Multidimensional Genetic Analysis of Repeated Seizures in the Hybrid Mouse Diversity Panel Reveals a Novel Epileptogenesis Susceptibility Locus.

Epilepsy has many causes and comorbidities affecting as many as 4% of people in their lifetime. Both idiopathic and symptomatic epilepsies are highly heritable, but genetic factors are difficult to characterize among humans due to complex disease etiologies. Rodent genetic studies have been critical to the discovery of seizure susceptibility loci, including mutations identified in both mouse and human cohorts.

Experimental evaluation and computational modeling of tissue damage from low-flow push-pull perfusion sampling in vivo.

Background: Neurochemical monitoring via sampling probes is valuable for deciphering neurotransmission in vivo. Microdialysis is commonly used; however, the spatial resolution is poor.

New Method: Recently push-pull perfusion at low flow rates (50nL/min) has been proposed as a method for in vivo sampling from the central nervous system.

Prior laparotomy or corticosterone potentiates lipopolysaccharide-induced fever and sickness behaviors.

Stimulating sensitized immune cells with a subsequent immune challenge results in potentiated pro-inflammatory responses translating into exacerbated sickness responses (i.e. fever, pain and lethargy).

Pain intensity and duration can be enhanced by prior challenge: initial evidence suggestive of a role of microglial priming.

Unlabelled: Activation of spinal microglia and consequent release of proinflammatory mediators facilitate pain. Under certain conditions, responses of activated microglia can become enhanced. Enhanced microglial production of proinflammatory products may result from priming (sensitization), similar to macrophage priming.