A recent study by Hadler and colleagues uncovered a novel form of plasticity of gamma oscillations in an ex vivo hippocampal slice preparation which they term 'gamma potentiation'. We discuss the potential cellular mechanisms of this form of plasticity and its functional and translational implications.
In a recent study, Clancy et al. elucidate a connection between activity patterns of the hippocampus (HC) and the broader functional connectivity networks associated with trauma-related intrusive memories (TR-IMs). This neurophenomenological methodology situates the HC within a larger neural framework and provides a nuanced exploration of the neurobiological underpinnings of distinct characteristics of TR-IMs.
Exercise training is an important strategy to counteract cognitive and brain health decline during aging. Evidence from systematic reviews and meta-analyses supports the notion of beneficial effects of exercise in cognitively unimpaired and impaired older individuals. However, the effects are often modest, and likely influenced by moderators such as exercise training parameters, sample characteristics, outcome assessments, and control conditions. Here, we discuss evidence on the impact of exercise on cognitive and brain health outcomes in healthy aging and in individuals with or at risk for cognitive impairment and neurodegeneration. We also review neuroplastic adaptations in response to exercise and their potential neurobiological mechanisms. We conclude by highlighting goals for future studies, including addressing unexplored neurobiological mechanisms and the inclusion of under-represented populations.
In a recent study, Ziak et al. employed precise sparse labeling and spatiotemporally controlled genetic manipulations to uncover novel regulators of axon branching of layer 2/3 mouse callosal projection neurons. The authors elucidated a cell-autonomous signaling pathway wherein glycogen synthase kinase 3β (GSK3β) phosphorylation of microtubule-associated protein 1B (MAP1B) restricts interstitial axon branching by modulating microtubule (MT) tyrosination status.
The descending-pain modulating circuit controls the experience of pain by modulating transmission of sensory signals through the dorsal horn. This circuit’s key output node, the rostral ventromedial medulla (RVM), integrates ‘top-down’ and ‘bottom-up’ inputs that regulate functionally defined RVM cell types, ‘OFF-cells’ and ‘ON-cells’, which respectively suppress or facilitate pain-related sensory processing. While recent advances have sought molecular definition of RVM cell types, conflicting behavioral findings highlight challenges involved in aligning functional and molecularly defined types. This review summarizes current understanding, derived primarily from rodent studies but with corroborating evidence from human imaging, of the role of RVM populations in pain modulation and persistent pain states and explores recent advances outlining inputs to, and outputs from, RVM pain-modulating neurons.
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