1988
DOI: 10.1016/0361-9230(88)90010-x
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Effects of interleukin-1 and arachiodonate on the preoptic and anterior hypothalamic neurons

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Cited by 115 publications
(29 citation statements)
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“…These effects may be mediated by the fast activation of the Nsphingomyelinase (N-Smase) and ceramide production (Mathias and Kolesnick, 1993;Nalivaeva et al, 2000). They are PGE2 independent and rapidly change the firing rates of neurons following binding of IL-1β to its receptor (Hori et al, 1988;Sanchez-Alavez et al, 2006;Wilkinson et al, 1993). Although the signaling molecules involved in the action of IL-1β upon defensive rage have not been identified, the observation that the maximum effect was observed at 60 minutes post injection suggests that the cyclooxygenase and PGE2 mediated pathway may be involved in IL-1β mediated potentiation of defensive rage in the cat.…”
Section: Discussionmentioning
confidence: 99%
“…These effects may be mediated by the fast activation of the Nsphingomyelinase (N-Smase) and ceramide production (Mathias and Kolesnick, 1993;Nalivaeva et al, 2000). They are PGE2 independent and rapidly change the firing rates of neurons following binding of IL-1β to its receptor (Hori et al, 1988;Sanchez-Alavez et al, 2006;Wilkinson et al, 1993). Although the signaling molecules involved in the action of IL-1β upon defensive rage have not been identified, the observation that the maximum effect was observed at 60 minutes post injection suggests that the cyclooxygenase and PGE2 mediated pathway may be involved in IL-1β mediated potentiation of defensive rage in the cat.…”
Section: Discussionmentioning
confidence: 99%
“…However, the brain site which senses blood-borne EPs/ IL-1 and the type of cells which are responsible for the release of PGE2 in response to EPs/IL-1 have not yet been determined. The hypothalamus, particularly the preoptic area (POA), has long been proposed as the primary site of action of EPs/IL-1 (Hori, Shibata, Nakashima, Yamasaki, Asami, Asami & Koga, 1988). However, the lack of evidence showing the actual entry of blood-borne EPs/IL-1 into the brain (Dinarello, Weiner & Wolff, 1978) and the lack of a consistent relationship between the thermosensitivity and the PGE2 responsiveness of POA neurones (Stitt & Hardy, 1975;Boulant & Scott, 1986) do not support this, although EPs/IL-1, which is synthesized in the brain, might contribute, at least partly, to the development of fever (Fontana, Weber & Dayer, 1984;Hori et al 1988; Nakashima, Hori, Mori, Kuriyama & Mizuno, 1989).…”
Section: Itmentioning
confidence: 99%
“…For example, electrophoretically applied rhIL-1 decreased the activity of warm-sensitive neurons in the rat hypothalamus (Hori et al, 1988). Furthermore, electrophoretically applied rhTNF and rhIL-1 suppress the activity of glucose-sensitive neurons in the art lateral hypothalamic area and increase neuronal activity of glucoreceptor neurons in the rat ventromedial hypothalamic nucleus (Oomura, 1988).…”
Section: Discussionmentioning
confidence: 98%
“…On the other hand, GABA is thought to be the predominant inhibitory transmitter in the brain and at most of its receptor sites elicits an increase in the membrane permeability to C1-as it does in bullfrog dorsal root ganglion and in Aplysia ganglia (Yarowsky and Carpenter, 1978;Hattori et al, 1983;Matsumoto et al, 1986;Oyama et al, 1990). Attention has focused on the influences of immune mediators (including the cytokines, IL-1, IL-2) on the firing rate of neurons in the central nervous system (CNS) of vertebrates (Hori et al, 1988;Oomura, 1988;Nistico and De Sarro, 1991). Cytokines may modulate the firing rate of CNS neurons by influencing membrane receptors.…”
Section: Introductionmentioning
confidence: 98%