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1 by increasing synaptic inhibition from local GABA neurons.
2 rrelated with the appearance of degenerating GABA neurons.
3 ropathic pain through NR1 phosphorylation in GABA neurons.
4 ected robust orexigenic potential for the ZI GABA neurons.
5 creased substance P NK1-R internalization on GABA neurons.
6 some direct synaptic influence on VTA DA and GABA neurons.
7 hat is likely to excite DA cells and inhibit GABA neurons.
8 h nAChRs that desensitize less than those on GABA neurons.
9 ification of all hippocampal interneurons as GABA neurons.
10 uced below a detectable level in a subset of GABA neurons.
11 uced below a detectable level in a subset of GABA neurons.
12 ill result in a powerful inhibition of these GABA neurons.
13 processed for immunocytochemical staining of GABA neurons.
14 oradrenaline (tyrosine hydroxylase; TH), and GABA neurons.
15 fonylureas increase transmitter release from GABA neurons.
16 n the development of embryonic monoamine and GABA neurons.
17 by analysis of immunoreactive 5-HT, TH, and GABA neurons.
18 re mediated by the activation of presynaptic GABA neurons.
19 hCpG methylation was detected in GLU versus GABA neurons.
20 cessing and is composed of dopamine (DA) and GABA neurons.
21 differences in eCB synthesis between DA and GABA neurons.
22 synergistic overinhibition of nigro-thalamic GABA neurons.
23 leus (DR), which contains both serotonin and GABA neurons.
24 ng-lasting polysynaptic complex EPSCs in SNr GABA neurons.
25 1)(-)/(-)) mice for CB(1) receptors in brain GABA neurons.
26 progenitors generated similar populations of GABA neurons.
27 nucleus incertus, a population of tegmental GABA neurons.
28 but showed TRH axons terminating on or near GABA neurons.
29 mRNAs, markers for gamma-aminobutyric acid (GABA) neurons.
30 of glutamatergic synaptic plasticity in VTA GABA neurons, a currently understudied cell type that is
32 inhibition of dopamine reuptake affected SNr GABA neuron activity in a D(1)-like receptor-dependent m
33 homologue of unc-47 is expressed by central GABA neurons and confers vesicular GABA transport in tra
34 in the opioid-induced inhibition of midbrain GABA neurons and consequent disinhibition of dopamine (D
35 ults revealed that social defeat engaged DRN GABA neurons and drove GABAergic sensitization that stre
36 sive disorder, implicate dendritic targeting GABA neurons and GABA synthesis, and, together, suggest
39 study the migrational trajectories of DA and GABA neurons and show that they occupy ventral mesenceph
40 ic, glutamatergic drive to both DRN 5-HT and GABA neurons and that this architecture was conducive to
41 mine neurons in embryonic rat brain, because GABA neurons and their receptors appear in brainstem dur
43 inhibited STN-triggered burst firing in SNr GABA neurons, and CP93129's inhibitory effect was strong
44 the magnitude of electrical coupling between GABA neurons, and GJ blockers increased the threshold fo
45 ted non-CpG sites were identified in GLU and GABA neurons, and non-CpG methylation was a better predi
46 inhibitory input onto VTA dopamine (DA) and GABA neurons, and that the GABAergic projection drives f
47 brane domains, that the gene is expressed by GABA neurons, and that the protein colocalizes with syna
48 the level of gene expression in a subset of GABA neurons, and the resulting changes in GABA neurotra
50 >SNr projection, reduces burst firing in SNr GABA neurons, and thus may play a critical role in movem
51 r this change is present in all or only some GABA neurons, and whether long-term treatment with halop
52 of a subpopulation of perisomatic-targeting GABA neurons, and, when activated, suppresses the releas
53 Given the critical role that PV-containing GABA neurons appear to play in regulating the cognitive
54 ptic terminals on the remaining dendrites of GABA- neurons appeared not to undergo major age-related
58 e observations show that, unexpectedly, ESR1-GABA neurons are only essential for the positive feedbac
60 noradrenergic and gamma-amino-butyric acid (GABA) neurones are implicated in the system's regulation
61 cystokinin class of gamma-aminobutyric acid (GABA) neurons, are lower in the dorsolateral prefrontal
62 pression is relatively unaltered in most PFC GABA neurons but is reduced below a detectable level in
64 ional deletion of CB(1) receptors from brain GABA neurons, but not from several other neuronal popula
65 s and indirectly inhibits them through local GABA neurons, but the relative magnitudes of the two mec
66 5-HT2CR expressing gamma-aminobutyric acid (GABA) neurons, but not 5-HT2CR expressing dopamine (DA)
67 eding and locomotor activity similar to LHA (GABA) neurons, but without inducing compulsive-like beha
69 hat the dynamic interplay between VTA DA and GABA neurons can control the initiation and termination
71 % of parvalbumin-containing septohippocampal GABA neurons colocalized the mu receptor, which at the u
73 e mesencephalon, where dopaminergic (DA) and GABA neurons constitute two major neuronal populations.
74 indings indicate that the discharging of VTA GABA neurons correlates with psychomotor behavior and th
75 sensory cortical development, and thus that GABA neurons could provide an important substrate for ex
76 investigate whether these same hypothalamic GABA neurons decrease their activity postcastration in f
77 Our results indicate that the mechanism of GABA neuron degeneration is calcium-dependent and requir
78 ath is also consistent with our finding that GABA neuron degeneration requires the mitochondrial fiss
79 ggered complex EPSCs and burst firing in SNr GABA neurons, demonstrating the effects of endogenous 5-
80 e intimate relationship between dopamine and GABA neuron development revealed here may offer novel in
82 r the selective ablation of GIRK channels in GABA neurons, diminished morphine-induced motor activity
83 Furthermore, optogenetic stimulation of VTA GABA neurons directly suppressed the activity and excita
84 Furthermore, optogenetic silencing of DRN GABA neurons disinhibited neighboring 5-HT neurons and p
85 w that in vivo optogenetic activation of VTA GABA neurons disrupts reward consummatory behavior but n
87 laterally stimulating ventral tegmental area GABA neurons dramatically reduces anticipatory licking t
89 doses of nicotine, by stimulating DA but not GABA neurons, exaggerates these phenotypes and produces
91 gy is the dysfunction of cortical inhibitory GABA neurons expressing parvalbumin, which are essential
94 mine, or halothane significantly reduced VTA GABA neuron firing rate and converted their activity int
96 and EPSC frequencies were increased in hilar GABA neurons from slices ipsilateral to the injury versu
97 model, we found that tangential migration of GABA neurons from the basal to the dorsal forebrain and
98 orter, but Prlr deletion from these dopamine/GABA neurons had no effect on feedback regulation of pro
99 ularly involving parvalbumin (PV)-expressing GABA neurons, has been proposed as a key mechanism under
101 arized GABA neurons including neuroendocrine GABA neurons identified by antidromic median eminence st
102 rter, a transcription factor that determines GABA neuron identity, a classic inhibitory GABA receptor
103 of a homogeneous population of presumed VTA GABA neurons, implicated in cortical arousal, increases
105 To solidify the importance of these VTA GABA neurons in behavioral function, we employed the neu
106 vidence is lacking for a causal role of vHPC GABA neurons in behaviors associated with schizophrenia.
107 se findings establish a causal role for vHPC GABA neurons in controlling behaviors relevant to schizo
108 lso generated a new mouse model for studying GABA neurons in narcoleptic mice, which could serve as a
110 altered in the majority of prefrontal cortex GABA neurons in schizophrenic subjects but is reduced be
111 MOR agonists could modulate the activity of GABA neurons in the Acb via receptors located mainly at
112 odulators reduces the activity of inhibitory GABA neurons in the ARC by multiple presynaptic and post
113 ncy within the TIDA population, the dopamine/GABA neurons in the arcuate nucleus represent a subpopul
114 These observations demonstrate that Sst-GABA neurons in the brainstem are crucial for regulating
116 ggest that swim stress engages CRF inputs to GABA neurons in the dorsolateral DR that function to inh
117 We provide the first characterization of GABA neurons in the DRN that monosynaptically inhibit 5-
119 hippocampus of mice in which BFCNs and some GABA neurons in the medial septum had been destroyed by
120 enic mice, we demonstrate that glutamate and GABA neurons in the MnPO/OVLT reciprocally regulate wate
124 Thus, a network of electrically coupled GABA neurons in the ventral brain may form the elusive n
128 w that inhibition of the terminals of the LH GABA neurons in ventral-tegmental area (VTA) facilitates
130 chemogenetic activation of LHA (Gal) or LHA (GABA) neurons in mice to compare their role in feeding b
132 a subpopulation of gamma-aminobutyric acid (GABA) neurons in the VTA increases in anticipation of BS
134 y reduced the firing rate and hyperpolarized GABA neurons including neuroendocrine GABA neurons ident
135 al that can act in the brain, also inhibited GABA neurons, including identified neuroendocrine cells,
136 pulations of DA and gamma-aminobutyric acid (GABA) neurons, including those projecting to the prefron
138 pulse ratio of the monosynaptic EPSCs in SNr GABA neurons, indicating a presynaptic 5-HT1B receptor-m
140 tory synaptic activity was detected in hilar GABA neurons ipsilateral to the injury after glutamate p
141 est that excitatory drive to surviving hilar GABA neurons is enhanced by convergent input from both p
142 tion in females showed that leptin action on GABA neurons is not necessary for estradiol-mediated sup
143 tered inhibition from parvalbumin-containing GABA neurons is thought to contribute to impaired gamma
148 alance between D1 and D2 receptors can alter GABA neuron migration from the basal forebrain to the ce
149 romotes and D2 receptor activation decreases GABA neuron migration from the medial and caudal ganglio
154 se 67)-synthesizing cells, we identified ARC GABA neurons (n > 300) and used whole-cell recording to
155 m the inhibition of the activity of NPY/AgRP/GABA neurons (NAG) in the arcuate nucleus of the hypotha
157 argets that included a preferential input to GABA neurons of both mesoaccumbens and mesoprefrontal po
165 ract the pronounced inhibitory effect of Sst-GABA neurons on vagal pre-motor neurons in the DMV that
167 other sub-populations of prefrontal cortical GABA neurons or abnormalities in the parvalbumin-contain
168 e zona incerta (ZI) gamma-aminobutyric acid (GABA) neurons or their axonal projections to paraventric
172 rphin-saporin (DS) to selectively lesion VTA GABA neurons prior to assessing spontaneous motor activi
174 ndelier subclass of gamma-aminobutyric acid (GABA) neurons provides potent inhibitory control over py
175 that this results from an action of SSRIs on GABA neurons rather than as a secondary consequence of m
176 ynaptic inputs from anterior neocortex while GABA neurons receive disproportionally higher input from
180 ic inhibition of LH gamma-aminobutyric acid (GABA) neurons restricted to cue presentation disrupts th
181 lts show that optogenetic stimulation of Sst-GABA neurons results in a robust inhibition of action po
182 However, examination of the proportion of GABA neurons revealed an unexpected late peak at postnat
183 s a direct correlation between increased VTA GABA neuron slowing and increased delta wave power.
185 Esr1(lox/lox) line to generate animals with GABA-neuron-specific or glutamate-neuron-specific deleti
186 (B)R signaling removes an intrinsic brake on GABA neuron spiking, which may augment GABA transmission
187 essels have greater disturbances in cortical GABA neurons suggests that these cell-type distinct path
190 ifferent but overlapping populations of vHPC GABA neurons that express either PV or GAD65 by selectiv
191 ns in parvalbumin-positive fast-spiking (FS) GABA neurons that may cause abnormal gamma oscillations.
192 at in distinct regions of the telencephalon, GABA neurons that react to cannabinoids may also be resp
193 he input sector by activation of hippocampal GABA neurons that terminate exclusively on apical dendri
194 urons induced a direct inward current in SNr GABA neurons that was sensitive to D(1)-like blockade.
196 roduce LHA (Gal) neurons as a subset of LHA (GABA) neurons that lack direct innervation of the ventra
197 eurons may represent a subpopulation of LHA (GABA) neurons that mediates food reward independent of d
198 he threshold for electrical coupling between GABA neurons, the degree of responding for IC self-stimu
199 lthough thought to contain only dopamine and GABA neurons, the VTA also includes a recently discovere
200 MDD, particularly affecting SST/NPY-related GABA neurons, thus linking the neurotrophic and GABA hyp
201 ivation of P2X receptors excited presynaptic GABA neurons to increase GABA release, which was excitat
202 ally released dopamine tonically excites SNr GABA neurons via D(1)-D(5) receptor coactivation that en
203 During exercise, muscle afferents excite NTS GABA neurons via substance P and microinjection of a sub
204 dose- and time-related selective loss of VTA GABA neurons was accomplished using this novel neurotoxi
207 GABAergic inputs from the NAc and local VTA GABA neurons were differentially modulated and activated
209 f the axon terminals of other populations of GABA neurons were not altered in the schizophrenic subje
211 Immunocytochemically labelled nonpyramidal GABA neurons were present from postnatal day 1 throughou
214 was found largely on nondopaminergic (i.e., GABA) neurons, whereas NOP mRNA was located on DA neuron
215 the axon terminals of parvalbumin-containing GABA neurons, which are known to have low levels of GAD6
216 tide and marker of gamma-amino butyric acid (GABA) neurons, which specifically inhibit pyramidal neur
218 suggests heterogeneity of both serotonin and GABA neurons with respect to the inputs they receive.
219 N15 suggest that some of the early-appearing GABA neurons within the developing molecular layer of th
220 aring population of gamma-aminobutyric acid (GABA) neurons within the developing molecular layer.
221 The absolute numbers of CR+, PV+, CB+, and GABA+ neurones within individual layers in a column of c
222 (Gal) neurons define a subpopulation of LHA (GABA) neurons without direct VTA innervation that mediat
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