In models of chronic migraine, neuronal complexity is diminished in head-pain processing regions but restored through HDAC6 inhibition, which increases tubulin acetylation and cytoskeletal flexibility, and CGRP receptor blockade.
The direct interaction of R-type Ca2+ channel Cav2.3 and GABAB receptor auxiliary subunits in the active zone of medial habenula terminals scales synaptic strength independent of GABAB receptor activation.
Immunohistochemical labeling of antigens deep within mouse brain tissue sections was achieved without the need for lipid permeabilization, thereby preserving tissue ultrastructure and enabling correlative light and electron microscopy studies.
An analysis of recent literature advances novel hypotheses and suggests new experimental approaches in order to build an integrated understanding of prefrontal neural architecture and behavioral repertoires during development.
The synaptic structure in mouse V1 is explained by a synergy of homeostatic plasticity in incoming and outgoing synapses of inhibitory interneurons, establishing a stimulus-specific balance of excitation and inhibition.