AB5561

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Showing 1-14 of 14 results for "AB5561" within Papers

AT1a influences GABAA-mediated inhibition through regulation of KCC2 expression.

George E Farmer et al.

American journal of physiology. Regulatory, integrative and comparative physiology, 315(5), R972-R982 (2018-08-30)

The median preoptic nucleus (MnPO) is an integrative site involved in body fluid homeostasis, cardiovascular control, thermoregulation, and sleep homeostasis. Angiotensin II (ANG II), a neuropeptide shown to have excitatory effects on MnPO neurons, is of particular interest with regard

Genetic Deletion of GABAA Receptors Reveals Distinct Requirements of Neurotransmitter Receptors for GABAergic and Glutamatergic Synapse Development.

Jingjing Duan et al.

Frontiers in cellular neuroscience, 13, 217-217 (2019-06-25)

In the adult brain GABAA receptors (GABAARs) mediate the majority of synaptic inhibition that provides inhibitory balance to excitatory drive and controls neuronal output. In the immature brain GABAAR signaling is critical for neuronal development. However, the cell-autonomous role of

Altered cortical GABAA receptor composition, physiology, and endocytosis in a mouse model of a human genetic absence epilepsy syndrome.

Zhou, C; Huang, Z; Ding, L; Deel, ME; Arain, FM; Murray, CR; Patel, RS; Flanagan, CD; Gallagher, MJ

The Journal of Biological Chemistry null

Dravet syndrome-associated mutations in GABRA1, GABRB2 and GABRG2 define the genetic landscape of defects of GABAA receptors.

Ciria C Hernandez et al.

Brain communications, 3(2), fcab033-fcab033 (2021-06-08)

Dravet syndrome is a rare, catastrophic epileptic encephalopathy that begins in the first year of life, usually with febrile or afebrile hemiclonic or generalized tonic-clonic seizures followed by status epilepticus. De novo variants in genes that mediate synaptic transmission such

GABA(A) receptor alpha1 subunit mutation A322D associated with autosomal dominant juvenile myoclonic epilepsy reduces the expression and alters the composition of wild type GABA(A) receptors.

Ding, L; Feng, HJ; Macdonald, RL; Botzolakis, EJ; Hu, N; Gallagher, MJ

The Journal of Biological Chemistry null

GABAA and GABAB receptor dysregulation in superior frontal cortex of subjects with schizophrenia and bipolar disorder.

S Hossein Fatemi et al.

Synapse (New York, N.Y.), 71(7) (2017-03-21)

Schizophrenia and bipolar disorder are complex psychiatric disorders that affect millions of people worldwide. Evidence from gene association and postmortem studies has identified abnormalities of the gamma-aminobutyric acid (GABA) signaling system in both disorders. Abnormal GABAergic signaling and transmission could

Differential molecular and behavioural alterations in mouse models of GABRG2 haploinsufficiency versus dominant negative mutations associated with human epilepsy.

Timothy A Warner et al.

Human molecular genetics, 25(15), 3192-3207 (2016-06-25)

Genetic epilepsy is a common disorder with phenotypic variation, but the basis for the variation is unknown. Comparing the molecular pathophysiology of mutations in the same epilepsy gene may provide mechanistic insights into the phenotypic heterogeneity. GABRG2 is an established

Loss of KCC2 in GABAergic Neurons Causes Seizures and an Imbalance of Cortical Interneurons.

Kirill Zavalin et al.

Frontiers in molecular neuroscience, 15, 826427-826427 (2022-04-05)

K-Cl transporter KCC2 is an important regulator of neuronal development and neuronal function at maturity. Through its canonical transporter role, KCC2 maintains inhibitory responses mediated by γ-aminobutyric acid (GABA) type A receptors. During development, late onset of KCC2 transporter activity

Differential expression of gamma-aminobutyric acid--a receptor subunits in rat dorsal and ventral hippocampus.

Evangelos Sotiriou et al.

Journal of neuroscience research, 82(5), 690-700 (2005-11-08)

Recent data demonstrate weaker gamma-aminobutyric acid (GABA)-ergic inhibition in ventral (VH) compared with dorsal (DH) hippocampus. Therefore, we examined possible differences regarding the GABAA receptors between VH and DH as follows: 1) the expression of the GABAA receptor subunits (alpha1/2/4/5

Expression of GABAA α2-, β1- and ε-receptors are altered significantly in the lateral cerebellum of subjects with schizophrenia, major depression and bipolar disorder.

S H Fatemi et al.

Translational psychiatry, 3, e303-e303 (2013-09-12)

There is abundant evidence that dysfunction of the γ-aminobutyric acid (GABA)ergic signaling system is implicated in the pathology of schizophrenia and mood disorders. Less is known about the alterations in protein expression of GABA receptor subunits in brains of subjects

Altered localization of the δ subunit of the GABAA receptor in the thalamus of α4 subunit knockout mice.

Zechun Peng et al.

Neurochemical research, 39(6), 1104-1117 (2013-12-20)

The α4 subunit of the GABAA receptor (GABAAR) is highly expressed in the thalamus where receptors containing the α4 and δ subunits are major mediators of tonic inhibition. The α4 subunit also exhibits considerable plasticity in a number of physiological

Amount of fear extinction changes its underlying mechanisms.

Bobae An et al.

eLife, 6 (2017-07-04)

There has been a longstanding debate on whether original fear memory is inhibited or erased after extinction. One possibility that reconciles this uncertainty is that the inhibition and erasure mechanisms are engaged in different phases (early or late) of extinction.

Modulating Endoplasmic Reticulum Chaperones and Mutant Protein Degradation in GABRG2(Q390X) Associated with Genetic Epilepsy with Febrile Seizures Plus and Dravet Syndrome.

Sarah Poliquin et al.

International journal of molecular sciences, 25(9) (2024-05-11)

A significant number of patients with genetic epilepsy do not obtain seizure freedom, despite developments in new antiseizure drugs, suggesting a need for novel therapeutic approaches. Many genetic epilepsies are associated with misfolded mutant proteins, including GABRG2(Q390X)-associated Dravet syndrome, which

Interneuron- and GABA(A) receptor-specific inhibitory synaptic plasticity in cerebellar Purkinje cells.

Qionger He et al.

Nature communications, 6, 7364-7364 (2015-07-17)

Inhibitory synaptic plasticity is important for shaping both neuronal excitability and network activity. Here we investigate the input and GABA(A) receptor subunit specificity of inhibitory synaptic plasticity by studying cerebellar interneuron-Purkinje cell (PC) synapses. Depolarizing PCs initiated a long-lasting increase

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