Mechanisms underlying excitatory amino acid-evoked calcium entry in cultured neurons from the embryonic rat spinal cord.
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Biomedical subjects
Publications and source records attributed to O Arancio.
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Rat soleus muscles were partially or totally denervated by sectioning the radicular nerve L5 or the radicular nerves L3 through L6, respectively. Three days after these procedures, fibrillation potentials were not observed in the case of partial denervation, whereas they were clearly detectable after total denervation. At later times, spontaneous spike activity also developed in the partially denervated muscles. The difference in time of onset of fibrillation between partially and totally denervated muscles was confirmed by a more gradual increase in the number of acetylcholine receptors and a greater sensitivity to tetrodotoxin of the former muscles. These differences between partially and totally denervated muscles are interpreted on the basis of the different amounts of nerve breakdown products generated in the two situations.
Resting membrane potentials (RMPs) have been recorded in vitro near the end-plate region of rat soleus muscles reinnervated with tetrodotoxin-inactive nerves and compared with those of denervated muscles whose reinnervation had been prevented. The two muscle groups exhibited the same low values of RMP typical of denervated muscles. In control muscles of rats in which impulse conduction was left unimpaired, reinnervation induced the expected increase in RMP values towards normal. It is suggested that, at least for this property, reinnervation restores to normal the muscle fibre membrane essentially through the return of activity.
Two brothers with motor retardation since the first months of life presented waddling ataxic-gait with lumbar lordosis, joint contractures and generalized muscle weakness. Both presented altered cerebellar tests and scanning speech. Creatine kinase, electromyography (EMG) and muscle biopsy pointed to muscular disease while CT scanning and NMR imaging showed cerebellar vermis agenesis. On this evidence we diagnosed the unusual association of vermian agenesis and congenital muscular dystrophy.
Two cases of familial myasthenia gravis are reported. One patient is a typical case of autoimmune myasthenia with positive anti acetylcholine receptor antibodies, while in the second patient the impairment of neuromuscular transmission is likely to be due to antibodies directed against determinants other than the acetylcholine receptors.
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Among the compartmental syndromes the necrosis of peroneal muscles is unusual. We report a case in which the swelling of peroneal muscle causes a compression of the common peroneal nerve below the peroneal head. A disturbance of both the motility and sensibility of the deep and superficial peroneal nerve is present with different pathogenesis. In fact, EMG suggested a muscular damage of the peroneal compartment and a denervation of the pretibial muscle. Interfascicular neurolysis along the peroneal nerve was performed to decompress the common and the deep peroneal nerve. A recovery in the territory of the tibialis anterior deep peroneal nerve confirmed the different mechanisms of paralysis.
Two populations of neurons are present in the dorsal root ganglia: i) the first which is connected with the neuromuscular spindles is localized in the mediodorsal (MD) part of the ganglion; ii) the second which is connected with the cutaneous receptors is localized in the ventrolateral (VL) part of the ganglion. The growth of MD but not of VL neurons in vitro is dependent upon the presence of the NGF. In order to study the presence in vivo of such differential effect of the NGF on the two neuronal populations, we have injected rat embryos with NGF antiserum (AS-NGF) and recorded the compound action potentials of different hindlimb nerves. We found that the sensory component, in the studied muscular nerves of the hindlimb, is seriously depressed in treated animals. These results indicate that the animals treated with AS-NGF suffer of a depression of activity in the afferents from the muscle spindles. This is probably due to a decrease in the number of these fibers in their muscle nerves.
Weanling and adult rats were intraperitoneally injected with D-carnitine for 40 days. After 15 days of treatment a statistically significant depletion in the muscle levels of free and total L-carnitine was observed, but after 40 days this depletion became slight and statistically not significant. These findings suggest the presence of a compensatory mechanism acting on the inhibition of L-carnitine transport into skeletal muscle fibres.
Previous results have suggested that cGMP is involved in hippocampal long-term potentiation (LTP), perhaps as the presynaptic effector of a retrograde messenger. However, other studies have failed to replicate some of those results, making the role of cGMP uncertain. We therefore reexamined this question and identified several variables that can affect the contribution of cGMP. First, brief perfusion with 8-Br-cGMP before weak tetanic stimulation produced long-lasting potentiation in the CA1 region of hippocampal slices, but more prolonged perfusion with 8-Br-cGMP before the tetanus did not produce long-lasting potentiation. Second, the activity-dependent long-lasting potentiation by cGMP analogs was reduced when NMDA receptors were completely blocked, indicating that NMDA receptor activation contributes to, but is not required for, the potentiation. The amount of reduction of the potentiation differed with different protocols, and in some cases could be complete. Third, LTP produced by strong tetanic stimulation in the stratum radiatum of CA1 (which expresses eNOS) was blocked by inhibitors of soluble guanylyl cyclase or cGMP-dependent protein kinase, but LTP in the stratum oriens (which does not express eNOS) was not. The results of these experiments should help to explain some of the discrepant findings from previous studies, and, in addition, may provide insights into the mechanisms and functional role of the cGMP-dependent component of LTP.