1,721,065 research outputs found
[Role of NGF in the development of primary sensory neurons in the rat]
No full textTwo 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
Fibrillatory activity and other membrane changes in partially denervated muscles
No full textRat 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
Furoxans (1,2,5-Oxadiazole-N-Oxides) as Novel NO Mimetic Neuroprotective and Procognitive Agents
No full textFuroxans (1,2,5-oxadiazole-N-oxides) are thiol-bioactivated NO-mimetics that have not hitherto been studied in the CNS. Incorporation of varied substituents adjacent to the furoxan ring system led to modulation of reactivity toward bioactivation, studied by HPLC-MS/MS analysis of reaction products. Attenuated reactivity unmasked the cytoprotective actions of NO in contrast to the cytotoxic actions of higher NO fluxes reported previously for furoxans. Neuroprotection was observed in primary neuronal cell cultures following oxygen glucose deprivation (OGD). Neuroprotective activity was observed to correlate with thiol-dependent bioactivation to produce NO2-, but not with depletion of free thiol itself. Neuroprotection was abrogated upon cotreatment with a sGC inhibitor, ODQ, thus supporting activation of the NO/sGC/CREB signaling cascade by furoxans. Long-term potentiation (LTP), essential for learning and memory, has been shown to be potentiated by NO signaling, therefore, a peptidomimetic furoxan was tested in hippocampal slices treated with oligomeric amyloid-beta peptide (A beta) and was shown to restore synaptic function. The novel observation of furoxan activity of potential therapeutic use in the CNS warrants further studies
Nerve stump effects in muscle are independent of synaptic connections and are temporally correlated with nerve degeneration phenomena.
No full textClose or distant denervation of the rat soleus muscle indicated that (1) longer soleus nerve stumps delay the onset of axon terminal degeneration and of muscle membrane changes (spike resistance to TTX) by strictly comparable times, and (2) the stump-induced delay of the muscle effect is independent of synaptic connections, because it is also obtained (RMP fall and TTX-resistance development) when sectioning a foreign nerve previously transplanted on the soleus surface but not making synaptic contacts. Both lines of evidence are consistent with the interpretation that, as far as the extrajunctional membrane properties are concerned, the effect of the length of the nerve stump on muscle is mediated by nerve terminal breakdown
Effects of reinnervation with normal and tetrodotoxin-inactive nerves on resting membrane potential of rat skeletal muscle
No full textResting 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
Acute peroneal compartmental syndrome: report of a case
No full textAmong 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
Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits
No full textAccording to the prevailing "amyloid cascade hypothesis," genetic dementias such as Alzheimer's disease and familial Danish dementia (FDD) are caused by amyloid deposits that trigger tauopathy, neurodegeneration, and behavioral/cognitive alterations. To efficiently reproduce amyloid lesions, murine models of human dementias invariably use transgenic expression systems. However, recent FDD transgenic models showed that Danish amyloidosis does not cause memory defects, suggesting that other mechanisms cause Danish dementia. We studied an animal knock-in model of FDD (FDDKI/+) genetically congruous with human cases. FDDKI/+ mice present reduced Bri2 levels, impaired synaptic plasticity and severe hippocampal memory deficits. These animals show no cerebral lesions that are reputed characteristics of human dementia, such as tangles or amyloid plaques. Bri2(+/-) mice exhibit synaptic and memory deficits similar to FDDKI/+ mice, and memory loss of FDDKI/+ mice is prevented by expression of WT BRI2, indicating that Danish dementia is caused by loss of BRI2 function. Together, the data suggest that clinical dementia in Danish patients occurs via a loss of function mechanism and not as a result of amyloidosis and tauopathy
Preparation of oligomeric β-amyloid 1-42 and induction of synaptic plasticity impairment on hippocampal slices
No full textImpairment of synaptic connections is likely to underlie the subtle amnesic changes occurring at the early stages of Alzheimer s Disease (AD). β-amyloid (Aβ), a peptide produced in high amounts in AD, is known to reduce Long-Term Potentiation (LTP), a cellular correlate of learning and memory. Indeed, LTP impairment caused by Aβ is a useful experimental paradigm for studying synaptic dysfunctions in AD models and for screening drugs capable of mitigating or reverting such synaptic impairments. Studies have shown that Aβ produces the LTP disruption preferentially via its oligomeric form. Here we provide a detailed protocol for impairing LTP by perfusion of oligomerized synthetic Aβ1-42 peptide onto acute hippocampal slices. In this video, we outline a step-by-step procedure for the preparation of oligomeric Aβ 1-42. Then, we follow an individual experiment in which LTP is reduced in hippocampal slices exposed to oligomerized Aβ 1-42 compared to slices in a control experiment where no Aβ 1-42 exposure had occurred
Congenital muscular dystrophy and cerebellar vermis agenesis in two brothers
No full textTwo 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. © 1988 Masson Italia Editori
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