Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress

In the present study, we examined the effect of pertussis toxin (PTX) administered centrally in a variety of stress-induced blood glucose level. Mice were exposed to stress after the pretreatment of PTX (0.05 or 0.1 µg) i.c.v. or i.t. once for 6 days. Blood glucose level was measured at 0, 30, 60 and 120 min after stress stimulation. The blood glucose level was increased in all stress groups. The blood glucose level reached at maximum level after 30 min of stress stimulation and returned to a normal level after 2 h of stress stimulation in restraint stress, physical, and emotional stress groups. The blood glucose level induced by cold-water swimming stress was gradually increased up to 1 h and returned to the normal level. The intracerebroventricular (i.c.v.) or intrathecal (i.t.) pretreatment with PTX, a Gi inhibitor, alone produced a hypoglycemia and almost abolished the elevation of the blood level induced by stress stimulation. The central pretreatment with PTX caused a reduction of plasma insulin level, whereas plasma corticosterone level was further up-regulated in all stress models. Our results suggest that the hyperglycemia produced by physical stress, emotional stress, restraint stress, and the cold-water swimming stress appear to be mediated by activation of centrally located PTX-sensitive G proteins. The reduction of blood glucose level by PTX appears to due to the reduction of plasma insulin level. The reduction of blood glucose level by PTX was accompanied by the reduction of plasma insulin level. Plasma corticosterone level up-regulation by PTX in stress models may be due to a blood glucose homeostatic mechanism.

Effect of chronic forced swimming stress on whole brain radiation induced cognitive dysfunction and related mechanism / 中华放射医学与防护杂志

Objective To explore whether chronic forced swimming stress could improve whole brain radiation induced cognitive dysfunction and possible mechanism. Methods Thirty-nine one month old male Sprague-Dawley rats were randomized into sham control group ( C ) , swimming group ( C-S ) , radiation group( R) , and radiation plus swimming group( R-S) . Radiation groups were given a single dose of 20 Gy on whole-brain. Rats in the swimming groups were trained with swimming of 15 min/d, 5 d/w. Rat behavior was performed 3 months after radiation in an order of free activity in an open field and the Morris water maze test including the place navigation and spatial probe tests. Then, the protein expressions of BDNF, P-ERK, T-ERK, P-CREB and T-CREB in the rat hippocampus tissue were assayed by Western blot. Results On the day 2, in the place navigation test of Morris water maze, the latency of swimming group was significantly shorter than that of sham group, the latency of sham group was significantly shorter than that of radiation group, and the latency of radiation swimming group was significantly shorter than that of radiation group(P0?05). Western blot assay showed that the expressions of BDNF and its downstream signals including P-ERK and P-CREB were markedly reduced by radiation ( P < 0?05 ) , but this reduction was attenuated by the chronic forced swimming stress. Conclusion The chronic forced swimming stress could improve whole brain radiation induced cognitive dysfunction by up-regulating the expressions of BDNF and its downstream signal molecules of P-ERK and P-CREB in hippocampus.

Changes of behavior, Ca~(2+)/CaMKⅡ in hippocampus of rats with chronic forced swimming stress model / 解剖学报

Objective To observe the changes of behavior, intracellular free calcium and the expression of calmodulin dependent protein kinase Ⅱ(CaMKⅡ) in the hippocampal neurons of chronic forced swimming stress rats. Methods Male Wistar rats were randomly divided into control group and chronic forced swimming stress group. The behavior was examined using sucrose preference test, open-filed test and Morris water maze. The intracellular free calcium was examined by fluorescence spectrophotometer. The expression of CaMKⅡ was detected using colloidal gold immunoelectron microscopy technique, Western blotting and RT-PCR. Results The consumption of sucrose and erect quantity of chronic forced swimming stress group were lower than those of control group(P<0.01, P<0.05). The escape latency time in Morries water maze test of chronic forced swimming stress group was higher than that of control group(P<0.01). The intracellular free calcium level and the expression of CaMKⅡ in the hippocampus was higher than that of control group(P<0.01).Conclusion The lasting dysfunction of Ca~(2+)/CaMKⅡ signaling cascades in hippocampus may play important roles in the pathogenesis of chronic forced swimming stress rats.

Changes of renal peripheral benzodiazepine receptor in the stress/anxiety response

Peripheral benzodiazepine receptor(PBR) has been identified in various peripheral tissues including kidney. The physiological and pharmacological functions of PBR are still uncertain, although it has been suggested that these are associated with the regulation of stress/anxiety response. Diazepam progeny, which were exposed to diazepam perinatally, was reported to be an animal model of chronic anxiety. However, PBR in the diazepam progenies are not known yet. In the present study, therefore, we examined the changes of PBR in the stress/anxiety response. Dams of rats were given injection of diazepam or vehicle during puerperium. Diazepam progenies showed increased level of anxiety on the performance of elevated plus maze, and increased Bmax of PBR. Saturation experiments followed by scatchard analysis of the results showed that the increase in the density of PBR and the affinity of the PBR remained unchanged. Forced swim stress increased anxiety on the plus maze in both groups of rats. In contrast to control, diazepam progenies did not show further upregulation of renal PBR immediately after swimming stress, but still higher than control. From the above results, it may be concluded that upregulation of renal PBR is associated with chronic anxiety as well as stress-induced response.

The Induction of Suppressor Cells in Murine Spleensby Stress and Its Effect on the Responsive for the Mitogen / 中国免疫学杂志

In this paper, it has been found that such stressors as operation or swimming in cold watermay suppress the mitogenic response of murine spleen cells to ConA or LPS, whichis closely related to the action of suppressor cells.Using the plastic-adherence method, the plastic-adherence cells in spleen(PAC)was removed or obtained. The difference of mitogenic responsivebefore and after the removal of PAC is very apparent in stressed mice, being much lower thannormal before the renioval of PAC and near to normal after removing PAC. It is interestingthat the lymphocyte transformation stimulated by LPS is suppressed predominantly after swim-ming stress instead of those by ConA in operation stress.It has also been observed that theindomethacin may block the induction of suppressor PAC by stress, which means that the pro-staglandins may play an important role in the induction and action of suppressor PAC.