2,634 research outputs found
Motor reinnervation during muscular activity
No full textMotor reinnervation during muscular activity
Sartini S, Bartolini F, Lattanzi D, Ciuffoli S, Ambrogini P, Cuppini R
Dept. Human, Environmental, Natural Scieces, University of Urbino “Carlo Bo”, Italy.
Following nerve injury and regeneration, a transient phase of multiple innervation of muscle cells occurs. Successively, 1:1 ratio of innervation is progressively reached. Two mechanisms has been proposed to explain these processes: nerve-terminal competition for muscle released growth factors and the different pattern of axon activity. We showed running to enhance muscle expression of BDNF, a trophic factor inducing sprouting. Thus we investigated the role of running early in post-traumatic reinnervation.
We used intracellular recordings and miography to evaluate the reinnervation of soleus muscle following nerve crush, in running and sedentary rats.
In sedentary rats, about 10% of recorded muscle cells was found to be multiply innervated from 7 to 45 days from nerve crush. In runners, multiple innervation reached 34% 10 days after nerve crush and this percentage gradually decreased during the following days, although it remained significantly higher with respect to sedentary group. This effect of running was reversible.
Both in runner and sedentary rats all axons were showed to be regenerated 10 days after nerve crush, but in runners recovery of muscle strength was higher and muscle reinnervation was almost complete.
On the basis of present results, we hypothesize that intense motoneuron-muscle activity might induce up-regulation of one or more neurotrophic factors released by muscle cells, that might induce motor nerve terminal sprouting and consequent massive muscle cell multiple innervation. This model allow to link nerve-terminal competition and axon activity hypotheses and is intriguing considering the importance of physical activity during rehabilitation and the correlated exercise protocol planning
FGF2 modulates the voltage-dependent K+ current and changes excitability of rat dentate gyrus granule cells.
No full textFibroblast growth factor 2 (FGF2) is involved in hippocampus-dependent learning. In this study, the effects of FGF2 on the excitability were investigated in granule cells of rat dentate gyrus. Hippocampal slices were used to perform patch clamp recordings in granule cells. Extracellularly applied FGF2 early quenched the depolarization-induced repetitive firing, suggesting a decreased excitability under these conditions. Consistently, transient and sustained voltage-gated K(+) currents decreased in a dose-dependent manner, repolarization phase of action potential was slowed down, afterhyperpolarization was reduced, and membrane resistance was decreased. These effects were not mediated by tyrosine kinase FGF2 receptors. Moreover, an involvement of G protein signaling was ruled out, as well as an intracellular action of FGF2. Considering the relationship between FGF2 and hippocampal functions, the modulation of neuron excitability by activity-driven FGF2 release may be regarded as a part of a homeostatic mechanism of self-regulation of hippocampal activity
Exploration-addressed physical activity induces synaptogenesis anticipation onto adult-generated neurons in dentate gyrus
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Creatine protects and improves the morpho-functional differentiation of neuroblasts in spinal cord primary cultures
No full textAim:
Creatine (Cr) is an essential component of Cr/Cr-phosphate system. Recent papers on different cell lines showed that Cr supplementation protects from cell death following radical insult by improving cell energy balance and/or exerting an antioxidant action. Neurons are known to have a low capacity to synthesize Cr and the relevance of oxidative stress-related mechanisms in the pathogenesis of several neurodegenerative diseases (ALS, Ataxia, Parkinson) is known. We studied the effects of Cr supplementation on primary cell cultures obtained from chick spinal cord embryo following oxidative stress.
Methods:
Neuroblast cultures were evaluated for viability (MTT test), morphological differentiation by Neuron J software and functional differentiation by whole-cell patch-clamp, in control conditions and following a treatment with hydrogen peroxide.
Results:
Hydrogen peroxide (20 mM) caused a significant decrease of viability and neurite/neuroblast extension length. Both actions were fully reversed by preincubation with Cr 10 mM. Protective effect of Cr was absent if Cr membrane transporters were blocked by b-guanidine propionic acid, thus demonstrating a cytosolic action of Cr. Moreover, electrophysiological studies demonstrated that Cr supplementation increases Na+ e K+ currents with respect to controls.
Conclusions:
Our results suggest that Cr is able to protect neurons from oxidative stress. Moreover, the increase in Na+ e K+ currents recorded in neuroblasts leads to suppose a higher number of voltage-dependent ion channels in membrane, indicating a possible role of Cr in functional differentiation of neurons
Who is the author of the 1876 Stefano manuscript?
No full textFor over one hundred years the Stefano manuscript was a private document in the possession of the Baccich family and descendants. It told a story of the 1875 Stefano shipwreck as narrated by the shipwreck survivor and the founding family patriarch Miho Baccich. In these circumstances the question of authorship of the manuscript was immaterial and did not arise as an issue. However, with the publication of the manuscript the author‟s name, or names, need to be formally attributed to it. It turns out that this is not such a clear-cut matter.
As we shall see, all informed sources attributed the authorship, and the ownership, of the manuscript to Miho Baccich. But the manuscript itself was written by Canon Stjepan Skurla – a priest from Miho‟s hometown of Dubrovnik. The question then arises: should Skurla also be considered as an author of the manuscript, or, even as the sole author (as some would have it)
Age-related naturally occurring depression of hippocampal neurogenesis does not affect trace fear conditioning
No full textNew neuron production throughout adulthood in granule cell layer (GCL) of rat hippocampus is a well-known phenomenon. A role of new neurons in hippocampal learning has been proposed, but the question is still open. A reduction of neural precursor proliferation in GCL of 2-month-old rats to about 20%, induced by the cytostatic agent methylazoxymethanol, was found to cause impairment in trace conditioning, suggesting a role of immature neurons in this kind of hippocampus-dependent learning (Shors et al., Hippocampus 2002;12:578-584). Neurogenesis decreases with increasing age. In this study, neural precursor proliferation and newborn cell survival were evaluated in GCL of adult rats within a range of ages following development and preceding old age. In 5-month-old rats, neural precursor proliferation was reduced to 57% and newborn cell survival was reduced to 40% in comparison to rats of 2 months of age; in 12-month-old rats, the decrease was to 5 and 4%, respectively. Consistently, the density of immature neurons decreased to 41 and 13% in 5- and 12-month-old rats, respectively. The role of neurogenesis in trace fear conditioning was studied in this natural model of neurogenesis depression. No impairment in trace fear conditioning was found both in 5- and 12-month-old rats in comparison to 2-month-old rats, notwithstanding the decrease of neurogenesis that is marked in 12-month-old rats. This finding shows that a lower rate of neurogenesis is sufficient for learning in 12-month-old rats in comparison to young rats
MATERNAL DIETARY LOADS OF ALPHA-TOCOPHEROL DIFFERENTIALLY INFLUENCE FEAR CONDITIONING AND SPATIAL LEARNING IN ADULT OFFSPRING
No full textα-Tocopherol, the main component of vitamin E, is well known to be a radical scavenger, so an increased intake of vitamin E is recommended in complicated pregnancy, to prevent possible fetus damage by free radical. In a previous work, we found that maternal α-tocopherol supplementation affects PKC-mediated cellular signaling and hippocampal synaptic plasticity in developing brain; the latter effect persists in adulthood. Here, adult rats maternally exposed to supranutritional doses of α-tocopherol were evaluated for Contextual Fear Conditioning and spatial learning in Morris Water Maze, two different hippocampus-dependent learning tasks. Moreover, anxiety, spontaneous activity, and explorative drive were also evaluated as factors potentially affecting learning performance. Treated rats showed a different behavior with respect to controls: performance in Contextual Fear Conditioning was improved, while spatial learning tested in Morris Water Maze, was impaired. The improvement of fear response was not ascribable to differences in anxiety level and/or spontaneous activity; thus it appears to be a specific effect of α-tocopherol overloading during brain development. On the contrary, the impaired performance in Morris Water Maze exhibited by treated rats can be in part explained by their enhanced explorative drive. Although extrapolation from rats to humans is difficult, a caveat in assuming supranutritional doses of vitamin E in pregnancy arises from this study
Maternal dietray loads of alpha-Tocopherol can affect PKC signaling and synaptic plasticity in postnatal developing hippocampus thereby affecting spatial memory in adult offspring.
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