-directed method of mRNA analysis is applied to HSV infected ganglia with the specific aim of identifying transcripts that may be associated with CD8+ T cell activity in the nervous system. / Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1997

Dorsal root ganglia (DRG) cell preparations are commonly used to study the properties of sensory neurons in relation to nociception. A typical DRG cell preparation contains both neurons and glial cells, and in addition to a conventional supportive role of glial cells, an increasing volume of literature has reported interactions between neurons and accompanying glial cells. A typical mixed DRG cell preparation can be separated into a neuron-enriched cell fraction and a preparation of purified glial cells. Using these purified cell fractions, we can study the relative contributions and interactions between neurons and glial cells in regulating neurite outgrowth and adenylyl cyclase-dependent cell signalling activity in vitro. / From our previous studies, pretreating DRG cell cultures with pertussis toxin (PTx) caused neurite retraction over a period of 2 h following the initial stimulus of removal from incubator. The purpose of the current study was to investigate whether this PIx-dependent response was specific to anyone of the three subpopulations of DRG neurons. Interestingly, no neurite retraction response was observed in enriched DRG cultures, including cultures enriched with isolectin B4 (IB4)-positive neurons or IB4-negative neurons. Addition of glial cells or conditioned medium from glial cells to IB4-negative cultures was necessary to restore the PTx-dependent neurite retraction response, which was then only observed in large diameter proprioceptive neurons. To conclude, glial cells constitutively release factor/s that stimulate neurite retraction in larger diameter neurons, and is counterbalanced by neuroprotective Gilo protein signalling pathway. / From our studies, we have provided evidence of bidirectional interactions between neurons and glial cells, with glial cells regulating neurite outgrowth and neurons regulating adenylyl cyclase activity in glial cells. These findings reveal the properties of glial cells in regulating neurite outgrowth and in producing prostanoid-stimulated responses. Moreover, our fmdings provide foundation to understand complex neuron-glia interactions in vivo which will eventually help to overcome obstacles in promoting neurite regeneration and in controlling pain. / In a parallel study, we proved that hyperalgesic agents such as prostaglandin E2 (PGE2) and the prostacyclin (PGI2) mimetic (cicaprost) stimulate cAMP production in DRG cell culture via EP4 and IP receptors, respectively. These prostanoids were presumed to act only on the neurons in typical mixed cell cultures, but since we had acquired purified glial cell preparation, we tested for involvement of glial cells in measurement of agonist-stimulated cAMP production. Interestingly, a purified glial cell cultures also produced EP4 and IP-dependent responses. The expression of EP4 and IP receptors by DRG glia was further confirmed by the detection of EP4 and IP-like immunoreactivity and mRNA. Moreover, these agonist-stimulated responses were greatest in the glial cell preparation, and surprisingly weakest in the neuron-enriched cell cultures. Furthermore, the presence of neurons significantly inhibited both EP4 and IP receptor-dependent signalling in glial cells, but was without effect on forskolin (agonist-independent) stimulation of adenylyl cyclase. In order to characterize this neuron-glia interaction, we tested the adenylyl cyclase activities in glial cell cultures which were treated with conditioned medium derived from neurons or were separated from physical contact with neurons plated on transwell membrane. These studies further suggest that the neuron-glia interactions were dependent on both soluble factors and cell-cell contact. / Ng, Kai Yu. / Adviser: Helen Wise. / Source: Dissertation Abstracts International, Volume: 73-04, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 152-172). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.