摘要:

Benzodiazepine receptor binding in vivo, as determined by the uptake of the high-affinity specific benzodiazepine receptor ligand [3H]Rol 5-1788, was examined following acute and chronic defeat stress in male mice aged 6 weeks, 7 months and 1 year. Specific uptake in 6-week-old mice was increased from control values only in the cerebellum following acute but not chronic stress. Specific uptake in the cortex and hypothalamus was unchanged from control values following both acute and chronic stress. Seven-month-old mice demonstrated an increased specific uptake in the cortex and cerebellum when measured immediately following both acute stress and the final session of chronic stress. This enhanced binding returned to baseline levels by 24 h after stress. One-year-old mice demonstrated no change in specific uptake when measured after acute stress, while binding was enhanced in all brain regions after the final session of chronic stress. This increased binding was still evident at 24 h after the cessation of chronic stress. Changes in benzodiazepine binding differ as a response to acute and chronic stress, and this response varies markedly with age.

ISSN:0031-7012    

DOI:10.1159/000138796

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The effect of inhibition of brain histamine synthesis by α-fluoromethylhistidine (α-FMH) on the pituitary adrenocortical activity stimulated by D-Ala-·D-Leu-enkephalinamide (DADL) and morphine was investigated indirectly through corticosterone secretion in conscious rats. α-FMH (20 mg/kg i.p.) drastically reduced the whole brain histamine content, measured 2 h later. The same pretreatment also considerably reduced the corticosterone response induced by DADL or morphine injected into cerebral ventricles, and abolished the response to morphine given intraperitoneally. When α-FMH was administered intracerebroventricularly (50 μg), the maximum inhibition of the corticosterone response to DADL and morphine occurred 4 h after administration, which may suggest a weaker accessibility of α-FMH from the cerebral venticle to the brain structures involved in pituitary-adrenocortical stimulation. The corticosterone responses were not related to the core temperature changes. These results indicate that inhibition of brain histamine synthesis by α-FMH considerably impairs the pituitary-adrenocortical response to the opioid δ- and μ-receptor agonists DADL and morphine. They also suggest that neuronal histamine is significantly involved in the central stimulation of the pituitary-adrenal axis b

ISSN:0031-7012    

DOI:10.1159/000138797

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The intracerebroventricular injection of the cholecystokinin-A receptor antagonist L-364,718, at the doses of 0.5, 5, 10 or 20 μg/mouse, while having no effect on pain threshold (hot plate, 51 °C), antagonized the analgesic activity of morphine (10 mg/kg, i.p.). This effect was obtained with a dose of 10 μg/mouse and was associated with a reduction of brainstem opiate-binding sit

ISSN:0031-7012    

DOI:10.1159/000138798

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Recent studies have shown that muscarinic stimulation causes an increase in the breakdown of glucose and glycogen leading to an increase in lactate and CO2 production and a decrease in the ratio of NADH/NAD. Similar studies using palmitate as substrate showed that bethanechol did not change the rate of palmitate oxidation. Using both isolated strips of rabbit bladder dome, and the rabbit in vitro whole-bladder model, the present study compares the ability of glucose, pyruvate, palmitate, succinate and malate to support contraction and correlates the results with the intracellular concentration of high-energy phosphates. The results can be summarized as follows. In the absence of substrate, the peak response of muscle strips to field stimulation (32 Hz, 80 V, 1 ms) decreased progressively with time to 85% of the initial response at 60 min and 72% at 160 min. In contrast, the plateau phase of the response decreased to 45 and 23% of the initial response at 60 and 160 min, respectively. When glucose was present in the incubation medium, the peak and plateau tensions were 86 and 73% of the initial values at 160 min. Similar experiments with pyruvate as substrate showed that at 160 min both peak and plateau were elevated above initial values (peak = 119%; plateau = 123%). In the presence of palmitate, succinate or malate, the peak and plateau tensions decreased with time at a similar rate as in the absence of substrate. The reduction in tissue content of preformed high energy phosphates was similar for zero substrate and when palmitate, succinate or malate were present in the bath. At the end of 160-min incubation, the ability of the in vitro whole bladder to empty following field stimulation was reduced by 95% in the absence of substrate or in the presence of palmitate, succinate or malate compared to 25% in the presence of glucose or pyruvate. Thus, the ability to empty was suppressed to a much greater extent by substrate deprivation than the phasic increase in intravesical pressure. These results indicate that phasic force generation and the ability to maintain tension may have separate metabolic properties. The phasic response being mediated by high energy phosphates, while the tonic phase of the response is linked to aerobic, oxidative metabolism.

ISSN:0031-7012    

DOI:10.1159/000138799

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Dopamine receptors of the DA1 subtype have been identified in mesenteric blood vessels, stimulation of which leads to vasodilation. In this study, we have determined the anatomical localization of dopexamine-hydrochloride-binding sites and carried out functional characterization of responses to this DA1-receptor and β2-adrenoceptor agonist in rat mesenteric vasculature. Autoradiographic studies showed the presence of [3H]-dopexamine-binding sites in all the different layers of the mesenteric artery. The DA1 receptor antagonist, SCH 23390 (IC50 = 4.9 μmol/l), and the β-adrenoceptor antagonist, propranolol (IC50 = 6.0 μmol/l), inhibited the binding of dopexamine. The inhibitory effect of these compounds on dopexamine binding was selective for different regions of the mesenteric artery. Also, dopexamine produced concentration-related increases in cAMP formation in membrane particles from superior mesenteric artery and its main branches. The presence of both SCH 23390 and propranolol was required to completely abolish dopexamine-induced increases in cAMP formation. In functional studies, dopexamine (1 and 3 μg/kg/min) produced dose-related increases in mesenteric blood flow (23 and 38%, respectively) which were accompanied by concomitant decreases in the calculated mesenteric vascular resistance. As seen with increases in cAMP, the vascular responses to dopexamine could be completely abolished only by prior treatment with both SCH 23390 and propranolol. These results suggest that in mesenteric vasculature of rat dopexamine binds primarily to DA1 receptors and β2-adrenoceptors. The activation of these receptors by dopexamine leads to vasodilation which is mediated by an increase in the intracellular levels of

ISSN:0031-7012    

DOI:10.1159/000138800

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Ginsenosides, the saponins of ginseng, are bioactive ingredients which exert many beneficial effects. One ginsenoside, Rb1, extracted from North American ginseng (Panax quinquefolium L.), partially prevents the memory deficits induced by a cholinergic agent (scopolamine) in rats. In vitro studies show that Rb1 has no effect on quinuclidinyl benzylate binding or on acetylcholinesterase activity, but facilitates the release of acetylcholine (ACh) from hippocampal slices. The increase in ACh release is associated with an increased uptake of choline into nerve endings; however, calcium influx is unaltered. The ability of Rb1 to prevent memory deficits may be related to facilitation of ACh metabolism in the central nervous system.

ISSN:0031-7012    

DOI:10.1159/000138801

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The present investigation was undertaken to clarify the in vitro effect of β-alanyl-L-histidinato zinc (AHZ) on bone metabolism in tissue culture. Calvaria were removed from weanling rats (3-week-old male) and cultured for periods up to 96 h in Dulbecco’s modified Eagle medium (high glucose, 4.5%) supplemented with antibiotics and bovine serum albumin. The experimental cultures contained 10–8 to 10–4 mol/l AHZ. The bone cellular zinc content was significantly increased in cultures with concentrations of AHZ greater than 10–6 mol/l. With 10–5 mol/l zinc sulfate, the bone cellular zinc content was significantly elevated. Bone calcium content was significantly increased by the presence of 10–7 to 10–4 mol/l AHZ. This increase was blocked by the presence of 10–7 mol/l cycloheximide. Bone alkaline phosphatase activity was elevated in the presence of AHZ (10–7 to 10–4 mol/l), whereas it did not significantly alter acid phosphatase activity. Bone collagen and DNA contents were significantly increased by 10–7 to 10–5 mol/l AHZ, while they were not significantly elevated by zinc sulfate (10–7 and 10–6 mol/l). The AHZ (10–5 mol/l)-induced increase in bone alkaline phosphatase activity and DNA content were prevented by 10–4 mol/l dipicolinate, a chelator of zinc. Furthermore, the AHZ (10–5 mol/l)-induced increase in bone alkaline phosphatase activity, collagen and DNA contents were blocked by 10–7 mol/l cycloheximide. These findings indicate that AHZ had a direct stimulatory effect on bone mineralization in vitro, and that bone protein synthesis was a necessary component of this response. The AHZ effect was more

ISSN:0031-7012    

DOI:10.1159/000138802

出版商:S. Karger AG    

年代:1991

数据来源: Karger