Topic: GABAergic neurotransmission

Gut microbiota perturbation and motor dysfunction have been reported in steatosis patients. Rats with mild liver damage (MLD) also show motor dysfunction mediated by neuroinflammation and altered GABAergic neurotransmission in the cerebellum. The extracellular vesicles from mesenchymal stem cells (MSC-EVs) have emerged as a promising therapeutic proxy whose molecular basis rely partly upon TGFbeta action. Therefore, this study aimed to assess if MSC-EVs improve motor dysfunction in rats with MLD and analyze underlying mechanisms, including the role of EVs, TGFbeta, neuroinflammation, and gut m

Parkinson’s disease (PD) affects more than 6 million people worldwide, and will affect more in coming decades. There are no drugs available for PD that alter progression of disease. Current symptomatic treatments provide limited relief and have side effects. Enhanced GABAergic neurotransmission contributes to Parkinson’s disease (PD) pathogenesis and to some motor and non-motor symptoms. In animal models, GABA levels are increased in substantia nigra pars compacta, leading to reduced expression of tyrosine hydroxylase (TH) in neurons which contributes to the behavioural deficits. The aim was t

Neuronal circuits universally recognize novel stimuli, but unpredicted features in a stimulus amplify its importance, shaping attentive reactions. Habituation, the gradual reduction of responses to repetitive stimuli, and its counterpart, dishabituation, the reversal of habituated responses upon exposure to novel stimuli, are fundamental processes that organisms employ to navigate their environment efficiently. Although mechanisms driving Habituation/Dishabituation remain partly understood, the communication within neuronal circuits, which ostensibly underlies these choices, is an emerging fie

GABAergic neurotransmission generates two types of inhibitions: the transient activation of synaptic GABA receptors, or phasic inhibition, which elicits inhibitory postsynaptic currents, and the activation of extrasynaptic GABA receptors by “ambient” GABA which causes a persistent, “tonic”, inhibition that finely tunes cellular excitability of target neurons. Change in GABA synaptic efficacy is a crucial mechanism that underlies experience-dependent modifications of brain function. Several forms of GABA synaptic plasticity require retrograde signaling by endocannabinoids (eCB) through the acti

GABAergic neurotransmission is enhanced in the cerebellum of hyperammonemic rats, an animal model of hepatic encephalopathy, and this induces motor incoordination. There is an interplay between neuroinflammation and GABAergic neurotransmission, but the underlying mechanisms remain unclear. This work aimed to unveil the molecular mechanisms by which GABAergic neurotransmission modulates neuroinflammation in the cerebellum.Ex-vivo experiments were performed using cerebellar slices from control and hyperammonemic rats treated or not with bicuculline. We analyzed by immunohistochemistry microglia