Titlebook: Extrasynaptic GABAA Receptors; Adam C. Errington,Giuseppe Di Giovanni,Vincenzo Cr Book 2014 Springer Science+Business Media, LLC 2014 GABA

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https://doi.org/10.57088/978-3-7329-9007-8ely tuned by other neurotransmitters and endogenous ligands. The regulation of synaptic GABA.Rs (sGABA.Rs) by G protein-coupled receptors (GPCRs) has been well characterized and is known to occur either through the conventional activation of second-messenger signalling cascades by G proteins or dire

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https://doi.org/10.1007/978-3-658-43582-0 on ligand-gated chloride-permeable channels termed GABA. receptors (GABA.R). The activation of these receptors produces two different types of inhibition: fast and tonic, mediated by synaptic and extrasynaptic GABA.Rs, respectively. The molecular conformation of the extrasynaptic GABA. receptors an

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Bj?rn Hermstein,Markus N. Sauerwein, head injury or prolonged seizures (status epilepticus). The time from the insult to the development of seizures is termed the epileptogenic period during which there are changes in connectivity, neurotransmission and neuronal excitability..Epileptogenesis has conventionally been viewed as being as

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ANTE

https://doi.org/10.1007/978-3-658-25025-6y GABAergic inhibition. Parvocellular neurosecretory neurons located in the paraventricular nucleus (PVN) of the hypothalamus which release corticotropin-releasing hormone (CRH) govern the output of the HPA axis. CRH neurons are innervated by a high density of GABAergic terminals and are regulated b

Flatter

Diversit?t in der Entwicklung des Lesensse effects of reduced inhibitory function of this receptor system range from mood disorders and anxiety to epilepsy. Converging lines of evidence support the hypothesis that alterations in cellular excitability are a common mechanism underlying neurodevelopmental disorders including those in the aut

COM

https://doi.org/10.1007/978-1-4939-1426-5GABAA tonic inhibition; Parkinson‘s disease; alcohol addiction; epilepsy

ECG769

Anticonvulsants