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1 eroid binding sites in the human alpha1beta3 GABAA receptor.
2 ines are secreted peptides that modulate the GABAA receptor.
3 g domains through which propofol acts on the GABAA receptor.
4 d by clonazepam, a positive modulator of the GABAA receptor.
5 y via a pentameric chloride ion channel, the GABAA receptor.
6 ibuting to neurosteroid interaction with the GABAA receptors.
7 such as hetero-oligomeric alpha1beta2gamma2 GABAA receptors.
8 oactive steroids potentiate a wider-range of GABAA receptors.
9 els, in particular, by enhancing activity of GABAA receptors.
10 ts, abolished by pharmacological blockade of GABAA receptors.
11 r type 1, oxytocin, ionotropic glutamate and GABAA receptors.
12 modulator of both synaptic and extrasynaptic GABAA receptors.
13 synaptic trapping of glycine (GlyR) but not GABAA receptors.
14 ical structure acting as a PAM at particular GABAA receptors.
15 uld be compensated for by an upregulation of GABAA receptors.
16 dation process remains poorly understood for GABAA receptors.
17 ric activation of synaptic and extrasynaptic GABAA receptors.
18 ines the hyperpolarizing action of GABA) and GABAA receptors.
19 etic with putative actions on the inhibitory GABAA receptors.
20 the effect was shown to be mediated via the GABA(A) receptor.
21 aria and a potent orthosteric agonist of the GABA(A) receptor.
22 tamate transporters EAAT1 and EAAT2, and the GABA(A) receptor.
23 ibits the human alpha (2) beta (3) gamma (2) GABA(A) receptor.
24 to the modes of action of these drugs on the GABA(A) receptor.
25 ty for brain gamma-aminobutyric acid type A (GABAA) receptors.
26 reversal potential of inhibitory glycine and GABA(A) receptors.
27 ious stimulation of the colon, primarily via GABA(A) receptors.
28 lular stores are necessary for modulation of GABA(A) receptors.
29 ch has focused on studying alpha5-containing GABA(A) receptors.
30 atory AMPA receptors (AMPARs) and inhibitory GABA(A) receptors.
31 property associated with outward rectifying GABA(A) receptors.
32 o the activity-induced dispersal of synaptic GABA(A) receptors.
33 protein (GABARAP) to stabilize cell surface GABA(A) receptors.
34 pha5beta3gamma2 over other alphaxbeta3gamma2 GABA(A) receptors.
35 ogical and pharmacological properties of the GABA(A) receptors.
36 tonic GABA current mediated by extrasynaptic GABA(A) receptors.
37 onses of the gamma-aminobutyric acid type A (GABA(A)) receptor.
38 mprising the gamma-aminobutyric acid type A (GABA(A)) receptor.
40 lcohol as a positive allosteric modulator of GABA(A) receptors, a decrease in dopamine function, and
43 Excitation of GABA neurons was mediated by GABAA receptor activation and involved stress-induced fu
45 pathomimetics, pancreatic lipase inhibitors, GABAA receptor activators, a serotonin 2C receptor agoni
46 was to provide a model-based description of GABA(A) receptor activity under steady-state conditions
47 ats by locally concentrating and releasing a GABA(A) receptor agonist from ultrasound-controlled carr
48 ute treatment with a peripherally restricted GABA(A) receptor agonist that acts directly on mechanose
49 n rats by microinjection of small amounts of GABAA-receptor agonists into an upper brainstem region n
51 tional relationship between delta and gamma2 GABA(A) receptors akin to that of slow NMDA and fast AMP
54 he hypotheses, indicating that loop C of the GABA(A) receptor alpha-subunit is the dominant molecular
55 These findings implicate movement of the GABAA receptor alpha1 subunit's beta1 strand during agon
57 -1 (~20%) levels, as well as TLR4 binding to GABA(A) receptor alpha2 subunits (~60%) and MyD88 (~40%)
58 associated with increased expression of the GABA(A) receptor alpha2 subunits by 93%, and these chang
60 ry approaches, we compared effects of mutant GABAA receptor alpha5 and alpha1 subunits on the propert
62 g to (i) the orthosteric binding site of the GABA(A) receptor and (ii) the high-affinity GHB binding
64 ) affinity selectivity for alpha5-containing GABA(A) receptors and show atom-level structure predicti
66 the postsynaptic clustering of gephyrin and GABAA receptors and the strength of inhibitory, but not
67 antibodies against NMDAR, LGI1, CASPR2, the GABAA receptor, and the AMPA receptor using live cell-ba
69 the NMDA receptor antagonist MK-801 and the GABA(A) receptor antagonist bicuculline methiodide while
70 tructurally dense (1.64 mcbits/ angstrom(3)) GABA(A) receptor antagonist bilobalide, intermediates en
72 intra-BLA administration of a low dose of a GABA(A) receptor antagonist, but not an NMDA/AMPA/kainat
73 Gabazine, a gamma-aminobutyric acid type A (GABA(A)) receptor antagonist, has previously been report
80 der both physiologic and clinical conditions GABA(A) receptors are exposed to multiple agonists, incl
85 y and arrangement of synaptic alphabetagamma GABAA receptors are generally accepted as 2alpha:2beta:1
87 ents mediated by high-affinity extrasynaptic GABAA receptors, are increasingly recognized as importan
88 itive modulators of chloride (Cl-) permeable GABAA receptors, are indicated as first-line treatment,
90 nd its encoded beta3 subunit is critical for GABAA receptor assembly and trafficking as well as stem
91 eurons, where it interacts directly with the GABA(A) receptor-associated protein (GABARAP) to stabili
92 teracting at the NCA site in the pore of the GABA(A) receptor at a location that is overlapping but n
93 ficient per se, for efficient recruitment of GABA(A) receptors at GABAergic synapses in C. elegans Th
95 nted gamma2 subunits from incorporating into GABAA receptors at synapses, although by different cellu
97 for three de novo missense mutations in the GABAA receptor beta3 subunit gene (GABRB3) identified in
98 , 5-7, displayed moderate GAT activities and GABA(A) receptor binding affinities in the mid-nanomolar
99 s with the high-affinity GHB and orthosteric GABA(A) receptor binding sites differently and that dist
101 ecular mechanisms that might link defects in GABAA receptor biophysics and biogenesis to patients wit
102 In long-term bioluminescence recordings, GABAA receptor blockade desynchronized the Fbxl3(+/+) bu
103 were sustained by GABAergic signaling, as a GABA(A) receptor blocker stopped them in 2 of 3 slices.
104 tagonist) or by (2) bicuculline (a preferent GABA(A) receptor blocker), suggesting a GABAergic activa
105 esent cryo-electron microscopy structures of GABA(A) receptors bound to intravenous anaesthetics, ben
106 receptor, oxytocin, ionotropic glutamate or GABAA receptors but instead involves a close relationshi
109 dy, we analyzed modulation of the human rho1 GABA(A) receptor by several neurosteroids, individually
110 been used to describe the activation of the GABA(A) receptor by the transmitter, GABA, and drugs tha
111 on of the GABA signaling and blockage of the GABAA receptor by the specific inhibitors both significa
112 the EC50 for activation of the GABA type A (GABAA) receptor by the transmitter GABA and basal activi
113 nding isotherms from recombinant alpha1beta3 GABA(A) receptors can be qualitatively predicted using e
114 In nonrhythmic conditions, antagonizing GABA(A) receptors can initiate this synchronization whil
116 be related to the extent of the reduction of GABAA receptor channel function and the differential dom
117 apses primarily on dendritic spines, whereas GABAA receptors cluster at inhibitory synapses mainly on
118 se gamma2 subunits are critical for synaptic GABAA receptor clustering, this provides an important cl
119 onal gray matter increases were explained by GABAA receptor concentration in addition to T1 relaxatio
120 rogate marker of water content, but not with GABAA receptor concentration, a surrogate of neuronal in
121 ontent, and not to any substantial degree by GABAA receptor concentration, an indirect marker of neur
122 ay matter increases were partly explained by GABAA receptor concentration, indicating some form of ne
123 e activity is associated with a reduction in GABAA receptor conductance and Cl- extrusion capability.
125 with wild-type alpha1beta2gamma2L receptors, GABAA receptors containing a mutant gamma2 subunit had r
128 a, DCUK-OEt acted primarily on extrasynaptic GABAA receptors containing the alpha1 subunit and genera
129 g mechanism involves membrane-shunting tonic GABA(A) receptor current; it does not have to rely on I(
130 e tonically active and enhance extrasynaptic GABA(A) receptor currents in cerebellar granule cells.
131 uding extrasynaptic delta subunit-containing GABA(A) receptors (delta-GABA(A)Rs) that mediate tonic i
132 ions of interest, we found no differences in GABA(A) receptor densities between ASD and TD groups.
134 eous acquisitions of GABA concentrations and GABA(A) receptor densities can identify objective molecu
135 Low-threshold cutaneous afferents evoke a GABA(A)-receptor-dependent form of PSI that inhibits sim
137 ervation is particularly interesting because GABAA receptor disturbances, leading to altered behavior
138 quantify and predict the loss of activatable GABA(A) receptors due to desensitization in the presence
139 rrecting the disrupted driving force through GABA(A) receptors during the CP in cortical neurons rest
144 results suggest a complex interplay between GABA(A) receptor expression by spinally projecting C1 an
145 and D1 receptor activation result in minimal GABAA receptor expression and activity and greatly dimin
146 steric modulator of gamma-aminobutyric acid (GABAA) receptors, for the treatment of post-partum depre
147 e brain during CO2 compensation could change GABAA receptor function and account for the behavioural
148 ssing, impaired synaptic clustering, reduced GABAA receptor function and decreased GABA binding poten
149 play a role in ethanol-induced sedation and GABAA receptor function, but does not regulate excessive
153 vity of interneurons and the distribution of GABA(A) receptor (GABA(A) R) subtypes, distinguished by
154 steroid-binding sites in the alpha(1)beta(3) GABA(A) receptor (GABA(A)R) contributes to neurosteroid
155 ering of seizures at room temperature by the GABA(A) receptor (GABA(A)R) positive allosteric modulato
156 ndently, of retinal environment age on their GABA(A) receptor (GABA(A)R) responses, elicited by musci
157 4 and 11 during pharmacological blockade of GABA(A) receptors (GABA(A) Rs) and/or glycine receptors
158 tameric ligand-gated ion channels, including GABA(A) receptors (GABA(A)R) and nicotinic acetylcholine
164 Oligodendrocytes (OLs) express functional GABA(A) receptors (GABA(A)Rs) that are activated by GABA
165 ent positive allosteric modulators (PAMs) of GABA(A) receptors (GABA(A)Rs) with in vivo anesthetic, a
166 n in the brain is mediated by GABA acting on GABA(A) receptors (GABA(A)Rs), which provides inhibitory
168 ctional modulators of heterologous expressed GABAA receptor (GABAAR) isoforms (synaptic alpha1beta3ga
171 we report a mechanism of KCC2 regulation by GABAA receptor (GABAAR)-mediated transmission in mature
172 experience depolarization upon activation of GABAA receptors (GABAAR) because their intracellular chl
173 ition in the brain is mediated by ionotropic GABAA receptors (GABAARs) and metabotropic GABAB recepto
174 n the brain is mediated mostly by ionotropic GABAA receptors (GABAARs), but their essential component
176 mpaired postsynaptic clustering of wild-type GABAA receptor gamma2 subunits and prevented gamma2 subu
177 s, the closed and desensitized states of the GABA(A) receptor gating cycle, and the basis for alloste
179 A (gamma-aminobutyric acid) to extrasynaptic GABA(A) receptors generates tonic inhibition that acts a
180 fect is mediated by the loss of postsynaptic GABA(A) receptors, gephyrin, and neuroligin 2 and does n
183 e accurate structural models for heteromeric GABA(A) receptors have been hampered by the use of engin
185 the blockade of both glutamatergic NMDA and GABA(A) receptors improved neuronal selectivity of delay
186 ich the full-length human alpha1beta3gamma2L GABA(A) receptor in lipid nanodiscs is bound to the chan
187 he central nervous system, alpha5-containing GABA(A) receptors in airway smooth muscles are considere
189 tions, a major risk factor for CVD, increase GABA(A) receptors in RVLM, including its rostral extensi
190 as been used to evaluate the distribution of GABA(A) receptors in the brain, and studies of modulatio
193 duces its anesthetic effect, largely via the GABAA receptor in the CNS, and also reduces the N-formyl
194 nant alpha5beta3gamma2 and alpha1beta3gamma2 GABAA receptors in both neuronal and non-neuronal cells
195 s the function of synaptic and extrasynaptic GABAA receptors in physiologic and pathologic conditions
196 ale for targeting synaptic and extrasynaptic GABAA receptors in the development of therapies for pati
199 irregularity; (iii) conversely, blockade of GABAA receptors in the KF of healthy rats mimicked the R
200 BAA receptors, the nanoscale distribution of GABAA receptors in the postsynaptic area is a crucial de
201 ively low-affinity gamma2 subunit-containing GABAA receptors in the thalamus, which can contribute to
202 ostsynaptic currents (EPSCs) are followed by GABA(A) receptor-independent outward currents, reflectin
203 R)mutation renders alpha1-subunit containing GABAA receptors insensitive towards benzodiazepines.
206 munoreactivity for the alpha2 subunit of the GABAA receptor is higher in layers 2/superficial 3 of th
207 larizing inhibition mediated by type A GABA (GABAA) receptors is dependent on chloride extrusion by t
208 th human alpha1beta3gamma2L-a major synaptic GABA(A) receptor isoform-that is functionally reconstitu
210 esthetic drugs that modulate the heteromeric GABA(A) receptor, it maintains a rich and multifaceted s
211 ences in the distribution and composition of GABAA receptors may account for distinct effects and sid
212 he postpartum period, the brain's inhibitory GABAA receptors may not recover in time following their
214 rent views suggest gamma2 subunit-containing GABA(A) receptors mediate phasic IPSCs while extrasynapt
218 altered mouse line (PC-Deltagamma2) in which GABA(A) receptor-mediated signaling at MLI to Purkinje c
219 ovel role for NO in strengthening inhibitory GABA(A) receptor-mediated transmission in molecular laye
222 sporter KCC2 (SLC12A5) tunes the efficacy of GABAA receptor-mediated transmission by regulating the i
224 c coagonists at pentameric alpha1beta3gamma2 GABA(A) receptors, modulating channel activation via fou
227 s able to rescue the deficits in AMPA, NMDA, GABA(A) receptors, mTOR and p-mTOR induced by CORT.
229 that precise functional genomic analyses of GABA(A) receptor mutations using concatenated constructs
230 sion by systemic administration of an alpha5-GABA(A) receptor negative allosteric modulator, L-655,70
231 eptors expressed in HEK293 cells, and native GABAA receptors of cerebellar granule cells, hippocampal
233 tes increases the expression and activity of GABAA receptors on the dendrites of the cells and that s
234 ates the molecular principles of heteromeric GABA(A) receptor organization and provides a reference f
239 is not associated with meaningful changes in GABA(A) receptor potency, mean channel open-time, open p
242 ts and mediated by alpha5 subunit-containing GABA(A) receptors rescues both NMDAR activation and syna
244 s, we inactivated the gamma2 subunit gene of GABAA receptors selectively in these neurons (SSTCre:gam
245 ntly decreases the hyper-excitable action of GABAA receptor signaling and restores network homeostati
251 nzotriazine, already identified as selective GABAA receptor subtype ligands endowed with anxiolytic-l
254 t it is not clear whether targeting distinct GABA(A) receptor subtypes will have disproportionate ben
256 itulated the memory deficits and had reduced GABA(A) receptor subunit alpha2 (GABRA2) expression in l
257 ine neurons and the expression of the alpha6 GABA(A) receptor subunit at the mossy fiber-granule cell
259 g on the cell type studied, their respective GABAA receptor subunit compositions, and critically, on
261 ith 480 epilepsy-related genes including all GABAA receptor subunit genes (GABRs), and we identified
267 stry, we investigated the distribution of 10 GABA(A) receptor subunits (alpha1, alpha2, alpha3, alpha
268 (i.e. exploratory behavior) and whole-brain GABA(A) receptor subunits (gabra1, gabra2, gabrd, & gabr
269 ome (Scn1a(+/-) ), and in which the alpha(2) GABA(A) receptor subunits are expressed at higher levels
272 s coping style and that expression of select GABA(A) receptor subunits may be one of the underlying m
273 osed fish had altered relative expression of GABA(A) receptor subunits, suggesting that some other st
274 amic principal neurons were found to express GABAA receptor subunits alpha1 , alpha3 , beta2/3 , gamm
276 regional staining intensity for all positive GABAA receptor subunits from the dorsolateral pole to ve
277 ere performed, and subcellular expression of GABAA receptor subunits was analyzed semiquantitatively.
280 s more sensitive to GABA than enhancement by GABAA receptors, suggesting GABAB receptors may be activ
281 have been explored experimentally using the GABA(A) receptor, summarize analytical expressions for a
282 ed the S-SCAM overexpression-induced loss of GABA(A) receptors, supporting that GABAergic synapse los
283 romotes the recruitment and strengthening of GABA(A) receptor synapses via Ca(2+)/calmodulin-dependen
284 tely selective for alpha5-subunit-containing GABA(A) receptors, the derivative SH53d-acid shows super
285 that, in addition to the number of synaptic GABAA receptors, the nanoscale distribution of GABAA rec
286 odulation of gamma-aminobutyric acid type A (GABA(A)) receptors to dampen neuronal activity in the br
287 potentiation of the human alpha1beta2gamma2L GABAA receptor to demonstrate that: 1) curvilinear isobo
288 the Cb-mediated recruitment of gephyrin and GABAA receptors to developing inhibitory postsynapses an
289 properties of recombinant alpha1beta2gamma2L GABAA receptors transiently expressed in HEK293T cells.
290 he potassium-chloride cotransporter KCC2 and GABAA receptors, undergo remarkable fluctuations within
291 icating perhaps increased neuronal matter or GABAA receptor upregulation and inflammatory edema.
295 hemical technology to individually study the GABA(A) receptor, which specifically expands the toolbox
296 clarifies a Grp94-mediated ERAD pathway for GABAA receptors, which provides a novel way to finely tu
297 mediated by type A gamma-aminobutyric acid (GABAA) receptors, which are Cl(-)-permeable, ligand-gate
299 mma2, alpha5beta3gamma2 and alpha1beta3delta GABAA receptors, while having no significant PAM effect
300 this deficit by overexpression of the alpha5-GABA(A) receptor within the ventral hippocampus (vHipp).