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The central nervous system, by a variety of mechanisms engages in constant surveillance of the peripheral immune system. Alterations in the status of the peripheral immune system induced by an invading pathogen for example, are quickly detected by the central nervous system, which then responds by altering physiological processes and behavior in an attempt to support the immune system in its efforts to eliminate the pathogen. Sleep is one of several behaviors that are dramatically altered in response to infection. Immune-active substances such as the pro-inflammatory cytokines interleukin-1 and tumor necrosis factor, either directly or indirectly via interactions with neurotransmitters or neurohormones are involved in the regulation of sleep. Because these cytokines increase during infection, they are likely candidates for mediating the profound alterations in sleep that occur during infection. Since regulation of behavior is the function of the central nervous system, infection-induced alterations in behavior provide a unique model for the study of neuro-immune interactions.
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Neurotensin is a 13-amino acid hormonal peptide which was first isolated from bovine hypothalamus. It is present in the digestive tract as well as in the central nervous system. It has a variety of biological activities as a central neurotransmitter or neuromodulator, and a peripheral hormone. NT receptors have been characterized in a variety of tissues and cell lines of peripheral and central organs. The physiological functions of NT include stimulation of pancreatic and biliary secretion, stimulation of colonic motility, inhibition of small bowel and gastric motility, trophic effect on numerous tissues of the gastrointestinal tract. NT exerts hypothermic and analgesis effect when injected into the central nervous system. From a clinical standpoint, studies with NT have led to implications of its involvment in schizophrenia, Parkinson's disease and Alzheimer's disease.
EN
The sympathetic nervous system evokes complex effects at multiple target organs in response to external, internal as well as mental stimuli. This output involves an interplay between the actions of a number of transmitters and modulators and a the postsynaptic and presynaptic sites of the autonomic ganglia and the sympathetic preganglionic neurons (SPNs). This review concerns particularly the SPNs of the cat and neonatal rat, studied by means of electrophysiological and immunohistochemical methods. Four types of responses may be elicited, the fast EPSP and IPSP, and their currents and the slow ESPSPs and IPSPs, and their currents. Glutamate and glycine appear to mediate the fast excitatory and inhibitory responses, respectively; peptides and amines seem to be responsible for generating the slow excitatory response, while the slow inhibitory response, found so far only in the cat, appears to be mediated by norepinephrine. Finally, glutamate, enkephalin and GABA, but not glycine attenuate the release of the inhibitory and excitatory transmitters from the nerve terminals abutting on the SPNs. The supraspinal efferent and afferent projections which may release the transmitters and modulators in question are discussed, as well the mechanisms that ensure appropriate programming and moment-to-moment regulation of the autonomic output.
EN
A form of activity dependent, functional plasticity can be induced in the barrel cortex by sensory deprivation without damage to the sensory receptors. Changes of cortical representation of a spared C3 vibrissa, when all other whiskers were plucked out, were mapped with 2-deoxyglucose autoradiography in mice and rats after a short-lasting deprivation. An increase in the volume of cortical column activated by the spared vibrissa was found previously that if deprivation is commenced immediately after birth, yhe changes in cortical representation of the spared whisker appeared in the third week of life. In search of a possible reason for the delayed expression of functional plasticity in neonatal animals we examined the developmental curves of neurotransmitter receptor binding for several transmitters thought to be involved in plstic processes of the cerebral cortex. We found that the beta noradrenergic and miscarinic cholinergic receptor binding increased rapidly at the end of the second postnatal week and subsequently remained high. By contrast, the metabotropic glutamate receptor binding decreased during the first month of postnatal development. The AMPA receptors binding values rose during the first two weeks of life, and then decreased. Together with our previous data on the development of NMDA and GABA receptor and voltage dependent calcium channel binding, the results suggest that slow development of functional plasticity in neonatal animals may be due to low levels of receptors of several neurotransmitters implicated in brain plasticity.
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