GABAA Receptor Channels

Macdonald, Robert L.; Botzolakis, Emmanuel J.

doi:10.1016/b978-0-12-374373-2.00014-5

Cited by 103 publications

(144 citation statements)

References 290 publications

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“…3). Another GABAA receptor antagonist, bicuculline methiodide [8], was also effective in inhibiting the PrPres formation dose-dependently but at almost a thousand times higher dose than that of salicylidene salicylhydrazide (Fig. 3b).…”

Section: Effects Of Gabaa Receptor-related Compoundsmentioning

confidence: 99%

“…These subunits were chosen from the following facts. Most GABAA receptors contain two a subunits, two b subunits, and either one c subunit or one d subunit [8]. The a5 subunit is reportedly upregulated in the brain when prion is inoculated into the mice expressing anchorless PrP [17].…”

Section: Effects Of Gabrb1 Gene Silencingmentioning

confidence: 99%

“…4). The compounds tested in this study included an antagonist, picrotoxin [8], and agonists such as GABA [8], muscimol [8], pentobarbital [8], ethanol [20], and isoguvacine hydrochloride [21].…”

Section: Effects Of Gabaa Receptor-related Compoundsmentioning

confidence: 99%

“…We report here a possible linkage of c-aminobutyric acid A receptor b1 (gabrb1) with the formation of PrPres. In fact, gabrb1 is a subunit of c-aminobutyric acid type A (GABAA) receptors responsible for most of the fast inhibitory synaptic transmission in mammalian brain [8]. Belonging to the ligand-gated ion channels, they are formed by the pentameric assembly of homologous subunits.…”

Section: Introductionmentioning

confidence: 99%

“…Belonging to the ligand-gated ion channels, they are formed by the pentameric assembly of homologous subunits. Numerous GABAA receptor subunits have been identified (a1À6, b1À3, c1À3, d, p, e, and h), all of which are products of separate genes, and most GA-BAA receptors contain two a subunits, two b subunits and either one c subunit or one d subunit [8]. It has been well documented that GABAergic neurons are affected by prion infection [9][10][11][12][13][14][15], but it is not clear whether GABAA receptors are involved in PrPres formation.…”

Section: Introductionmentioning

confidence: 99%

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GABAA receptor subunit β1 is involved in the formation of protease‐resistant prion protein in prion‐infected neuroblastoma cells

et al. 2010

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Edited by Jesus AvilaKeywords: Prion GABAA receptor gabrb1 siRNA Antagonist a b s t r a c t c-Aminobutyric acid type A (GABAA) receptor b1 (gabrb1), a subunit of GABAA receptors involved in inhibitory effects on neurotransmission, was found to associate with the formation of proteaseresistant prion protein in prion-infected neuroblastoma cells. Silencing of gabrb1 gene expression significantly decreased the abnormal prion protein level but paradoxically increased the normal prion protein level. Treatment with a gabrb1-specific inhibitor, salicylidene salicylhydrazide, dose-dependently decreased the abnormal prion protein level, but silencing of other GABAA receptor subunits' gene expression and treatments with the receptor antagonists and agonists did not. Therefore, gabrb1 involvement in abnormal prion protein formation is independent of GABAA receptors.

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Section: Effects Of Gabaa Receptor-related Compoundsmentioning

confidence: 99%

Section: Effects Of Gabrb1 Gene Silencingmentioning

confidence: 99%

Section: Effects Of Gabaa Receptor-related Compoundsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

GABAA receptor subunit β1 is involved in the formation of protease‐resistant prion protein in prion‐infected neuroblastoma cells

et al. 2010

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GABRG1 variant as a potential novel cause of epileptic encephalopathy, hypotonia, and global developmental delay

Williams

Cooney

Segal

et al. 2022

American J of Med Genetics Pt A

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Epileptic encephalopathies (EEs) are severe brain disorders with excessive ictal (seizure) and interictal (electrographic epileptiform discharges) activity in developing brain which may result in progressive cognitive and neuropsychological deterioration. In contrast to regular epilepsy where the treatment goal is to prevent the seizure (ictal) recurrence, in patients with EE the goal is to treat both ictal as well as interictal activity to prevent further progression. With the introduction of genetic sequencing technologies over the past 20 years, there is growing recognition of the genetic basis of EE, with the majority due to monogenic causes. Monogenic etiologies of EE include pathogenic variants in the γ‐aminobutyric acid type A receptor (GABA‐A) encoding gene family. We present a 2‐year‐old patient with EE, hypotonia, and global developmental delays. Clinical trio exome sequencing showed a novel, de novo variant in GABRG1. GABRG1 encodes the γ1 subunit of the GABA‐A receptor. To date, there has not been an association of EE with pathogenic variants in GABRG1. This variant is predicted to be damaging to protein structure and function, and the patient's phenotype is similar to those with pathogenic variants in other members of the GABA‐A receptor encoding gene family.

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Tranexamic acid–associated seizures: Causes and treatment

Lecker

Wang

Whissell

et al. 2015

Annals of Neurology

208

158

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Antifibrinolytic drugs are routinely used worldwide to reduce the bleeding that results from a wide range of hemorrhagic conditions. The most commonly used antifibrinolytic drug, tranexamic acid, is associated with an increased incidence of postoperative seizures. The reported increase in the frequency of seizures is alarming, as these events are associated with adverse neurological outcomes, longer hospital stays, and increased in‐hospital mortality. However, many clinicians are unaware that tranexamic acid causes seizures. The goal of this review is to summarize the incidence, risk factors, and clinical features of these seizures. This review also highlights several clinical and preclinical studies that offer mechanistic insights into the potential causes of and treatments for tranexamic acid–associated seizures. This review will aid the medical community by increasing awareness about tranexamic acid–associated seizures and by translating scientific findings into therapeutic interventions for patients. ANN NEUROL 2016;79:18–26

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GABAA Receptor Channels

Cited by 103 publications

References 290 publications

GABAA receptor subunit β1 is involved in the formation of protease‐resistant prion protein in prion‐infected neuroblastoma cells

GABAA receptor subunit β1 is involved in the formation of protease‐resistant prion protein in prion‐infected neuroblastoma cells

GABRG1 variant as a potential novel cause of epileptic encephalopathy, hypotonia, and global developmental delay

Tranexamic acid–associated seizures: Causes and treatment

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