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The motor representation of the body musculature was studied in 11 adult mice by using ICMS. The motor responses elicited from both granular and agranular cortical fields showed that the mouse motor cortex is topographically organized; however, within the representation of individual body-parts the movements are multiply represented. In addition, several sites were encountered where more than one movement was elicited at the same stimulus threshold. The locations of pyramidal cells contributing axons to the pyramidal tract were examined by means of retrograde tracing with HRP injected into the cervical enlargement. This procedure labeled neurons only in lamina V in granular and agranular cortical fields. The similarities between the organization of motor cortex demonstrated in this study and the organization in the rat suggest that the rat and mouse share a common plan of rodent motor cortical organization.

Phorbol ester-induced translocation of the calcium/phospholipid-dependent protein kinase, protein kinase C (PKC), from soluble to particulate cell fractions was inhibited in primary cultures of hepatocytes isolated from rats chronically exposed to the liver tumor promoter phenobarbital (PB). Inhibition of translocation (34%) was significant after a 15-min treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA, 500 nM); an 85% inhibition was observed after 60 min. In contrast, the translocation responses to two non-phorbol ester activators of PKC, ATP (1 mM) and arginine-vasopressin (0.1 microM), were not significantly impaired. Assessment of total PKC specific activity revealed that translocation induced by TPA and the two nonphorbol activators was not associated with PKC degradation in hepatocytes from either control or PB-exposed rats. The defect in TPA-induced translocation was correlated with an impaired down-regulation of the hepatocyte surface receptor for epidermal growth factor in hepatocytes from PB-exposed rats. Chronic exposure to PB did not affect the total content or specific activity of PKC in whole liver, nor did it affect the distribution of PKC activity between soluble and particulate fractions in unstimulated liver or hepatocytes. However, both the diminished epidermal growth factor receptor response and the inhibition of TPA-induced PKC translocation were reversed by withdrawal of PB for 2 to 4 weeks. Hepatocytes isolated from female rats were found to contain a 3- to 4-fold greater PKC specific activity and content than hepatocytes from male rats. However, no sex-related differences were observed in PKC distribution or in the modulation of translocation by chronic PB exposure and withdrawal. Immunoblotting of partially purified liver extracts revealed that the defect in phorbol ester-induced translocation was not caused by altered expression of PKC isozymes. PKC isozymes II and III, but not I, were detected, and their amounts were unaffected by PB exposure, although higher levels were detected in female relative to male livers. These data demonstrate reversible inhibition of phorbol ester-induced PKC activation by the liver tumor promoter, PB, and suggest that PB alters a component of the PKC-signaling pathway other than the expression of PKC isozymes.

The effect of the uncoupler of oxidative phosphorylation, FCCP (carbonylcyanide p-trifluoromethoxyphenylhydrazone), on the tight junction of Madin-Darby canine kidney cells was examined. FCCP induced an abrupt decrease in the transepithelial electrical resistance of the confluent monolayers over a period of 20 s. When FCCP was withdrawn from the incubation medium, the monolayer resistance recovered to close to the original level in less than 2 h. Staining of the tight junction-associated protein ZO-1 showed that the changes in transepithelial electrical resistance were accompanied by a diffusing of the protein away from cell peripheries and a reconcentration to the tight junction areas following resistance recovery. Intracellular pH was decreased by FCCP on a similar time-scale with no obvious changes in ATP levels over this time-course. These data suggest that the uncoupler FCCP has a profound effect on tight junction permeability and cellular distribution of the tight junction protein ZO-1 in the epithelial cells and that it probably acts by breaking down proton gradients and altering intracellular pH.

We studied the distribution of the peripheral nerves innervating the distal forepaw by recording receptive fields from fascicles of the ulnar, radial, and median nerves and compared this result with the peripheral nerve representation in primary somatosensory (SI) cortex of cat. Our findings suggest that SI cortex receives input, in large part, from multiple peripheral nerves even when those nerves do not show a strong overlapping pattern in the periphery. This overlap pattern observed in SI cortex may be responsible, in part, for the immediate reorganization which is known to follow peripheral nerve deafferentation.

A high molecular weight tight junction-associated protein, ZO-1, has been demonstrated in liver (hepatocytes) and in both epithelium and endothelium. We carried out studies to examine the presence of the protein in vascular endothelial cell cultures and several other types of cultured cells, and the relationship between the ZO-1 protein content and confluency of endothelial cell monolayers. Immunofluorescence labelling of endothelial monolayers and two types of epithelial monolayers, IEC-6 and MDCK, with monoclonal antibody against ZO-1 protein localized the protein to the cell peripheries. Its association with the cell periphery only occurred when cells had contact with one another as demonstrated in endothelial cells. We have been able to show a positive correlation between the ZO-1 content of the cells and the extent of monolayer confluency in the endothelial cells by immunoblotting. The protein is much less expressed in nonconfluent endothelial cell monolayers and totally absent from mouse myeloma cultures. The presence and confluence-related expression of the protein in endothelium give support to the hypothesis that tight junctions exist in confluent endothelial cells and that the ZO-1 protein is expressed under the conditions where tight junction interactions occur.

A retrospective analysis of 20 cases of orbital fistula in Shanghai showed the causes to be trauma with foreign-body retention, osteomyelitis, mucocele, and dermoid cyst. Half the patients were children younger than 10 years old. Cicatricial ectropion, ptosis, and extraocular motility disturbance constituted the common clinical findings. Treatment according to the various causes included surgical removal of the foreign body, oral administration of antibiotics combined with local irrigation, radical extraction of all the epithelium lining the fistula, and excision of the fistula.

The effects of water soluble extract of Liriope spicata on acute hemodynamics were studied in anesthetized cats. The results showed that LV dp/dt max was increased by 87%, whereas t-dp/dt max was shortened by 28% after administration of WSEL (1.75 g/kg, iv). At the same time CO, CI, SI, and SVWI were increased by 146, 151, 153, and 194%, respectively. HR was declined slightly. SVR was reduced by about 48%. WSEL (0.7 g/kg, iv) induced an increase of 38% in LV dp/dt max, 44% in CO, 50% in SI and a decrease of 20% in t-dp/dt max and 20% in SVR. Preliminary results indicated that WSEL increased ventricular contractile force and might increase cardiac pump function.

Protected nonapeptide--Delta Sleep-Inducing Peptide (DSIP) formula: see text has been synthesized by classical method. The product has been treated with TFA and purified on DEAE-Sephadex-A25 column, pure free nonapeptide obtained and alpha to beta transposition of Asp-residue found to be absent. It has been assayed by electrophoresis at pH 3.8, microcrystallinecellulose TLC and HPLC. The physiological activities of synthetic DSIP are performed on rabbits by using intravenous administration or mesodiencephalic ventricular infusion. Its function of intensifying delta and sigma waves on rabbit's electroencephalogram (EEG) is evident. There is no concomitant increase of delta- and sigma-enhancing effect following mesodiencephalic ventricular infusion of 10 or 20 times higher than 5 microgram/rabbit doses. Results of 6-day consecutive intravenous administration (50 microgram/kg) indicate that there is no obvious sign of adaptation to DSIP. Results suggest that the physiological function of endogenous sleep-inducing peptide is different from that of general sleeping draught.