Nature neuroscience最新文献

The Ca²⁺/calmodulin (CaM)-dependent protein kinase II (CaMKII) plays a fundamental role in learning and possibly also in memory. However, current mechanistic models require fundamental revision. CaMKII autophosphorylation at Thr286 (pThr286) does not provide the molecular basis for long-term memory, as long believed. Instead, pThr286 mediates the signal processing required for induction of several distinct forms of synaptic plasticity, including Hebbian long-term potentiation and depression and non-Hebbian behavioral timescale synaptic plasticity. We discuss (i) the molecular computations by which CaMKII supports these diverse plasticity mechanisms, (ii) alternative CaMKII mechanisms that may contribute to the maintenance phase of LTP and (iii) the relationship of these mechanisms to behavioral learning and memory.

Perceiving substrate-borne vibrations is a fundamental component of tactile perception. How location (somatotopy) and frequency tuning (tonotopy) of vibrations are integratively processed is poorly understood. Here we addressed this question using in vivo electrophysiology and two-photon calcium imaging along the dorsal column–medial lemniscal pathway. We found that both frequency and location are organized into structured maps in the dorsal column nuclei (DCN). Both maps are intimately related at the fine spatial scale, with parallel map gradients that are consistent across the depth of the DCN and preserved along the ascending pathway. The tonotopic map only partially reflects the distribution of end organs in the skin and deep tissue; instead, the emergence of the fine-scale tonotopy is due to the selective dendritic sampling from axonal afferents, already at the first synaptic relay. We conclude that DCN neural circuits are key to the emergence of these two fine-scale topographical organizations in early somatosensory pathways.

Seizures are made up of the coordinated activity of networks of neurons, suggesting that control of neurons in the pathologic circuits of epilepsy could allow for control of the disease. Optogenetics has been effective at stopping seizure-like activity in non-human disease models by increasing inhibitory tone or decreasing excitation, although this effect has not been shown in human brain tissue. Many of the genetic means for achieving channelrhodopsin expression in non-human models are not possible in humans, and vector-mediated methods are susceptible to species-specific tropism that may affect translational potential. Here we demonstrate adeno-associated virus–mediated, optogenetic reductions in network firing rates of human hippocampal slices recorded on high-density microelectrode arrays under several hyperactivity-provoking conditions. This platform can serve to bridge the gap between human and animal studies by exploring genetic interventions on network activity in human brain tissue.

Nasal dermoid cyst is a rare benign lesion. The mainstay of treatment for a nasal dermoid cyst is surgical excision, which aims to remove the cyst and associated structures to prevent recurrence. We report a case of a 30-year-old man with nasal dermoid cyst, without intranasal or intracranial extension. The patient underwent open rhinoplasty technique for dermoid cyst excision. He had an uneventful postoperative recovery and was discharged well. The cyst and associated structure were successfully removed. There was no evidence of recurrence and complications postoperatively after 2 years of follow-up.