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1 nsgenic mouse model that specifically labels GABA cells.
2 ated and regulated by neighboring inhibitory GABA cells.
3 th immunocytochemistry to distinguish DA and GABA cells.
4 ned excitatory plasticity in fluorescent VTA GABA cells.
5 y is far greater in excitatory cells than in GABA cells.
6 th GluR3 and GluR6 subunits not expressed by GABA cells.
7 influences on the serotonin-accumulating and GABA cells.
8 this being the first report of iLTD onto VTA GABA cells.
9 cally innervating aversion-encoding midbrain GABA cells.
10 adual transition of RG cells into CalR(+) or GABA(+) cells.
11                                 We show that GABA cell activation only promotes cataplexy attacks ass
12 lied Delta(9)-tetrahydrocannabinol depressed GABA cell activity, therefore downstream dopamine cells
13 alter behavior through regulating VTA DA and GABA cell activity.
14 tribute to the activity of dopamine (DA) and GABA cells and, hence, to the affective and cognitive fu
15 s a novel form of synaptic plasticity in VTA GABA cells, and the synaptic remodeling that can occur a
16                             Ventral thalamus GABA cells are derived from a region connecting the vent
17 physiological studies indicate that cortical GABA cells are modulated by a variety of afferents.
18 not been possible to record selectively from GABA cells, because they have no defining morphological
19 duced by stimulation of LH GABA terminals or GABA cell bodies in this peri-LC region.
20 tory influence on both mesoprefrontal DA and GABA cells but a divergent impact on mesoaccumbens neuro
21 d) cells were also found but no new Cr(+) or GABA(+) cells colabeled with a mature neuron marker, Neu
22 the trisynaptic pathway, so that subtypes of GABA cells could be defined by their location in various
23 gic studies reporting reduced glial cell and GABA cell density in the prefrontal cortex in individual
24  we found that excitatory synapses on DA and GABA cells display several differences.
25                                              GABA cell dysfunction in both schizophrenia (SZ) and bip
26                     In contrast, synapses on GABA cells exhibit a facilitation in response to repetit
27 ntify GABA cells, we observed that these VTA GABA cells experience either inhibitory GABAergic long-t
28 yramidal cells and gamma-amino butyric acid (GABA) cells; GluR2/3 immunoreactivity is preferentially
29 mouse line that enables genetic targeting of GABA cells in orexin(-/-) mice.
30 y excitatory synapses that innervated DA and GABA cells in rough proportion to their representation w
31 s the first functional evidence to implicate GABA cells in the amygdala as regulators of cataplexy tr
32  stimuli may trigger cataplexy by activating GABA cells in the CeA.SIGNIFICANCE STATEMENT Although ca
33 bers from the MD and different subclasses of GABA cells in the PFC are not known.
34 n which excitatory synaptic inputs to DA and GABA cells in the VTA can be modulated have potentially
35       Previous studies demonstrated that the GABA cells intrinsic to the VTA receive insufficient syn
36 R4 immunoreactivity is largely restricted to GABA cells; NMDA receptor subunit immunoreactivity is fa
37                                    Intrinsic GABA cells of dorsal thalamus may, therefore, derive fro
38 w hypotheses regarding the regulation of the GABA cell phenotype in the hippocampus of SZ and BD.
39 accumbens GABA neurons are well studied, VTA GABA cell plasticity, specifically inhibitory inputs to
40 ut affecting their duration, suggesting that GABA cells play a functional role in initiating but not
41 , we identified two molecularly distinct LDT(GABA) cell populations.
42                                              GABA+ cells represented a mean of 16.2% (14.8-17.2%) of
43 askets target the somas of certain GABA+ and GABA- cells, resembling cortical axosomatic synapses.
44                                To manipulate GABA cells specifically, we developed a new mouse line t
45     A novel CB1-dependent LTD was induced in GABA cells that was dependent on metabotropic glutamate
46  some population of gamma-aminobutyric acid (GABA) cells that, in turn, innervates DA neurons.
47 ing, gamma-aminobutyric acid (GABA) (PFC(Sst-GABA)) cells that responded to sleep deprivation.
48 tion and/or genomic integrity of hippocampal GABA cells varies according to diagnosis and their locat
49 ctrophysiology in GAD67-GFP mice to identify GABA cells, we observed that these VTA GABA cells experi
50               The serotonin-accumulating and GABA cells were affected as they were drastically reduce
51 logical type, whereas VAChT(+) synapses onto GABA cells were more frequently symmetric (presumed inhi
52                                  CalR(+) and GABA(+) cells were apparent for the first time after 3 d
53                    After 24 h, no CalR(+) or GABA(+) cells were seen in cultures, whereas 5-10% cells
54 um (ganglionic eminence) generate CalR(+) or GABA(+) cells, whereas this was not the case with RG cel
55 rs and altered integration among hippocampal GABA cells with extrinsic and intrinsic afferent fiber s
56                           Then, we show that GABA cells within the CeA are responsible for mediating
57 ity of both dopaminergic (DA) and GABAergic (GABA) cells, yet little is known about the basic propert