Neuroscience
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After myocardial infarction (MI), ovariectomized (OVX) female rats develop depression-like behaviors and an increase of pro-inflammatory cytokine (PIC) levels in the prefrontal cortex (PFC). We hypothesized that inhibition of neuroinflammation by the PIC synthesis inhibitor, pentoxifylline (PTX) would prevent depression-like behaviors induced by heart failure (HF) post-MI in OVX female rats. PTX treatment was initiated in female Wistar rats, 1 week after ovariectomy, and 1 week before MI by occlusion of the left anterior descending artery. ⋯ These findings show that OVX female rats post-MI exhibit an increase in both peripheral and central inflammation. PTX treatment prevents increases in PIC levels in plasma and PVN but does not attenuate the progression of cardiac dysfunction. In contrast, PTX prevents enhanced PIC production in the PFC, as well as limits depression-like behaviors induced by MI in OVX female rats.
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Understanding and predicting the intentions of others through limb movements are vital to social interaction. The processing of biological motion is unique from the processing of motion of inanimate objects. Presently, there is controversy over whether visual consciousness of biological motion is regulated by visual attention. ⋯ Late processing was localized to frontal-parietal regions, such as the right dorsal superior frontal gyrus, the left medial superior frontal gyrus, and the occipito-temporal regions. Congruency-related processing occurred in the 246-260-ms window and was localized to the right superior occipital gyrus. In summary, due to its complexity, biological motion awareness has a unique neural basis.
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We have recently shown that the efficiency of stopping a response is correlated with GABAergic activity in primary motor cortex (M1) measured using the short interval intracortical inhibition (SICI) protocol. However, this finding was observed when SICI was measured in left M1 and when stopping efficiency was measured with a bimanual response task. The aim of the present study was to examine the extent to which the relationship between SICI and stopping is lateralized to the hemisphere controlling the response (e.g. left M1 and stopping a right hand response) and/or reflects bilateral inhibitory mechanisms (as might be seen between left M1 and left hand stopping). ⋯ We found that SICI was significantly correlated between hemispheres (r = 0.51) and stopping efficiency was correlated between hands (r = 0.77). When controlling for other relevant variables, we found that stopping efficiency in each hand was uniquely predicted by SICI in the contralateral hemisphere, but not the ipsilateral hemisphere. These results suggest that there is a hemispheric-specific contribution of SICI to stopping efficiency.
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Exposure to commonly used anesthetics is associated with widespread neuroapoptosis in neonatal animals. Vulnerability of developing hippocampal dentate gyrus granule cells to anesthetic neurotoxicity peaks approximately 2 weeks after cell birth, as measured by bromodeoxyuridine birth dating, regardless of the age of the animal. The present study examined whether the vulnerable window can be further characterized by utilizing a transgenic approach. ⋯ Apoptotic EGFP- granule cells more frequently expressed the immature neuronal marker calretinin (75.4% vs 45.0%, P < 0.001) and less frequently the late progenitor marker NeuroD1 (21.9% vs 87.9%, P < 0.001) than EGFP+ granule cells. Although EGFP- granule cells were more mature in immunostaining than EGFP+ granule cells, their electrophysiological properties partially overlapped in terms of input resistance, resting membrane potential and action potential amplitude. Our results revealed the POMC stage, when GABA acts as an excitatory neurotransmitter, only partly captures susceptibility to anesthetic neurotoxicity, suggesting the vulnerable window of anesthesia-induced neuroapoptosis extends from the end of POMC+ stage to the post-POMC+ stage when depolarizing glutamatergic inputs emerge.
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Temporal lobe epilepsy is triggered by an initial insult, such as status epilepticus, that initiates the process of epilepsy development. Heat shock protein 70 (Hsp70) is a ubiquitously expressed molecular chaperone, involved in the inflammatory response that is upregulated after status epilepticus. Hsp70 has been described as an endogenous intracellular ligand of Toll-like receptor 4. ⋯ No colocalization with the astrocytic marker GFAP or the microglia marker Iba1 was found. The intense neuronal Hsp70 upregulation during the early post-insult phase might contribute to the onset of excessive inflammation triggering molecular and cellular reorganization and generation of a hyperexcitable epileptic network. Therefore, development of multi-targeting strategies aiming at prevention of epileptogenesis should consider Hsp70 modulation in the early days following an epileptogenic insult.