Neuroscience
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During the early developmental period, long-term potentiation (LTP) can be induced in both vertical and horizontal connections in the rat visual cortex. However, the temporal difference in LTP change between the two pathways during animal development remains unclear. In this study, LTP in vertical (from layer IV to layer II/III) and horizontal (from layer II/III to layer II/III) synaptic connections were recorded in brain slices from the same rats, and the developmental changes of LTP in both directions were compared within the animals' eye-opening period. ⋯ The data show that the weak PS, which failed to induce H-LTP alone, was able to induce H-LTP effectively while V-LTP was performed on P10. Our results suggest that V-LTP can strengthen H-LTP induction in the visual cortex during the early developmental period. In contrast, the regulatory effect of H-LTP on V-LTP was much weaker.
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Acute stress impairs the hippocampus-dependent spatial memory retrieval, and its synaptic mechanisms are associated with hippocampal CA1 long-term depression (LTD) enhancement in the adult rats. Endogenous hydrogen sulfide (H2S) is recognized as a novel gasotransmitter and has the neural protective roles. However, very little attention has been paid to understanding the effects of H2S on spatial memory retrieval impairment. ⋯ Dithiothreitol (DTT, a disulfide reducing agent) abolished a decrease in the glutamate uptake caused by acute stress, and NaHS eradicated the decreased glutamate uptake caused by 5,5'-dithio-bis(2-nitrobenzoic)acid (DTNB, a thiol oxidizing agent), collectively, revealing that exogenous H2S increases glutamate uptake by reducing disulfide bonds of the glutamate transporters. Additionally, NaHS inhibited the increased expression level of phosphorylated c-Jun-N-terminal kinase (JNK) in the hippocampal CA1 region caused by acute stress. The JNK inhibitor SP600125 eliminated spatial memory retrieval impairment, hippocampal CA1 LTD enhancement and the decreased glutamate uptake caused by acute stress, indicating that exogenous H2S exerts these roles by inhibiting the activation of JNK signaling pathway.
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The study explored unintentional force changes elicited by removing visual feedback during cyclical, two-finger isometric force production tasks. Subjects performed two types of tasks at 1Hz, paced by an auditory metronome. One - Force task - required cyclical changes in total force while maintaining the sharing, defined as relative contribution of a finger to total force. ⋯ This finding is in contrast to most earlier studies that demonstrated only two stable patterns, in-phase and out-of-phase. We interpret the results as consequences of drifts of parameters in a dynamical system leading in particular to drifts in the referent finger coordinates toward their actual coordinates. The relative phase desynchronization is caused by the right-left differences in the hypothesized drift processes, consistent with the dynamic dominance hypothesis.
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The incidence of sudden unexpected death in epilepsy (SUDEP) is highest in people with chronic and drug-resistant epilepsy. Chronic spontaneous recurrent seizures cause cardiorespiratory autonomic dysfunctions. Pituitary adenylate cyclase-activating polypeptide (PACAP) is neuroprotective, whereas microglia produce both pro- and anti-inflammatory effects in the CNS. ⋯ We did not notice changes in microglial morphology or changes in a number of M2 phenotype in epileptic nor control rats in the vicinity of RVLM neurons. Our findings establish that microglial activation, and not PACAP, at the IML accounts for higher SNA and proarrhythmogenic changes during chronic epilepsy in rats. This is the first experimental evidence to support a neurotoxic effect of microglia during chronic epilepsy, in contrast to their neuroprotective action during acute seizures.
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The prefrontal cortex (PFC), amygdala and hippocampus display a coordinated activity during acquisition of associative fear memories. Evidence indicates that PFC engagement in aversive memory formation does not progress linearly as previously thought. Instead, it seems to be recruited at specific time windows after memory acquisition, which has implications for the treatment of post-traumatic stress disorders. ⋯ This effect was associated with a reduction in DA turnover in the PFC following retrieval 5days after training. We also observed that post-conditioning infusion of CBD reduced c-fos and zif-268 protein expression in the hippocampus, PFC, and thalamus. Our findings support that CBD interferes with contextual fear memory consolidation by reducing PFC influence on cortico-limbic circuits.