Melanin concentrating hormone projections to the nucleus accumbens enhance the reward value of food consumption and do not induce feeding or REM sleep.

Regulation of food intake and energy balance is critical to survival. Hunger develops as a response to energy deficit and drives food-seeking and consumption. However, motivations to eat are varied in nature, and promoted by factors other than energy deficit.

Melanin concentrating hormone projections to the nucleus accumbens enhance the reward value of food consumption and do not induce feeding or REM sleep.

Regulation of food intake and energy balance is critical to survival. Hunger develops as a response to energy deficit and drives food-seeking and consumption. However, motivations to eat are varied in nature, and promoted by factors other than energy deficit.

Medial septum parvalbumin-expressing inhibitory neurons are impaired in a mouse model of Dravet Syndrome.

Dravet syndrome (DS) is a severe neurodevelopmental disorder caused by pathogenic variants in the gene, which encodes the voltage-gated sodium channel Na 1.1 α subunit. Experiments in animal models of DS - including the haploinsufficient mouse - have identified impaired excitability of interneurons in the hippocampus and neocortex; this is thought to underlie the treatment-resistant epilepsy that is a prominent feature of the DS phenotype.

Allele-Specific Editing of a Dominant SCN8A Epilepsy Variant Protects against Seizures and Lethality in a Murine Model.

Objective: Developmental and epileptic encephalopathies (DEEs) can result from dominant, gain of function variants of neuronal ion channels. More than 450 de novo missense variants of the sodium channel gene SCN8A have been identified in individuals with DEE.

Methods: We studied a mouse model carrying the patient Scn8a variant p.