The Roles Of HSD2 Neurons In The NTS To Participate In The Regulation Of Sodium Appetite And Its Adjusyment In Rat Central Nucleus Of The Amygdala

Sodium ion is the importance electrolyte in the living organism,as well as plays an important role in maintaining the cell homeostasis and the balance between water and sodium.When the body appears in the absence of sodium ions,the animal appears to find and ingest a large number of sodium-containing solution or food and this goal-oriented behavior is called Sodium Appetite.Studies have shown that low sodium diet increase the activity of aldosterone sensitive nerve in NTS of rats and HSD2 neurons in NTS maybe involved in the descending modulation from the Ce A,while we still have no clear idea about its mechanism.For human,strong sodium appetite leads to excessive intake of sodium,which will impair people's health seriously.Salt restriction will be an important basis for the treatment and improvement of various chronic disease,especially cardiovascular and cerebrovascular diseases.Therefore,further clarifying the mechanism of sodium to control has important practical significance and clinical value.ObjectiveToinvestigate the regulation of Ce A on the uptake behavior of normal rats and hyponatremia rats and to explore whether the changes of sodium uptake of CeA are related to the activity of aldosterone-sensitive neurons?HSD2 neurons?in NTS and its regulation.MethodsThrough damaging the CeA,fake damaged and not damaged CeA,we observe the changes of the amount of 0.3M Nacl solution before and after low sodium diet and analyze the consumption of 0.3M NaCl solution of 1/3/6/12/24 hours after 14 days low sodium diet.The expression of HSD2 neurons in NTS was observed by immunofluorescence labeling.Immunofluorescence tracer was used to investigate whether neurons in CeA were involved in the regulation of HSD2 neurons and the nature of this regulation.Results 1.Effects of chronic cementation of Ce A and low sodium diet on sodium tolerance in rats.After 14-days low sodium diet,the double bottle taste test showed that the intake of 0.3M Nacl solution has significantly increased?22.55±1.56 mlVS 7.73±1.44ml,P<0.001?,the consumption of DW has reduced?17.22±1.64mlVS 34.75±2.59ml,P<0.001?.However,the total fluid intake has no significant changes?39.77±1.20ml VS 42.48±1.31ml,P>0.05?.The liquid of 1/3/6/12/24 hours cumulative consumption resulted that 50%0.3M NaCl solution was taken during the first 12 hours,andthe consume of DW was only 30%.Ater 14-days low sodium diet,we analyzed the cumulative liquid intake of 0.3M NaCl solution,distilled water and total liquid in the 1/3/6/12/24 hours intervals of rats:CeA-Lesioned-L,CeA-Sham lesioned-S and CeA-Normal-N.The results showed that the intake of 0.3M NaCl solution in group S and group N was significantly higher than that in L group at 1h,3h,6h,12h and 24h?P<0.001?.The cumulative intake of DW solution in the three groups was significantly lower than that in the L group?P<0.001?at 12hour and 24 hour after the low sodium diet.In addition,we analyzed the intake of 0.3M Na Cl,DW and total fluid in the three groups of rats at 24h.We found that the intake of 0.3M NaCl in S group and N group was significantly higher than that in L group?P<0.001?,and the intake of DW was significantly decreased?P<0.001?.However,there is no significant difference among the total fluid intake in the three groups.2.HSD2 neurons to participate in the activities of rat sodium appetiteIn this experiment,rats were divided into CeA-Lesioned-L and CeA-Shamed-S.After 14 days low sodium diet,the expression of HSD2 neurons in NTS was significantly higher than that in normal diet?P<0.05?,and the difference was statistically significant.However,for low sodium model rats or normal fed rats,whether CeA is damaged or not,it did not affect the expression of HSD2 neurons in NTS,and the expression level of HSD2 neurons did not show any significant difference.3.The regulation of Aldosterone sensitive neurons and its property in rat CeANeurons projected into NTS in CeA have fluorescent gold from NTS retrograde tracing,and this neuron has GABA neurotransmitters.In addition,there are a large number of GABA_A receptors in NTS and GABA_A receptors on HSD2 neurons.Indicating that the neurons in the NTS receive GABAergic nerve fibers from CeA,and the peripheral GABA neurotransmitters can act on GABA_A receptors on aldosterone-sensitive neurons?HSD2 neurons?within NTS.Conclusion1.The low-sodium diet increases the intake of high-salt solution in rats,but does not increase the intake of the total fluid,suggesting that the sodium is essentially a result of an increase in the taste of the high salt solution.2.The damage of CeA reduced the amount of salt in low sodium rats,suggesting that it was involved in the regulation of sodium in low sodium rats,which is that Ce A damage inhibited the sodium activity of low sodium rats.In addition,HSD2 neurons in brain stem NTS were involved in the changes of sodium activity.3.CeA has a fluorescent gold from the NTS retrograde tracer.And GABA on neurons suggests that neurons within NTS may accept down-regulation from CeA and this regulatory nature is GABAergic?inhibitory?.