Topic: GluK1

Early life stress (ELS) is one of the key risk factors in the development of mental health disorders, strongly impacting the limbic system. Kainate receptors and GluK1 specifically have been previously shown to be affected, and potentially mediate some of the effects of ELS on GABAergic interneurons. Aims: To study the effects of the ELS on the circuitry of the ventral hippocampus (vHPC) and assess the potential of GluK1 as a tool for phenotype rescue.Methods: Limited bedding and nesting model of ELS was used in WT and PV-Cre mice and validated using standard behavioral tests in adults. Electr

Kainate receptors are ionotropic glutamate receptors, involved in modulation of synaptic transmission in developing and adult brain. Genetic disruption of all five kainate receptor subunits reduces cortico-striatal synaptic connectivity and leads to OCD-related pathological behavior. The aim of the project is to evaluate if the OCD-like pathology arises due to the deficit in the development of cortico-striatal projections due to the lack of the kainate receptor subunit 1 (GluK1). We characterized the expression of GluK1 during the development of the cortico-striatal circuitry using immunohisto

Research has shown that individuals with Down syndrome experience altered pain sensitivity, with varying results depending on the type of nociceptive stimulus. GRIK1, a gene coding for the GluK1 subunit of kainate receptors is triplicated in Down syndrome. This subunit is heavily expressed in Dorsal Root Ganglion neurons and has been implicated in modulating pain perception. To investigate this further, we have conducted experiments in the Ts2Cje mouse model of Down syndrome, comparing them to mice lacking Grik1. The results suggest that altered pain perception in Down syndrome is dependent on