Production of aldosterone by the regenerated adrenal gland after neonatal autograft in the normal, and the sodium deprived rat]

The suppression of the adrenal medulla by bilateral neonatal autograft in Sprague-Dawley male rat involves important changes in plasma aldosterone concentration: it falls of about 50% in animals with control diet; on the contrary, it is doubled in sodium depleted rats. Changes in adrenal aldosterone level are slight and non significant. The mechanism of effect of adrenal medulla on aldosterone production is discussed.     

Triple staining of normal and degenerating nervous tissue.

A method of counterstaining sections impregnated according to a previously reported modification of the Glees silver impregnation is described. The basis for this counterstain is the Klüver-Barrera luxol fast blue technique. The results are illustrated and the advantages and disadvantages of the procedure are discussed.     

Levels of myo-inositol in normal and degenerating peripheral nerve

—Free inositol was measured in peripheral nerves of the monkey, rabbit, rat, frog and lobster; levels in mammalian nerve were similar, and two to three times greater than in the other species. Concentrations of myo-inositol in rabbit tibial nerve increased from proximal to distal segments; in optic nerve the concentrations decreased with greater distance from the retina. In the early stages of Wallerian degeneration rabbit tibial nerve contained 25 per cent less free myo-inositol, rat nerve 50 per cent less. Rabbit nerves were analysed at 2 and 5 weeks after section; by 5 weeks levels of myo-inositol had increased to 50 per cent above normal. Similar changes were found in degenerating rabbit optic nerve. The combination of galactose feeding and nerve section resulted in reduction of the myo-inositol in rat sciatic nerve to one-fifth of the control value; galactitol in the nerve decreased by 50 per cent after section. The evidence suggests that myo-inositol in nerve is located mainly in Schwann cells or glia.     

Immunocytochemical localization of S-100b protein in degenerating and regenerating rat sciatic nerves

We studied the cellular and subcellular distribution of S-100b protein in normal, crushed, and transected rat sciatic nerves by an immunocytochemical procedure. In uninjured nerves, S-100b protein was restricted to the cytoplasm and membranes of Schwann cells, with no reaction product present in the nucleus or in axons. Similar images were seen from the first to the thirtieth day after the crush in activated Schwann cells during the degeneration period, i.e., up to the seventh post-lesion day, and in normal Schwann cells reappearing during the regeneration period, i.e., after the seventh post-lesion day, in the zone of the crush and proximal and distal to it. By the technique employed, there seemed to be no differences in the intensity of the immune reaction product in normal and activated Schwann cells. Also, similar images were seen in the proximal stump of transected nerves. Only a slight S-100b protein immune reaction product could be observed in the rare activated Schwann cells present in the distal stump around the seventh post-lesion day, the majority of cell types being represented by fibroblasts and elongated cells at this stage and thereafter. By immunochemical assays, similar results as those presented here have been reported and interpreted as indicative of the presence of S-100 protein in axons or, alternatively, of axonal control over expression of S-100 protein in Schwann cells. Our immunocytochemical data clearly show that the strong reduction in the S-100 protein content of the distal stump of transected nerves is owing to the paucity of Schwann cells and to the decrease in the S-100 protein content of these cells, rather than to degeneration of axons.     

Conduction velocity and excitability of A and C fibers of cat mesenteric nerves

The conduction velocity and excitability of fibers running from the mesenteric into the splanchnic nerves were studied in experiments on cats. Among the A fibers of these nerves there were shown to be: 1) fibers with an excitation threshold of 0.06–0.10 V (stimulus duration 0.1 msec) and a maximal conduction velocity of 48–85 m/sec; 2) fibers with an excitation threshold of 0.3–0.7 V, impulses of which form up to five waves in the composition of the action potential, with maximal conduction velocities of between 8–10 and 33–39 m/sec; 3) fibers with an excitation threshold of over 1 V and a conduction velocity of between 1.8 and 7 m/sec. The excitation threshold of the group C fibers was 6–8 V. Impulses of these fibers form a low-amplitude wave in the composition of the action potential of the mesenteric and splanchnic nerves with a conduction velocity of 1.0–1.8 m/sec, several waves of higher amplitude with a conduction velocity of 0.5–1.2 m/sec, and several low-amplitude waves with a conduction velocity of 0.35–0.55 m/sec. The results of experiments with different combinations of arrangement of the stimulating and recording electrodes on the mesenteric and splanchnic nerves indicate that sympathetic postganglionic C fibers of the mesenteric nerves occur only in the second group, whereas afferent C fibers occur in all three of the groups distinguished.Institute of Normal and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 7, No. 3, pp. 272–278, May–June, 1975.     

Protein synthesis-independent plasticity mediates rapid and precise recovery of deprived eye responses

Monocular deprivation (MD) for a few days during a critical period of development leads to loss of cortical responses to stimulation of the deprived eye. Despite the profound effects of MD on cortical function, optical imaging of intrinsic signals and single-unit recordings revealed that deprived eye responses and orientation selectivity recovered a few hours after restoration of normal binocular vision. Moreover, recovery of deprived eye responses was not dependent upon mRNA translation, but required cortical activity. Interestingly, this fast recovery and protein synthesis independence was restricted to the hemisphere contralateral to the previously deprived eye. Collectively, these results implicate a relatively simple mechanistic process in the reactivation of a latent set of connections following restoration of binocular vision and provide new insight into how recovery of cortical function can rapidly occur in response to changes in sensory experience.     

Anoxic block and recovery of axoplasmic transport and electrical excitability of nerve

Axoplasmic transport of cat sciatic nerves was studied in vitro in a chamber in which maximal α action potentials could also be elicited. After initiation of N₂ anoxia, electrical responses fell to zero at an average time of 22 min. A shorter time to zero of 11 min was seen during a second period of anoxia. A good recovery of both action potential responses and axoplasmic transport occurs after a period of anoxia lasting 1–1.5 hr. An apparent failure of recovery of axoplasmic transport was seen after 2 hr of anoxia with a good recovery of electrical responses. Axoplasmic transport tended to return toward normal when more time was allowed for recovery after anoxia. An adequate supply of ～P was shown to be present by measurement of ATP and creatine phosphate levels. The delay in recovery of transport thus signifies a failure of utilization of ～P by the transport mechanism. Longer periods of anoxia and recovery were limited in vitro and for this reason, ischemic anoxia was produced in vivo. Blood pressure cuffs were placed on the upper thigh of cats and maintained for times of 1–8 hr at pressures of 300–310 mm Hg. Then, recovery times up to 7 days were allowed. It was shown that axoplasmic transport could gradually recovery after an anoxia lasting up to 6–7 hr if sufficient recovery times were allowed. A possible explanation for the delay in the recovery of axoplasmic transport and the disassociation in the earlier recovery of electrical responses as against the recovery of transport was discussed.