Effect of interleukin-1b on subdiaphragmatic vagal efferents in the rat (original) (raw)
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Effect of interleukin-1beta on subdiaphragmatic vagal efferents in the rat
Autonomic Neuroscience
Interleukin-1b (IL-1b) is an important mediator of fever and illness. Recent studies have demonstrated that IL-1b (2 mg kg ) increases gastric vagal afferent activity. The peripheral mechanisms of the action of lower doses were studied by recording the mass efferent and afferent activity of the gastric branch of the ventral vagal nerve in anesthetized rats. Twenty min after i.v. administration of 21 IL-1b (1 mg kg ) the efferent activity of the vagal nerve was decreased to 6266% in totally but not in partly vagotomized rats.
Effect of interleukin-1β on subdiaphragmatic vagal efferents in the rat
Autonomic Neuroscience Basic Clinical, 2000
Interleukin-1b (IL-1b) is an important mediator of fever and illness. Recent studies have demonstrated that IL-1b (2 mg kg) increases gastric vagal afferent activity. The peripheral mechanisms of the action of lower doses were studied by recording the mass efferent and afferent activity of the gastric branch of the ventral vagal nerve in anesthetized rats. Twenty min after i.v. administration of 21 IL-1b (1 mg kg) the efferent activity of the vagal nerve was decreased to 6266% in totally but not in partly vagotomized rats. 21 21 Preadministration of indomethacin (5 mg kg) 30 min before IL-1b blocked this reduction. Administration of 1 mg kg of IL-1b had no effect on the afferent activity of the gastric branch of the vagal nerve. The present results suggest that the subdiaphragmatic vagal afferents modulate the parasympathetic efferent outflow in response to IL-1b partly through prostaglandin dependent mechanisms and that supradiaphragmatic afferents or central sites are more sensitive to the low doses of IL-1b which becomes evident after elimination of the subdiaphragmatic vagal input.
Journal of the autonomic nervous system, 1997
The response of mass activity of the gastric vagal afferent nerve to intravenous administration of interleukin-1 beta (IL-1 beta) and the involvement of cholecystokinin (CCK) in the response were investigated in pentobarbital-anesthetized rats. Intravenous administration of 2 micrograms.kg-1 of IL-1 beta caused an increase in the afferent activity, which reached 150% of control activity by 30 min after administration and persisted for more than 80 min. The increase in the nerve activity was significantly reduced in animals pretreated with a type A CCK receptor antagonist. IL-1 beta also significantly increased the CCK concentration in systemic blood. Furthermore, it was confirmed that intravenous administration of CCK produced an increase in the nerve activity via the type A CCK receptor. These findings suggest that systemically applied IL-1 beta increases CCK concentration in systemic blood secreted from mucosal endocrine cells of the small intestine, and that in turn CCK in the ga...
We have shown that systemic administration of interleukin-1b (IL-1b) excites gastric vagal afferent activity in part via stimulation of type A cholecystokinin (CCK-A) receptors in rats. The present study was undertaken to determine whether the response of the gastric vagal afferent nerve to systemic IL-1b is altered in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which lack CCK-A receptors. The response was compared with that of the control strain, Long-Evans Tokushima Otsuka (LETO) rats. All animals were anesthetized with pentobarbital and arti®cially ventilated. Intravenous administration of 4 mg/kg of IL-1b increased gastric vagal afferent activity in both LETO and OLETF rats, whereas a smaller dose of 2 mg/kg of IL-1b increased activity only in the OLETF rats. The present results demonstrate that the response of the gastric vagal afferent activity in CCK-A receptor de®cient OLETF rats was more sensitive to intravenous administration of IL-1b than was in control LETO rats. q
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
Intravenous administration of interleukin-1 (IL-1) activates central autonomic neuronal circuitries originating in the nucleus of the solitary tract (NTS). The mechanism(s) by which bloodborne IL-1 regulates brain functions, whether by operating across the blood-brain barrier and/or by activating peripheral sensory afferents, remains to be characterized. It has been proposed that vagal afferents originating in the periphery may monitor circulating IL-1 levels, because neurons within the NTS are primary recipients of sensory information from the vagus nerve and also exhibit exquisite sensitivity to blood-borne IL-1. In this study, we present evidence that viscerosensory afferents of the vagus nerve respond to intravenously administered IL-1. Specific labeling for mRNAs encoding the type 1 IL-1 receptor and the EP3 subtype of the prostaglandin E2 receptor was detected in situ over neuronal cell bodies in the rat nodose ganglion. Moreover, intravenously applied IL-1 increased the number of sensory neurons in the nodose ganglion that express the cellular activation marker c-Fos, which was matched by an increase in discharge activity of vagal afferents arising from gastric compartments. This response to IL-1 administration was attenuated in animals pretreated with the cyclooxygenase inhibitor indomethacin, suggesting partial mediation by prostaglandins. In conclusion, these results demonstrate that somata and/or fibers of sensory neurons of the vagus nerve express receptors to IL-1 and prostaglandin E2 and that circulating IL-1 stimulates vagal sensory activity via both prostaglandindependent and -independent mechanisms.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998
Intravenous administration of interleukin-1 (IL-1) activates central autonomic neuronal circuitries originating in the nucleus of the solitary tract (NTS). The mechanism(s) by which blood-borne IL-1 regulates brain functions, whether by operating across the blood-brain barrier and/or by activating peripheral sensory afferents, remains to be characterized. It has been proposed that vagal afferents originating in the periphery may monitor circulating IL-1 levels, because neurons within the NTS are primary recipients of sensory information from the vagus nerve and also exhibit exquisite sensitivity to blood-borne IL-1. In this study, we present evidence that viscerosensory afferents of the vagus nerve respond to intravenously administered IL-1beta. Specific labeling for mRNAs encoding the type 1 IL-1 receptor and the EP3 subtype of the prostaglandin E2 receptor was detected in situ over neuronal cell bodies in the rat nodose ganglion. Moreover, intravenously applied IL-1 increased the ...
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
Intraperitoneal administration of the cytokine interleukin-1 (IL-1) induces brain-mediated sickness symptoms that can be blocked by subdiaphragmatic vagotomy. Intraperitoneal IL-1 also induces expression of the activation marker c-fos in vagal primary afferent neurons, suggesting that IL-1 is a key component of vagally mediated immune-to-brain communication.
Interleukin-1beta sensitizes the response of the gastric vagal afferent to cholecystokinin in rat
Neuroscience Letters
Interleukin-1b (IL-1b) and cholecystokinin (CCK) are important mediators in the development of anorexic response during disease. The role of IL-1b and CCK in the peripheral mechanisms of anorexia was studied by recording the mass afferent activity of the gastric vagal nerve in anesthetized rats. The i.v. administration of CCK (1 nmol) increased the activity of the vagal nerve, and this response was raised by 55-72% 2 h after i.v. injection of IL-1b. It is proposed that IL-1b-induced anorexia is mediated via the sensitization of type A CCK receptors in the periphery.
Interleukin-1b sensitizes the response of the gastric vagal afferent to cholecystokinin in rat
Interleukin-1b (IL-1b) and cholecystokinin (CCK) are important mediators in the development of anorexic response during disease. The role of IL-1b and CCK in the peripheral mechanisms of anorexia was studied by recording the mass afferent activity of the gastric vagal nerve in anesthetized rats. The i.v. administration of CCK (1 nmol) increased the activity of the vagal nerve, and this response was raised by 55–72% 2 h after i.v. injection of IL-1b. It is proposed that IL-1b-induced anorexia is mediated via the sensitization of type A CCK receptors in the periphery.