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Local brain functional activity reductions in bvFTD follow the distribution of serotonergic, GABAergic, and norepinephrinergic neurotransmitter systems, indicating a selective vulnerability and providing novel insights into the underlying disease mechanisms.

In the SOD1^G93A mouse model of amyotrophic lateral sclerosis (ALS), expression of transmembrane signaling molecule ephrinB2 in spinal cord astrocytes contributes to motor neuron damage and loss of diaphragm function.

Δ⁹-Tetrahydrocannabinol (THC)-E-gel enables robust preclinical study of voluntary THC consumption in mice, revealing sex-dependent psychotomimetic effects that are valuable for understanding cannabimimetic responses.

Brain activity is modelled as a function of stimuli that evolve continuously in time, in experimental designs without repeated trials.

Analyses reveal that multiple NTS neuron types act cumulatively in the suppression of feeding, that the abrogation of food intake by multiple non-aversive populations fails to promote aversive responses, and that there exist additional NTS populations that modulate food intake.

Noradrenergic receptors can control the spontaneous electrical firing of neurons by inhibiting a Na⁺ channel known as NALCN using a pathway shared by metabotropic GABA receptors.

Silencing long-descending propriospinal neurons that connect C6 to L2 disrupts right-left alternation of both the forelimbs and hindlimbs in the intact animal, but leads to improved stepping after a mild-moderate thoracic contusion spinal cord injury.

MRI is sensitive to the increase in axonal caliber due to pathology and was used to detect widespread increase in the average axonal caliber in multiple sclerosis brains with short disease duration only.