Neuroscience
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Oxidative stress and the production of reactive oxygen radicals play a key role in neuronal cell damage. This paper describes an in vitro study that explores the neuronal responses to oxidative stress focusing on changes in neuronal excitability and functional membrane properties. This study was carried out in pyramidal cells of the motor cortex by applying whole-cell patch-clamp techniques on brain slices from young adult rats. ⋯ Most of the neurons, however, kept their repetitive discharge even though their maximum frequency and gain decreased. Furthermore, cancelation of the repetitive firing discharge took place at intensities that decreased with time of exposure to CH, which resulted in a narrower working range. We can conclude that oxidative stress compromises both neuronal excitability and the capability of generating action potentials, and so this type of neuronal functional failure could precede the neuronal death characteristics of many neurodegenerative diseases.
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To probe the mechanism underlying the auditory behavior-related response patterns of inferior collicular neurons to constant frequency-frequency modulation (CF-FM) stimulus in Hipposideros pratti, we studied the role of post-spike hyperpolarization (PSH) in the formation of response patterns. Neurons obtained by in vivo extracellular (N=145) and intracellular (N=171) recordings could be consistently classified into single-on (SO) and double-on (DO) neurons. ⋯ These data suggested that the PSH directly participated in the formation of SO and DO neurons, and the PSH elicited by the CF component was the main synaptic mechanism underlying the SO and DO response patterns. The possible biological significance of these findings relevant to bat echolocation is discussed.
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Sex- and season-specific modulation of hippocampal size and function is observed across multiple species, including rodents. Other non-hippocampal-dependent behaviors exhibit season and sex differences, and whether the associated brain regions exhibit similar variation with sex and season remains to be fully characterized. As such, we examined the brains of wild-caught Richardson's ground squirrels (RGS; Urocitellus richardsonii) for seasonal (breeding, non-breeding) and sex differences in the volumes of specific brain areas, including: total brain volume, corpus callosum (CC), anterior commissure (AC), medial prefrontal cortex (mPFC), total neocortex (NC), entorhinal cortex (EC), and superior colliculus (SC). ⋯ Only two simple main effects of sex were observed: males captured in the non-breeding season had significantly larger total brain volume than females captured in the non-breeding season, and females captured during the breeding season had larger volumes of the mPFC and EC than males captured in the breeding season. These results indicate that females have more pronounced seasonal differences in brain and brain region sizes. The extent to which seasonal differences in brain region volumes vary with behaviour is unclear, but our data do suggest that seasonal plasticity is not limited to the hippocampus and that RGS is a useful mammalian species for understanding seasonal plasticity in an ecologically relevant context.
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Spinocerebellar ataxia type 1 (SCA1) is an incurable, dominantly inherited neurodegenerative disease of the cerebellum caused by a polyglutamine-repeat expansion in the protein ataxin-1 (ATXN1). While analysis of human autopsy material indicates significant glial pathology in SCA1, previous research has focused on characterizing neuronal dysfunction. ⋯ Glial activation occurred in the absence of neuronal death, suggesting that glial activation results from signals emanating from dysfunctional neurons. Finally, in all different models examined glial activation closely correlated with disease progression, supporting the development of glial-based biomarkers to follow disease progression.
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Necrostatin-1 (Nec-1) is an inhibitor of necroptosis, playing an important role in inhibition of pathological death in the central nervous system (CNS). Our earlier study suggests that Nec-1 protects the injured spinal cord. In this study, we found that Nec-1 reduces the elevated Ca(2+) concentration in mitochondria post-injury and preserves the remarkably decreased mitochondrial membrane potential (MMP) level post-spinal cord injury (SCI). ⋯ It also inhibits the up-regulation of mitochondrial fusion genes Mnf1, Mnf2 within 6h post-injury and adjusts the abnormal expression of mitochondrial fission gene Fis1. All these results indicate the improvement of mitochondrial functions in injured spinal cord after the treatment of Nec-1. This research revealed the mechanisms of functional protection of Nec-1 by mitigating mitochondrial dysfunction post-SCI.