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1 as binding partners for ionotropic GABAA and GABAC receptors.
2 s docking to the homology models of GABAA or GABAC receptors.
3 scimol-PEG-qdot treatment of oocytes lacking GABAC receptors.
4  exhibited no significant effect on the rho1 GABA(C) receptor.
5  acts as a non-competitive antagonist on the GABA(C) receptor.
6 re observed for picrotoxin inhibition of the GABA(C) receptor.
7 perties confirmed the presence of functional GABA(C) receptors.
8 ack IPSCs, were mediated by both GABA(A) and GABA(C) receptors.
9 low concentrations that selectively activate GABA(C) receptors.
10 (A) receptors as well as expression of novel GABA(C) receptors.
11 ed in dark-adapted retinas by GABA acting at GABA(C) receptors.
12 and potency of agonists on intact functional GABA(C) receptors.
13 n exogenously expressed human rho1 homomeric GABA(C) receptors.
14  by bicuculline, indicating that it involved GABA(C) receptors.
15 hibitory feedback that activated presynaptic GABA(C) receptors.
16  been described, activating both GABA(A) and GABA(C) receptors.
17 ls, through both GABA(A) and GABA(B) but not GABA(C) receptors.
18 l bipolar cells, which have both GABA(A) and GABA(C) receptors.
19 ng GABAergic current mediated exclusively by GABA(C) receptors.
20 bution of GABA (gamma-aminobutyric acid) and GABA(C) receptors.
21 onal coupling between GAT-1 transporters and GABA(C) receptors.
22 ggesting the involvement of both GABA(A) and GABA(C) receptors.
23 ngs we observed for picrotoxin inhibition of GABA(C) receptors.
24 ain and the ligand for GABA(A), GABA(B), and GABA(C) receptors.
25 otropic receptors in the retina, GABA(A) and GABA(C) receptors.
26 zed, whereas much less is known about native GABA(C) receptors.
27 activity at GABA(A)-rho1 (also known as rho1 GABA(C)) receptors.
28 ockade of glutamate receptors, expression of GABA(C) receptors abolished the hyperactivity and the co
29 ith their relative contributions to L-IPSCs, GABA(C) receptor activation most effectively reduced the
30 ergic amacrine cells, thereby sustaining the GABAC receptor activation required for rod bipolar cell
31  A and E, but not F, involved in forming the GABA(C) receptor agonist binding pocket.
32                                          The GABA(C) receptor agonist CACA (200 microM) was without s
33 cked by muscimol, but not by baclofen or the GABAc receptor agonist cis-4-aminocrotonic acid, and the
34 rotonic acid (CACA), and isoguvacine are all GABA(C) receptor agonists.
35                                 Furthermore, GABA(C) receptors and MAP-1B co-localize at postsynaptic
36 ct oocyte expressing recombinant human rho 1 GABAC receptors and directly correlate the binding kinet
37 rough two ligand-gated channels, GABA(A) and GABA(C) receptors, and a third receptor, GABA(B) , which
38                                          The GABA(C) receptor antagonist (1,2,5,6-tetrahydropyridin-4
39                                              GABA(C) receptor antagonists did not block the effects o
40                                              GABA(C) receptor antagonists reduced inhibition attribut
41                 Surprisingly, GABA(A) and/or GABA(C) receptor antagonists restored the fast component
42 ethylphosphinic acid (TPMPA) and picrotoxin, GABAC receptor antagonists, reduced the ATPA effect.
43 es of GABA-induced currents to the GABAA and GABAC receptor antagonists.
44 cording and Western blot analysis using rho1 GABA(C) receptor antibodies revealed that recombinant rh
45                       Although native rodent GABA(C) receptors are composed of rho1 and rho2 subunits
46 A(C) receptor function in the retina because GABA(C) receptors are highly expressed on the axon termi
47          These data suggest that GABA(A) and GABA(C) receptors are highly unlikely to be synaptically
48     Experiments showed that both GABA(A) and GABA(C) receptors are involved in the masking inhibition
49                  gamma-Aminobutyrate type C (GABA(C)) receptors are ligand-gated ion channels that ar
50 endent process is receptor subtype specific: GABAC receptors are maintained, whereas GABAA receptors
51 smitter gamma-aminobutyric acid (GABA(A) and GABA(C) receptors) are the principal sites of fast synap
52 de-field amacrine cells, which stimulate the GABAC receptors at rod bipolar cell axons.
53 h previous findings, a complete model of the GABA(C) receptor binding pocket was proposed and discuss
54 ises in retinotectal axons were inhibited by GABA(C) receptor blockade.
55                                              GABA(C) receptor blockers reduced dim surround inhibitio
56  enhanced by sustained chloride currents via GABA(C) receptor channels.
57 al regions previously unexplored in the rho1 GABA(C) receptor, corresponding to the binding loops A,
58 (tau(decay)), 1.0 ms) in addition to a tonic GABA(C) receptor current.
59 1 GABA transporter, which strongly regulates GABA(C) receptor currents in BC terminals, fails to reve
60 ty at the ligand-binding pocket of expressed GABAC receptors, despite the presence of both the long P
61 shion, whereas PTX inhibition of glycine and GABA(C) receptors displays little or no use-facilitated
62                 Adenovirus-mediated neuronal GABA(C) receptor engineering, via its dual mechanism of
63      The pore diameter of the homomeric rho1 GABAC receptor expressed in oocytes was estimated to be
64 uscimol-PEG-qdot conjugate to homomeric rho1 GABAC receptors expressed in Xenopus oocytes.
65 elations were suppressed by antagonizing the GABA(C) receptor (expressed on bipolar terminals), and c
66 sion was selectively eliminated there was no GABA(C) receptor expression.
67 eek, and we evaluated: GABA(A), GABA(B), and GABA(C) receptor expression; intrahepatic bile duct mass
68                           Inhibition through GABAC receptors extracts spatial edges in neural represe
69 amate receptors, on heterologously expressed GABA(C) receptors formed by homomeric rho subunits.
70                                  We assessed GABA(C) receptor function in the retina because GABA(C)
71 a, Glu, or Lys, which experimentally disrupt GABAC receptor function, and repeating the simulation re
72    From noise analysis of the tonic current, GABA(C) receptor gamma is estimated to be 4 pS.
73 hree binding domains in the recombinant rho1 GABA(C) receptor have been recognized among six potentia
74  terminal of goldfish retinal bipolar cells, GABA(C) receptors have been shown to mediate inhibitory
75  strongly suggest that GABA(A) receptors and GABA(C) receptors have distinct functional roles in the
76              gamma-Aminobutyric acid type C (GABAC) receptors identified in retina appear to be compo
77 sed a model in which picrotoxin binds to the GABA(C) receptor in both channel open and closed states.
78 ells includes activation of both GABA(A) and GABA(C) receptors in an approximately equal ratio.
79 ies and localization of synaptic GABA(A) and GABA(C) receptors in BC terminals are likely to facilita
80                                  GABA(A) and GABA(C) receptors in BC terminals mediate currents with
81     Five days after infection, expression of GABA(C) receptors in hippocampal neurons significantly d
82 denovirus can be used to express recombinant GABA(C) receptors in hippocampal neurons.
83 ceptors in ON BSGCs, and by both GABA(A) and GABA(C) receptors in OFF BSGCs.
84  than OFF BSGCs, and was mediated largely by GABA(C) receptors in ON BSGCs, and by both GABA(A) and G
85                                  The role of GABA(C) receptors in retinotectal responses was also eva
86 ia gene targeting, results in the absence of GABA(C) receptors in the retina and selective alteration
87                           Expression of rho1 GABAC receptors in Xenopus oocytes and in HEK293 cells g
88 correlations were suppressed by antagonizing GABA(C) receptors, indicating that glutamate bursts from
89 s to GABA(A) or GABA(A0r) (formerly known as GABA(C)) receptors inhibited form-deprivation myopia.
90 uggests that the binding site for CTZ on the GABA(C) receptor is distinct from that for GABA, and tha
91  a cation-pi interaction with GABA, while in GABA(C) receptors it is a loop B residue.
92 r distribution on RBC axons is unaffected in GABAC receptor knockout mice.
93 genes; rho1 and rho2 that encode subunits of GABA(c) receptors, L7 that encodes Purkinje cell protein
94                              Thus, GABAA and GABAC receptor maintenance are regulated separately.
95                                      Because GABA(C) receptors may be specifically expressed by GABAe
96  cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate inhibition on axon terminals i
97 ies have shown that in Xenopus tectal cells, GABA(C) receptors mediate inhibition, in retinotectal ax
98 ndicates that two pharmacologically distinct GABAC receptors mediate feedback to bipolar cells.
99                                              GABAC receptors mediate inhibitory synaptic signaling at
100   Second, we showed, for the first time, how GABA(C) receptor mediated amacrine cell feedback to bipo
101 ow that different proportions of GABA(A) and GABA(C) receptor-mediated inhibition determined the kine
102 been used to define the roles of GABA(A) and GABA(C) receptor-mediated input in RF organization.
103      Furthermore, we find that the amount of GABA(C) receptor-mediated reciprocal feedback between bi
104                         We propose that this GABA(C) receptor-mediated standing current serves to reg
105 ating the retinas of transgenic mice lacking GABAc receptor-mediated presynaptic inhibition, we found
106 l rod bipolar cells (RBCs) receive GABAA and GABAC receptor-mediated synaptic inhibition.
107                                   Identified GABA(C) receptor mIPSCs exhibit a slow decay (tau(decay)
108                                          The GABA(C) receptor, normally found only in the retina, is
109 tion, quite different from the properties of GABA(C) receptors observed in native cells.
110 sly in Xenopus laevis oocytes, and on native GABA(C) receptors of perch bipolar cells.
111 y other GABA rho subunits, as well as on the GABA(C) receptors of retinal bipolar cells.
112  enhanced the light-evoked IPSCs mediated by GABA(C) receptors on bipolar cell axon terminals, which
113      Focal applications (puffs) of GABA onto GABA(C) receptors on bipolar cells terminals or GABA(A)
114            Blocking of GABA(A), GABA(B), and GABA(C) receptors prevented GABA inhibition of cholangio
115       The masking inhibition is subserved by GABAC receptors, probably on bipolar cell axon terminals
116      This result suggests that activation of GABA(C) receptors produces an increase in the synaptic e
117 sponses to micromolar GABA involve GABAB and GABAC receptor proteins.
118  that possess distinct glycine, GABA(A), and GABA(C) receptors (R).
119 meric receptor may not be the native retinal GABAC receptor reported previously.
120 n the closely related vertebrate GABA(A) and GABA(C) receptors, residues in distinct locations perfor
121 irus vector that expressed cDNA for both the GABA(C) receptor rho(1) subunit and a green fluorescent
122 function have been attributed to GABA(A) and GABA(C) receptors, specific retinal functions have also
123 adenovirus was generated with the human rho1 GABA(C) receptor subunit (adeno-rho).
124 I-, NO3-, Br- and HCO3- were higher for rho1 GABAC receptors than alpha1beta2gamma2L GABAA receptors.
125 loride currents mediated by both GABA(A) and GABA(C) receptors, the small-field bipolar cells showed
126 vertebrate counterparts, GABAA receptors and GABAC receptors, the binding of GABA to ionotropic insec
127 del of the amino-terminal domain of the rho1 GABA(C) receptor, they are facing toward the putative bi
128 We assessed the contributions of GABA(A) and GABA(C) receptors to inhibition at the dendrites and axo
129 Aergic response mediated by nondesensitizing GABA(C) receptors to two rapid glutamate puffs onto the
130  docked into the extracellular domain of the GABAC receptor to explain the molecular interactions of
131  L-IPSCs, but their relative roles differed; GABA(C) receptors transferred significantly more charge
132 ion suggests that the subunit composition of GABA(c) receptors vary during retinal development.
133                            CTZ inhibition of GABA(C) receptors was subunit specific; it produced a do
134          To determine the functional role of GABA(C) receptors, we eliminated their expression in mic
135                          However, functional GABA(C) receptors were also demonstrated.
136 ting that, when GABA uptake was blocked, the GABA(C) receptors were more strongly activated by spillo
137                         Homomeric human rho1 GABAC receptors were expressed in Xenopus oocytes and in
138  GABA-evoked responses, normally mediated by GABA(C) receptors, were eliminated, and signaling from r
139                           Unlike GABA(A) and GABA(C) receptors, which are chloride channels, GABA(B)
140                                              GABA(C) receptors, which are composed of rho-subunits, a
141 and acts at a variety of receptors including GABAC receptors, which are a subclass of GABAA receptors
142 ) are well suited to match the properties of GABAC receptors, which thus provide part of the prolonge
143        CTZ inhibited the open channel of the GABA(C) receptor with a time constant of about 0.4 s, bu
144 hought to contribute to the formation of the GABA(C) receptors with pharmacological and physiological
145 n though picrotoxin blocked both GABA(A) and GABA(C) receptors within a few seconds.

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