Alterations to brain network communication leading to a progressive loss in descending inhibitory modulation of the spinal cord is a key determinate of pain state development following peripheral nerve injury.
Disruption of the disease-associated synaptic adhesion molecule Neurexin1a in cortical excitatory neurons perturbs decision making and disrupts value-associated neural activity in downstream striatal circuits.
Compared to a sensory thalamocortical circuit, the mediodorsal thalamus preferentially innervates prefrontal cortical interneurons, and enhancing excitability of this thalamic structure drives prefrontal activity patterns that are dominated by inhibition.
Single cell RNA–sequencing and neuroanatomical methods reveal unexpected molecular diversity and highly segregated spatial organization of neuronal cell types within the mouse ventral posterior hypothalamus, including the mammillary nuclei.
M2 cortex-dorsolateral striatum circuit is functionally altered in Huntington's disease and, by boosting its activity, we reverse symptoms at behavioral, physiological, and morphological level in symptomatic mice.