| More and more evidences have shown that there is a complicated reciprocal relationship between nervous system and immune system. Immune system transfers the immune information into CNS during antigens challenge and influences the function of CNS. The CNS in turn can modulate the function of immune system. The background of this research is based on two facts: first, lipopolysaccharide (LPS) and staphylococcal enterotoxin B(SEB) have been widely used as immune stimuli to mimic some of the acute-phase immune responses. Systemic LPS or SEB administration triggers wide responses involved in nervous system, endocrine system and immune system. However, it is reported that the activity occurs in the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON) neuron induced by LPS and SEB also can be observed in many other cases triggered by different other stressors. Thus, whether the neuronal activities in CNS aroused by LPS and SEB only attributes to brain regulation to stress, or results from the co-operation of stress and immune stimuli, in other words, whether there is any differences about the activity of the relative brain region between non-immune stimuli and immune stimuli, need to be answered. The experiment in Part One of this thesis is an initial step to answer these questions.Secondly, the previous work from our lab has discovered an interestingphenomenon that following intraperitoneal (i.p.) administration of SEE, the Fos expression has greatly increased in many of brain regions such as PVN or SON whereas reduced in hippocampus and cingulated cortex, indicating the differences between the limbic structures and other brain regions in respect to the response to immune challenge. Thus in the Part Two of the thesis, we selected hippocampus as the target for study and observed the effect of fimbria transection on the activation of hypothalamic oxytocin (OT) neurons in the rats intraperitoneally administrated LPS. The aim is to reveal the mechanism how hippocampus regulate immunity. In addition, since fimbria transection itself was a CNS trauma, which inevitably aroused local immune reaction in brain, we observed the distribution of MHC- II antigen in the brain 21d after unilateral fimbria transection with immunohistochemical method.In Part One, using phosphorylation of extracellular signal-regulated protein kinase-1/2 (pERK1/2) as a maker, we observed the neuronal activation in CNS elicited by a peritoneal noxious stimulus, acetic acid. In the article, we only reported the activity of neurons in brainstem responsible to visceral sense and movement. pERKl/2-like immunoreactivity (LI) was enhanced in the neurons of the nucleus of the solitary tract (NTS) and dorsal motor nucleus of the vagus nerve (DMV) 8 min after an intraperitoneal injection of acetic acid in the mouse. The results suggest that ERK1/2 signal-transducting pathway is involved in conveying nociceptive visceral information. In the process of response to nociceptive stimulus, short circuit NTS project to DMV may be activated. The enhancement in pERKl/2-LI was suppressed after subdiaphragmatic vagotomy, However, the number of pERKl/2-like immunoreactive neurons in the acetic acid group was still more than that in saline-injection group. It indicates that additional route transmitting peritonealnoxious sensation might be co-existed. We also observed co-localization of tyrosine hydroxylase (TH) and peritoneal chemical stimuli-induced pERKl/2 in NTS neurons, which indicates catecholaminergic neurons in NTS mediate nociceptive signals from viscus. Whether ERK1/2 signaling pathway is necessary to the synthesis or release of catecholamine needs to be investigated in future. No co-localization of pERK with GFAP or OX-42, the marker of astrocyte and microglia respectively, was found in NTS and DMV, indicating that at least at 8 min after an intraperitoneal noxious stimulus, glial cells were either not activated, or activated through other signaling transduction pathway.Part Two of this article includes two experiments.
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