![]() 2013), indicating that Nlgn4 may contribute to information processing and function in the somatosensory barrel field (S1BF). 2015).įurther, genetic ablation of Nlgn4 has been reported to attenuate both glutamatergic and GABAergic synaptic transmission in L2/3 of mouse primary somatosensory (S1) cortex ( Delattre et al. However, loss of Nlgn4 causes hippocampal deficits at GABAergic synapses, suggesting a prominent function in maturation of inhibition ( Hammer et al. Currently available antibodies demonstrated a weak staining in cerebral cortex, hippocampus and most other forebrain areas, but all antibodies failed to detect a large proportion of the forebrain Nlgn4 pool. In retina Nlgn4 is involved in the postsynaptic clustering of glycine receptors, consequently glycinergic transmission is weakened in the Nlgn4-KO retina ( Hoon et al. In the retina, spinal cord, brainstem, thalamus, and globus pallidus, Nlgn4 is predominantly present at inhibitory synapses. The question whether Nlgn4 is localized in a specific subpopulation of synapses remains partly unresolved. 2004), and Neuroligin-3 at both excitatory and inhibitory synapses ( Budreck and Scheiffele 2007). 1999), Neuroligin-2 at GABAergic synapses ( Varoqueaux et al. Neuroligin-1 is localized at glutamatergic synapses ( Song et al. 2014).įour neuroligin isoforms are expressed at specific subpopulations of synapses. Genetic knockout (KO) of Nlgn4, a homologue of human Nlgn4X, in mice results in autism-like behavioral changes, including reduced social interaction and stereotypies, indicating Nlgn4-KO as a valid model of ASD ( El-Kordi et al. Human loss-of-function mutations of Neroligin-4X are among the most frequent monogenic causes of autism spectrum disorders (ASD) ( Jamain et al. 2003, 2008), which are expressed throughout the central nervous system (CNS) and play an important role in synaptic organization and function ( Varoqueaux et al. Neuroligin-4 (Nlgn4) is a member of the neuroligin family of postsynaptic adhesion proteins ( Bolliger et al. We conclude that Nlgn4-KO does not influence the incoming whisker-mediated sensory information to the barrel cortex, but modifies intracortical information processing.Īdhesion proteins, autistic spectrum disorders, short-termed plasticity, single-whisker stimulation Introduction However, Nlgn4 deficit strongly suppresses glutamatergic activity, shifting the excitation–inhibition balance to inhibition. Although Nlgn4-KO did not affect evoked EPSCs in layer 4 (L4) spiny stellate cells in acute thalamocortical slices elicited by electrical stimulation of thalamocortical inputs, it caused a lower frequency of both miniature (m) IPSCs and mEPSCs, and a decrease in the number of readily releasable vesicles at GABAergic and glutamatergic connections, weakening both excitatory and inhibitory transmission. Nlgn4-KO did not affect single-whisker-induced local field potentials, but suppressed the late evoked multiunit activity in vivo. Using Nlgn4-KO mice, we found that Nlgn4-KO increases the power in the alpha frequency band of spontaneous network activity in the barrel cortex under urethane anesthesia in vivo. The complex profile of cellular and circuit changes that are caused by Nlgn4-KO is still only partly understood. In mouse, Nlgn4 knockout (KO) perturbs GABAergic synaptic transmission and oscillatory activity in hippocampus, and causes social interaction deficits. ![]() ![]() Mutations in human NLGN4 are among the causes of autism spectrum disorders. Neuroligin-4 (Nlgn4) is a cell adhesion protein that regulates synapse organization and function.
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