The present investigation was undertaken to study the effect of hypothalamic stimulation on the pain response elicited by tail stimulation and pain-suggestive response evoked by midbrain stimulation (vocaliz-tion) in lightly anesthetized cat. In 45 hypothalamic stimulations testing its effect on CG-elicited vocalization, 22 inhibited the vocalization response, 6 facilitated it, and 17 showed no effect. In 22 hypothalamic stimu ations testing its effect on tail-elicited vocalizations, 18 inhibited the vocalization, 4 showed no effect Furthermore, in 5 spontaneously groaning cats, hypothalamic stimulations could successively inhibited the groaning. The result indicate that the hypothalamus-mid-brain continum is intimately related with pain modulation.

Present work was undertaken to investigate the effect of destruction of different non-mediobasal hypothalamic areas on the traumatic stress responses in 64 Sprague-Dawley rats.Leg break was used as a stressor.The plasma corticosterone levels before (Bo) and 20' after the legbreak (Bs) were determined using competitive protein binding assay.The values of Bs/Bo and Bs-Bo were taken as indicators for the magnitude of the stress responses.The animals were divided into 6 groups according to injured brain areas: sham operated group, PVH injured group, PVH partially injured group, PVH minimally injured group, anterior hypothalamic-preoptic area injured group, posterior hypothalamic area injured group.Having compared statistically all Bs/Bo and Bs-Bo values of 6 groups, and on the basis of the fact that in the 4 cases of complete bilateral PVH destruction the stress response could not be entirely abolished, we conclude. (1) In traumatic stress response of conscious animals, PVH plays an important role as compared with other non-mediobasal hypothalamic areas. (2) Some CRF-containing neurons outside the PVH may also participate in the above-mentioned stress response.

Unit discharges of neurons of the hypothalamic ventromedial nucleus region (HVM) and its surrounding structures including paraventricular nucleus, anterior hypothalamic area,and hypolhalamic dorsomcdial nucleus, were recorded in the ureth-ane-anesthetized and flaxidel-immobilized rats. In HVM,8 of 82 units showed periodical fluctuations in discharge rate, which could be categorized into two types: (1) With alternating active and silent phases 5 (2) with gradually waxing and waning phases. The duration of cach cycle varied from 1 to 5 minutes in different neurons. The periodicity disappeared after intraperitoneal injection of nembutal, while the average discharge rate was raised somewhat. This result suggested that the depressing pha-s of periodical activity of the HVM neuron might probably result from the inhibitory action in certain neuronal circuit, rather than from the intrinsic property of the recorded neurons. The effect of picrotoxin was contradictory. No periodical activity was noted in the 47 recorded neurons outside of the HVM.

AIM To investigate the nongenomic effects of steroids on glycine uptake in L 929 cells. METHODS L 929 cells were incubated with labeled glycine, steroids, and/or other reagents. With liquid scintillation technique, the labeled glycine in L 929 was measured. RESULTS Steroids could rapidly inhibit the glycine uptake. Action intensity of steroids was different. Effects of CORT and ALD were dose-dependent. There was no difference in effects between corticosterone 21-sulfate and B-BSA. Inhibitor for cytoplasm receptor of glucocorticoids could partially block the effect of CORT. Extracelullar Ca 2+ could influence the effect of CORT. CONCLUSION Effects of steroids on glycine uptake in L 929 cells are nongenomic. Steroids may take effect through membrane receptors. The receptors of CORT in membrane are similar to those of glucocorticoids in cytoplasm.

Objective To investigate the role of steroids on the intracellular signal transduction mechanism of nongenomic effects for L 929 cells to uptake glycine. Methods The labeled glycine in L 929 cells was measured by scintillation technique. After L 929 cells were incubated with labeled glycine and steroid and/or other chemical reagents, the effects of steroids and their mechanism were determined. Results Corticosterone, aldosterone, estradiol, dexamethone and hydrocortisone inhibited glycine uptake by L 929 cells to various extents. There was no substantial difference between the effects of bovine serum album conjugated corticosterone and corticosterone 21 sulfate on glycine uptake. The inhibitor of G protein, GDP ? S, could partially block the effects of corticosterone and aldosterone. The inhibitor of phospholipase C, neomycine, did not inhibit the effect of corticosterone. The inhibitor of protein kinase C, Chelerythrine, partially blocked the effect of corticosterone. The activator of protein kinase C (phorbol 12 myristate, 13, acetate) seemed to imitate the effect of corticosterone. The activator of cAMP, Forskolin, and the inhibitor of protein kinase A, H 89 , blocked the effect of corticosterone. Conclusion The rapid inhibitory effects of steroids on glycine uptake in L 929 cells are nongenomic, and their signal transduction is through the pathway of G protein protein kinase C.

Objective: To investigate the effect of glucocorticoid on high K + induced catecholamine secretion in PC12 cells. Methods: High performance liquid chromatography with electrochemical detection were used to measure catecholamine secreted by PC12 cells. Results:(1) After PC12 cells were pretreated with various concentration of corticosterone at 37℃ for 5 min and then stimulated with various concentration of high K + for different time periods, the inhibitory effect of corticosterone on catecholamine secretion was found in a dose dependent manner. (2) When the duration of high K + treatment was prolonged, the inhibitory effect of corticosterone on catecholamine secretion tended to be attenuated. Conclusion: Glucocorticoid can rapidly inhibit the catecholamine secretion induced by high K + in PC12 cells. [

The effect of stress with electric tail-shock on interleukin-1 (IL-1) production by peritoneal exudate jnacrophages of C57 BL/6 mice was studied. The results showed that IL-1 level was decreased to 63.7?5.5%, 59.2?4.8%, and 61.2?3.8% of that of control 6 h, 12h, and 20h after stress, respectively (P

17B~estradiol. Displacement experiments showed that when RU38486 concentration reached 100~280-fold that of [3H]corticosterone, it began to inhibit [3H]corticosterone binding, while low concentration of RU38486 had no inhibitory effect.

Effects of microiontophoretically applied transmitter receptor antagonists on the evoked response of “pain” units of PVN in rats by sciatic stimulation were observed. The results showed: (l)The evoked response of 7 out of 38 PVN “pain” units could be blocked by atropine (7/38); 5 out of 27 by hexamethonium; 6 out of 31 by phentolamine (6/31); and 4 out of 25 by propranolol (4/25). Seventeen out of 52 were blocked by cyproheptadine (17/52), but 3 out of 52 were augmented by cyproheptadine (3/52). (2) The evoked response of the same “pain” unit could be blocked by two antagonists: the evoked response of 2 out of 27 PVN “pain” units could be blocked by atropine and cyprohepadine; 3 out of 20 by hexamethonium and cyproheptadine; 2 out of 25 by prepamolol and cyproheptadine. These results suggest that the noxious somatic input to PVN involves 5-HT, cholinergic and adrenergic transmitter receptor mechanisms and that the convergence of various transmitter systems on PVN “pain” unit is indicated.

In 34 hypothalamic slices of rats, spontaneous discharging of 63 paraventricular neurons was extracellulariy recorded by glass microelectrode. When the slices were perfused with artificial cerebrospinal fluid (ACSF) containing noradrenaline (NA) (10-6 mol/L), firing rates of 20 units significantly increased, those of 8 units decreased or even ceased, and those of 35 units, not affected. When low Ca2+ high Mg2+-ACSF was applied to block synaptic transmission, of 20 units which were excited by NA, 14 units still had excitatory responses and 6 units had no significant response to NA. When synaptic transmission was blocked, of 8 units which were inhibited by NA, 7 units still had inhibitory responses and only one unit had no significant response to NA. The results of this experiment strongly suggest the existence of direct effects of NA on paraventricular neurons.