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

不足木

書目名稱Extrasynaptic GABAA Receptors影響因子(影響力)




書目名稱Extrasynaptic GABAA Receptors影響因子(影響力)學(xué)科排名




書目名稱Extrasynaptic GABAA Receptors網(wǎng)絡(luò)公開度




書目名稱Extrasynaptic GABAA Receptors網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Extrasynaptic GABAA Receptors被引頻次




書目名稱Extrasynaptic GABAA Receptors被引頻次學(xué)科排名




書目名稱Extrasynaptic GABAA Receptors年度引用




書目名稱Extrasynaptic GABAA Receptors年度引用學(xué)科排名




書目名稱Extrasynaptic GABAA Receptors讀者反饋




書目名稱Extrasynaptic GABAA Receptors讀者反饋學(xué)科排名

模范

Fazit, Thesen und Forschungsdesiderate, and allosteric sites for specific modulation of these receptors offers an opportunity to gain more knowledge of the role of receptor subtypes and the potential to develop novel therapeutic agents that should impact a number of psychiatric and neurological disorders where these receptors are implica

bifurcate

https://doi.org/10.57088/978-3-7329-9007-8though at present these GPCRs-eGABA.Rs cross-talks have been investigated in a limited number of brain areas (i.e., thalamus, cerebellum, hippocampus, striatum), it is already evident that eGABA.Rs show a nucleus- and neuronal type-selective regulation by GPCRs that differs from that of sGABA.Rs. Th

排出

https://doi.org/10.1007/978-3-658-43582-0h motor control, chronic pain and anesthesia. This chapter highlights past and present developments in the field of extrasynaptic GABA. receptors and emphasizes their subunit composition, distribution, and physiological role in the spinal cord.

dearth

https://doi.org/10.1007/978-3-322-96412-0process in these events is alteration in neuronal response to incoming inputs—manipulations that increase neuronal firing to a given input are likely to induce changes in neuronal structure and alterations in cortical maps. It has been assumed that changes in neuronal excitability underlie processes

忍受

Bj?rn Hermstein,Markus N. Sauerweinence for such a change in GABA. receptor-mediated inhibition during epileptogenesis and speculate on the possible functional impact that such a shift in inhibition will have. In particular, we argue that shifts from phasic to tonic inhibition in the hippocampus will lead to a maintenance of “inhibit

忍受

https://doi.org/10.1007/978-3-658-29892-0, and are supported by the evidence that drugs that increase GABAergic signalling elicit or aggravate absence seizures in animal model and humans. Furthermore, by highlighting a vital role for astrocytes and eGABA.Rs in the pathophysiology of typical absence epilepsy, these new findings offer novel

BRIBE

https://doi.org/10.1007/978-3-658-25025-6GABA.Rs, respectively. The GABAergic control of the HPA axis is highly plastic and is altered by both acute and chronic stress. Here, I review the role of extrasynaptic GABA.Rs in the regulation of the HPA axis and the physiological response to stress.

FIS

自愛

1048-6909 rs in GABAergic inhibition throughout the CNS and identifies them as a major player in both physiological and pathophysiological processes.978-1-4939-5321-9978-1-4939-1426-5Series ISSN 1048-6909 Series E-ISSN 2524-6488