| The gastric motility is mainly controlled by CNS (central nervous system) at the level of brainstem, through para- sympathetic and sympathetic ways. The pre-parasympathetic fibers concerned with gastrointestinal functions are mostly originated from DMV (dorsal motor nucleus of the vagus) .In CNS, the serotonergic system and noradrenergic system interplay and co-work extensively, while NRM and LC, also participate in many modulations and functions together, cooperating with each other.DMV accept afferent input from NRM (raphe magnus nucleus) and LC (Locus coeruleus), and there are 5-HT1 A 2A 5A receptor and α β receptor distribute in DMV. Electrophysiological experiments have shown that, gastric and intestinal -projecting DMV neurons can be excited or inhibited by 5-HT (5-hydroxytryptamine) and NE (norepinephrine) .Now there is no uniform conclusion about the effect of NRM stimulation on gastric motility, and a small quantity of researches about the modulation of LC on stomach. Further more, if NRM and LC regulate gastric motility through DMV remains indistinct and systematical investigation about the nucleus in brainstem regulated gastric motility is not much.In our research, we use nucleus location electric stimulation electric lesion and microinjection methods, record the average inter-gastric pressure and amplitude of gastric motility, intend to establish a parasympathetic local circuit among DMV (the central nucleus in parasympathetic way regulated gastric motility) LC (which contains the major group of noradrenergic perikarya of the brain) and NRM (which is also close related with modulation of brainstem on gastric motility) , which may worked as a neural center of gastric modulation in brainstem. The results are as follows: 1 Modulation on amplitude of the contractions of gastric motility. (1) NRM stimulation significantly reduced the amplitude of the contractions of gastric motility (P<0.05, P<0.01) , the effect could be abolished by pretreatment of DMV lesion. And all those above have no effect on the average inter-gastric pressure.(2) LC stimulation significantly reduced the amplitude of the contractions of gastric motility(P<0.05, PO.01), but has no effect on the average inter-gastric pressure. Pretreatment of DMV lesion decreased the effect of LC stimulation on amplitude, and we could seesignificant differences in the 20 min and the 40 min (PO.01) .Further more, LC stimulation after DMV lesion could decrease the average inter-gastric pressure significantly (PO.01) .(3) Microinjection of phentoramin into DMV increased the amplitude (PO.05, P<0.01.) and the average pressure (P<0.05), and a succeeding stimulation on LC could boost up the effect more (PO.05) .(4) Microinjection of ritanserin into DMV significantly reduced the amplitude about 80% (PO.01) and meanwhile decreased the average intra-gastric pressure(PO.05) . A subsequent stimulation onNRM had no effect on it, compared with stimulation only, there is no effect either.(5 ) Microinjection of ritanserin into LC could increase the amplitude of gastric motility compared with DMSO-mricroinjected group (PO.01) , and a subsequent stimulation on NRM could enhance the effect more. Pretreatment of LC lesion or microinjection of ritanserin into LC all had no effect on average pressure, and the reduction of gastric motility amplitude induce by NRM stimulation could not occur either.So we conclude:K NRM reduce the amplitude of gastric motility via DMV. Serotonergic projections originated from NRM work on 2 A receptor in LC, activate the noradrenergic neurons, and then restrain the DMV neurons, which could enhance the gastric motility normally, via a-receptor. The direct way between NRM and DMV via serotonergic projections and 2A receptor is inexistent. And NRM doesn't participate in the regulation on inter-gastric average pressure.2> LC stimulation reduce the amplitude of gastric motility via a receptor in DMV, and phentoramin could reverse the inhibiting effect of LC on gastric activity. It indicates that there would be other noradrenergic or nonadrenergic way exerting exciting process.3 > Microjection of ritanserin into DMV significantly reduced the amplitude to 20%, and meanwhile decrease the average intra-gastric pressure significantly. So 2A receptor on DMV may play an important exciting role in keeping the gastric motility amplitude normally.Above all, DMV is an important nucleus in gastric modulation mechanism, and works as a core among other related nucleus in brainstem. NRM and LC inhibit the gastric activity via DMV, and NRM communicate with DMV through LC. NRM and LC all exert inhibiting effect on gastric activity via adrenergic a-receptor in DMV. And there are 5-HT 2A-receptor and other non-adrenergic receptor distribute on DMV, exerting exciting effect, regulating the gastric activity with noradrenergic a-receptor together.
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