Projections from the lateral mammillary nucleus to the anterodorsal thalamic nucleus in the rat

There has been an abundance of research on the connections of the mammillary bodies but the projections from the lateral mammillary nucleus to the anterodorsal thalamic nucleus has remained a gray area due to a dearth of material which directly addresses the details of this pathway. This study seeks to further define the nature of this particular nerve connection within the mammillothalmic tract. The technique employed is fluorescent nerve tract tracing using two fluorescent tracers implanted separately into each anterodorsal thalamic nucleus then followed retrogradely to the soma of the neurons in the lateral mammillary nucleus. Fluorescent photomicrography allowed us to document the single and double labeled cells of the lateral mammillary nucleus. The single labeled cells can be categorized into ipsilaterally projecting neurons and contralaterally projecting neurons. About half of all labeled cells were bilaterally projecting double-labeled, a third was ipsilaterally projecting single-labeled and the remainder were contralaterally projecting single labeled-cells. There were no labeled cells traced to the medial mamillary nucleus. The mammillary bodies play an important role in the limbic circuitry and a part of the so-called "Papez Circuit". The pathway by which the mammillary body projects to the other structures of the limbic system and the way it connects the limbic system to other parts of the brain like the tegmentum is not fully understood. This clarification of the connection between the lateral mammilary nucleus and the anterodorsal thalamic nucleus is but one of the contemplated pathways.     

The high-affinity sulphonylurea receptor regulates KATP channels in nerve terminals of the rat motor cortex

The coexpression of sulphonylurea binding sites and ATP-sensitive K+(KATP) channels was examined in the rat motor cortex, an area of the CNS exhibiting a high density of sulphonylurea binding. These channels were not detected on neuronal cell bodies, but sulphonylurea-sensitive KATP channels and charybdotoxin-sensitive, large-conductance calcium-activated K+ BKCa channels were detected by patch clamping of fused nerve terminals from the motor cortex. Subcellular fractionation revealed that high-affinity sulphonylurea binding sites were enriched in the nerve terminal fraction, whereas glibenclamide increased calcium-independent glutamate efflux from isolated nerve terminals. It is concluded that neuronal sulphonylurea receptors and KATP channels are functionally linked in the motor cortex and that they are both selectively expressed in nerve terminals, where the KATP channel may serve to limit glutamate release under conditions of metabolic stress.     

Effect of prenatal haloperidol administration on anxiety patterns in rats

Haloperidol (0.1 mg/kg, i.p.) treatment was given from day 12 to 20 of gestation to pregnant rats, this being the critical period for neural development in this species. The pups born were subjected to open-field exploratory behaviour, tunnel-board exploratory behaviour, elevated zero-maze and elevated plus maze behaviour tests at 7-8 weeks of age. The results indicate that prenatal haloperidol treatment induces a significant increase in open-field ambulations and rearings, decrease in scratching and licking/washing behaviours whereas grooming and faecal droppings remain unchanged. Significantly reduced activity in the centre and increased activity in the periphery of the tunnel board was noted. These suggest presence of anxiety in these animals. Significant anxiogenic behavioural patterns were also observed on elevated zero-maze and plus-maze in the prenatally haloperidol treated offsprings. The results suggest that prenatal exposure of haloperidol leaves a lasting effect on offsprings resulting in hyper-emotional responsiveness and anxiety state.     

Different functional effect of Ro 15-4513 and Ro 19-4603 on synaptic responses of Purkinje cells in the rat cerebellar slice

The Sugiura operation has been reported to have low operative mortality, rebleeding, and encephalopathy rates when carried out in a predominantly nonalcoholic Japanese population with good liver function. A literature review of reports of the Sugiura procedure outside Japan reveals a high complication and mortality rate when it is used as an emergency procedure in patients with advanced liver disease, especially in those with alcoholic cirrhosis. Uncontrolled studies report results that differ little from the Japanese series when the operation is confined to good-risk patients in the elective situation. Our experience with the Sugiura operation supports its role in these circumstances, especially in patients with portal vein thrombosis and normal liver function. The only good prospective controlled trial has been carried out in patients with schistosomiasis and suggests that the Sugiura operation is far superior to total shunt and may have a slight advantage over the Warren shunt because of its low incidence of postoperative encephalopathy. More controlled trials are required to establish its role in good- to moderate-risk patients with alcoholic cirrhosis.     

Plasma patterns of tumor necrosis factor-alpha (TNF) and TNF soluble receptors during acute meningococcal infections and the effect of plasma exchange

In 39 patients with acute meningococcal infections, the plasma concentrations of tumor necrosis factor-alpha (TNF) and its soluble receptors (sRs) TNFsR-p55 and TNFsR-p75 were measured from admission till recovery. At admission, patients with shock had significantly higher TNF, TNFsR-p55, and TNFsR-p75 values than patients without shock. In addition, during the first 24 hours, patients with shock had higher TNFsR-p75 to TNFsR-p55 ratios, indicating that in shock the increase of TNFsR-p75 exceeds that of TNFsR-p55. TNF measured more than 12 hours after admission failed to differentiate between shock and nonshock because TNF concentrations normalized within 12-24 hours. However, because concentrations of TNFsRs remained elevated for 5-6 days, at that time plasma TNFsRs still differentiated between shock and nonshock. Plasma exchange or whole blood exchange (PEBE), performed in 20 patients with shock, accelerated the decrease of plasma TNFsRs. However, because of a rebound after each PEBE session, the overall half-lives of both TNFsRs were not affected by PEBE.     

Localization of gap junctions and tracer coupling in retinal Müller cells

BACKGROUND: The objective of this study was to evaluate the indications for percutaneous ethanol injection (PEI) performed in a single session under general anesthesia for treating patients with cirrhosis and large (tumors > 5 cm) hepatocellular carcinoma (HCC), and relevant survival curves. METHODS: Between November 1991 and November 1996, 108 patients were treated (a total of 128 procedures). They fell into 3 groups: 24 patients with single, encapsulated HCC measuring from 5-8.5 cm (Group A); 63 patients with single, infiltrating HCC measuring from 5-10 cm or multiple HCC (Group B); and 21 patients with advanced disease, either hepatic (Child's Class C) or neoplastic (symptomatic HCC or with portal thrombosis) type (Group C). The mean amount of ethanol injected was 62 mL. The average hospital stay was 3.8 days. The mean follow-up time was 40 months. RESULTS: The 1-, 2-, 3-, and 4-year survival rates were: 72%, 65%, 57%, and 44%, respectively, for Group A; 73%, 60%, 42%, and 18%, respectively, for Group B; and 46%, 25%, and 0%, respectively, for Group C. Mortality was 0.7% (bleeding from esophageal varices in a Child's Class C patient). The rate of major complications was 4.6% (1 case of peritoneal hemorrhage, 1 case of severe liver failure, 1 case of transient renal insufficiency, 1 case of peritoneal seeding, and 2 cases of infarctions of a segment adjacent to the tumor). CONCLUSIONS: Single session PEI has been proven to be a valid alternative in patients otherwise treated surgically or with transcatheter arterial chemoembolization who present with adverse prognostic factors or risks for these therapies, and may be an option for selected patients with advanced disease previously excluded from any therapy. Risk conditions are marked portal or pulmonary hypertension or esophageal varices at risk of bleeding, superficial tumors with severe coagulation disorders, hyperfibrinolysis, chronic renal insufficiency, and obstructive jaundice.     

Terikalant, an inward-rectifier potassium channel blocker, does not abolish the cardioprotection induced by ischemic preconditioning in the rat

Recent results have shown that the sulfonylurea receptor couples to several types of inward-rectifier potassium (KIR) channels, which suggests that sensitivity to blockade of a pathophysiological phenomenon such as ischemic preconditioning (PC) by glibenclamide may not be the result of this compound selectively blocking the ATP-sensitive potassium (KATP) channel. Therefore, to address this possibility, a role for myocardial KIR v KATP channels in ischemic PC was evaluated in the rat. To test this hypothesis, anesthetized, open-chest, male Wistar rats were assigned to one of seven experimental protocols. Animals assigned to group I (control) received 30 min of occlusion and 2 h of reperfusion. Ischemic PC was produced by 3x5-min occlusion and 2-h reperfusion periods (group II). Terikalant (TK), an inward-rectifier potassium channel blocker, was used to test the role of other K+ channels, most notably the KIR, in the cardioprotective effect of ischemic PC in the rat. TK was given at a dose of 3 mg/kg, i.v., 15 min before the prolonged occlusion and reperfusion periods (group III). In groups IV, V, and VI terikalant (1, 3 and 6 mg/kg, i.v.) was given 15 min before ischemic PC (lowTK+PC, medTK+PC and hiTK+PC, respectively). Group VII consisted of glibenclamide (0.3 mg/kg, i.v.) given 30 min prior to ischemic PC (GLY+PC). Infarct size (IS) as a percent of the area at risk (AAR) was measured using the histochemical stain, 2,3, 5-triphenyltetrazolium chloride. The average IS/AAR for the control was 49.9+/-2.1%. Ischemic PC markedly reduced infarct size (8.6+/-1. 8%; * P<0.05 v control). Terikalant (TK; 1, 3 and 6 mg/kg, i.v.) did not abolish the cardioprotective effect of ischemic PC at any dose (15.5+/-6.4, 16.4+/-5.2 and 8.8+/-1.6%, respectively; * P<0.05 v control). TK itself had no effect on infarct size. GLY completely abolished the cardioprotective effect of ischemic PC (48.2+/-6.4%). In addition, the high dose of TK significantly (P<0.05) increased the action potential duration at 50% repolarization from 48+/-3 to 64+/-4 ms and 30 microM of TK, a concentration which produced a 39% decrease in the inward-rectifier potassium channel current in isolated guinea-pig ventricular myocytes in the whole-cell patch-clamp mode did not block the increase in K ATP current produced by the KATP opener bimakalim (3 microM). These results demonstrate that although the myocardial KATP channel belongs to the K IR superfamily, the endogenous myocardial KIR channel does not mediate ischemic PC in the rat heart; however, the K ATP channel does mediate its cardioprotective effect.     

Characterisation of triacylglycerol hydrolase activities in human placenta

We examined whether high conductance Ca2+-activated K+ (BK(Ca)) channels are involved in the modulatory action of nitric oxide (NO) on the secretion of adrenal catecholamines in response to splanchnic nerve stimulation and acetylcholine in anesthetized dogs. The NO donor 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamin e (NOC 7), the BK(Ca) channel blocker charybdotoxin and acetylcholine were administered intraarterially (i.a.) into the adrenal gland. NOC 7 infusion (2 microg min(-1)) inhibited increases in catecholamine output induced by splanchnic nerve stimulation (1-3 Hz) and acetylcholine (0.75-3 microg). Charybdotoxin infusion (100 ng min(-1)) did not affect increases in catecholamine output induced by splanchnic nerve stimulation and acetylcholine. Charybdotoxin blocked the NOC 7-induced inhibition of increases in catecholamine output induced by splanchnic nerve stimulation but not by acetylcholine. These results suggest that NO may inhibit the secretion of adrenal catecholamines induced by splanchnic nerve stimulation through activation of BK(Ca) channels.