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1 rcuit comprised of AFD thermosensory and AIY interneurons.
2 ing a pathophysiological role for inhibitory interneurons.
3 a discrete subset of nociceptive, excitatory interneurons.
4 not caudal ganglionic eminence (CGE)-derived interneurons.
5 her parvalbumin (PV+) or somatostatin (SOM+) interneurons.
6 he majority of NK1R spinal neurons are local interneurons.
7 poptotic elimination of a third of GABAergic interneurons.
8 terns precisely fine-tuned through GABAergic interneurons.
9 tially encase parvalbumin-containing (PV(+)) interneurons.
10 apses were rare in nonfast-spiking GABAergic interneurons.
11 rmation is modulated by striatal cholinergic interneurons.
12 acts by reducing excitation from cholinergic interneurons.
13 ment is mediated by TRKB activation in PV(+) interneurons.
14  stem cells generate olfactory bulb-destined interneurons.
15 ayer 1 interneurons and other VIP(+)/ChAT(+) interneurons.
16 ed action potentials primarily in inhibitory interneurons.
17 cal inhibition of cholecystokinin-containing interneurons.
18  thus the majority of Tacr1(CreER) are local interneurons.
19 rd by a network of excitatory and inhibitory interneurons.
20 bumin-expressing and somatostatin-expressing interneurons.
21 glial activation and vulnerability of spinal interneurons.
22 ting somatostatin and inhibiting parvalbumin interneurons.
23 tor-dependent quinone reductase 2 pathway in interneurons.
24 ion of proper numbers of forebrain GABAergic interneurons.
25 ynchronized inhibition provided by GABAergic interneurons.
26 e ("hourglass waist") that consists of 10-15 interneurons.
27 in the ATP-to-ADP ratio in Cox6a2(-/-) PV(+) interneurons.
28 sed survival of parvalbumin and somatostatin interneurons.
29 l dynamics as the maturation of fast-spiking interneurons.
30 nied by enhanced axonaloutgrowth in immature interneurons.
31  and connections between cortical inhibitory interneurons.
32 tory parvalbumin (PV) and somatostatin (SST) interneurons.
33  motor neurons and abnormal migration of V2a interneurons.
34  are thought to occur via inhibition of GABA interneurons.
35 n intrinsic connections involving inhibitory interneurons.
36 ting somatostatin-expressing (SST) GABAergic interneurons.
37  associated with the activity of cholinergic interneurons.
38 naling in the antennal lobe inhibitory local interneurons.
39 he antRNs are inhibitory photoreceptor relay interneurons.
40  that alters the intrinsic properties of CA1 interneurons 3 h following learning, in a form of oxidat
41                    In contrast, fast-spiking interneuron ablation did not affect any index of water o
42  manipulation triggers rapid reduction of PV interneuron activity and disinhibition of excitatory neu
43 ain mnemonic processing, potentiation of SST interneuron activity represents an important causal mech
44            Disrupting either PV(+) or SST(+) interneuron activity, via either photoinhibition or phot
45  nutrition, and activity of certain AL local interneurons affect the magnitude of interfly behavioral
46 wed no obvious loss in any of the subsets of interneurons after TBI.
47 ivo opto-activation of cortical somatostatin interneurons alleviates motor symptoms in a parkinsonian
48 yramidal cells, unexpectedly the majority of interneurons also decreased their activity.
49 gether, GSK3beta inhibition in corticolimbic interneurons ameliorates the deficits in spatial working
50 one connectome, revealing a novel inhibitory interneuron, an amacrine cell, receiving excitatory glut
51 male mice reveal selective modulation of SST interneurons and a putative downstream circuit mechanism
52  release GABA strongly onto other inhibitory interneurons and acetylcholine sparsely onto layer 1 int
53 However, it is largely unknown how GABAergic interneurons and astrocytes interact and contribute to s
54  highlighting unexpected roles for both CCK+ interneurons and endocannabinoid modulation in hippocamp
55 n spiny neurons (MSNs), parvalbumin-positive interneurons and Iba1-positive microglia were all decrea
56 lpha-positive neurons are largely excitatory interneurons and many coexpress substance P, a marker fo
57 /inhibitory (E/I) ratio by recruiting SST(+) interneurons and modulates specific features of V1 spont
58 ding suprareticular inputs to control spinal interneurons and motoneurons.
59 rons and acetylcholine sparsely onto layer 1 interneurons and other VIP(+)/ChAT(+) interneurons.
60 and developmental factors affecting cortical interneurons and PFC function.
61  but still little is known about the role of interneurons and plasticity-related molecules on such me
62 segregated functional assemblies composed of interneurons and pyramidal cells are prominent in the so
63 f over 4,200 mouse visual cortical GABAergic interneurons and reconstructed the local morphologies of
64 research, given the alterations in PNNs, PV+ interneurons and their physiology described in different
65 tes PRs in the central retina in 1 week, but interneurons and their synapses are maintained for as lo
66 al (inhibitory interneurons inhibiting other interneurons) and feedforward (inhibitory interneurons i
67 migration and laminar deposition of cortical interneurons, and further implicates the JNK pathway as
68 s are the presynaptic dendrites of GABAergic interneurons, and GAD67-GFP interneurons are a source of
69 n neurons, including inputs from parvalbumin interneurons, and increased endocannabinoid tone.
70 s with reduced AKT signaling in Pcdhg mutant interneurons, and is rescued by genetic blockade of the
71 rough a highly recurrent network of about 80 interneurons, and it produces a coordinated output from
72     This aberrant pattern effectively blocks interneuron apoptosis, causing increased survival of par
73                                        These interneurons appear to antagonize the otolith circuit un
74 tes of GABAergic interneurons, and GAD67-GFP interneurons are a source of these presynaptic dendrites
75       Here, we confirm in mice that Pitx2(+) interneurons are active during fictive locomotion and th
76 ol in rodents, and that striatal cholinergic interneurons are an essential node of such circuitry.
77                                   Inhibitory interneurons are essential for proper brain development
78   Our model suggests that different types of interneurons are essential to unravel the mechanisms und
79 the dorsal telencephalon, whereas inhibitory interneurons are generated in its ventral portion.
80                            However, cortical interneurons are heterogeneous.
81  Abnormalities of or reductions in GABAergic interneurons are implicated in the pathology of severe n
82                  Parvalbumin (PV)-expressing interneurons are important for cognitive and emotional b
83           Yet the mechanisms by which viable interneurons are produced from progenitors remain poorly
84 in (PV+), and somatostatin (SOM+) expressing interneurons are prominent in layer 5 (L5) of infralimbi
85 CANCE STATEMENT Parvalbumin-expressing (PV+) interneurons are surrounded by specializations of the ex
86 udies point toward a dysfunction of cortical interneurons as a central element.
87 ccompanied by increased sensory pooling onto interneurons as well as species-specific central project
88 ked by GluN2B-NMDAR knockdown on GABA (Gad1) interneurons, as well as subtypes expressing somatostati
89                                          The interneurons associated with rapid escape circuits are a
90 erineuronal nets (PNNs) around many of these interneurons at the end of the critical periods reduces
91 radely inhibiting a pair of premotor command interneurons, AVA, that control cholinergic motor neuron
92                 Tonically active cholinergic interneurons become dysregulated during chronic L-DOPA a
93 tions, and conversely if activation of these interneurons blocks the rapid and sustained antidepressa
94                     Multiple neuropeptide-ir interneurons branched in ME4, connecting the AME to ME2.
95 ndings demonstrate that DREADD activation of interneurons brings about both short-term and long-term
96 a deficit in the recruitment of fast-spiking interneurons by excitatory inputs during adolescence.
97     Our study demonstrates modulation of SST interneurons by Lypd6 to achieve robust levels of cortic
98 er suggest that intense activation of SST(+) interneurons can enable the CA3 circuit to generate fast
99 onstrate that early genetic abnormalities in interneurons can interact with postnatal development dur
100 e, we predict that the silencing of anti-SWR interneurons can trigger SWRs.
101                       Spikes from inhibitory interneurons (cartwheel cell) and principal output neuro
102 hree and cholecystokinin expressing cortical interneurons (CCK(+)VGluT3(+)INTs) has prompted speculat
103                               CCK-expressing interneurons (CCK+INs) are crucial for controlling hippo
104 uses in the activity of striatal cholinergic interneurons (ChINs) are correlated with elevated activi
105 creases the survival of MGE-derived cortical interneurons (CINs) and changes their physiological prop
106                          Cortical inhibitory interneurons (cINs) are born in the ventral forebrain an
107                                     Cortical interneurons (cINs) are consistently observed to be abno
108                           Cortical GABAergic interneurons (CINs) are implicated in NF1 pathology, but
109                                     Cortical interneurons (CINs) originate in the ganglionic eminence
110    Here, we generated developmental cortical interneurons (cINs)-which are known to be affected in sc
111                                     Although interneuron classes have unique functional properties an
112 d activity dynamics of the major hippocampal interneuron classes in behaving animals.
113                                   Inhibitory interneurons comprise a fraction of the total neurons in
114 Parvalbumin-expressing striatal fast-spiking interneurons comprise ~1% of the total neuronal striatal
115  non-associative reorganization of pyramidal-interneuron connections triggered by the optogenetic mod
116 ies closely resembling those of fast-spiking interneurons, consistent with previous transcriptomic fi
117                            Since hippocampal interneurons control information processing, we tested w
118 lbumin- (PV) and somatostatin-(SST) positive interneurons control sound-evoked responses, temporal ad
119 e with highly restricted expression to PV(+) interneurons: Cox6a2, which codes for an isoform of a cy
120 , GPe cells (actor) and striatal cholinergic interneurons (critic) while monkeys performed a classica
121 l cord regions harboring Mc4r-expressing V2a interneurons, crucial components of the premotor network
122                             Although altered interneuron development and function are clearly demonst
123 eract with extracellular signals to regulate interneuron development is poorly understood.
124                                    Embryonic interneuron development underlies cortical function and
125                                   Individual interneurons did not display sustained firing but instea
126 e find that cell-autonomous mutations within interneurons disrupts morphophysiological development of
127 ethargus, altered activity of the locomotion interneurons during lethargus favors strong RIS activati
128 ngs provide evidence that cortical GABAergic interneuron dysfunction plays a key role in sensory hype
129 normalizing the function of GABAergic and PV interneurons, EA may represent a promising therapeutic s
130 1, GluA2, GluA3 selectively from MGE derived interneurons early in development.
131 is a segmentally arranged network of sensory interneurons electrically coupled to the central medial
132 s provides a potential circuit basis for SST interneuron-evoked disinhibition of medial prefrontal co
133                      We found desynchronized interneuron firing between the CA1 and dentate gyrus in
134 l medial giant fiber (MGF), the command-like interneuron for head withdrawal.
135 ransmembrane proteins that select inhibitory interneurons for survival and modulate the extent of PCD
136 s in distinct subpopulations of somatostatin interneurons from early postnatal stages of cortical dev
137  show that networks of striatal fast-spiking interneurons (FSIs) are capable of generating delta/thet
138 medium spiny neurons (MSNs) and fast-spiking interneurons (FSIs) encoded such information and that pr
139 realizing this enhancement uses fast spiking interneurons (FSIs) in the striatum to train striatal pr
140                         Molecules regulating interneuron function under redox control include NMDA re
141          Chemogenetic inhibition of all GABA interneurons (Gad1+), as well as Sst+ and Pvalb+ subtype
142 on-divergent circuit: cone -> midget bipolar interneuron -> midget ganglion cell (the "private line")
143 NCE STATEMENT NMDAR hypofunction in cortical interneurons has been linked to schizophrenia pathophysi
144 sorders in which alterations in PNNs and PV+ interneurons have been described.
145                        Cortical layer 1 (L1) interneurons have been proposed as a hub for attentional
146 izophrenia that exceed those caused by NMDAR interneuron hypofunction alone.SIGNIFICANCE STATEMENT NM
147 how an early NMDAR ablation in corticolimbic interneurons impacts on mPFC and ventral hippocampus fun
148 tracellular accumulation of tau in GABAergic interneurons impairs AHN by suppressing GABAergic transm
149 bsets of all known dendrite targeting CCK(+) interneurons in addition to the expected basket cells, a
150 rive from low-threshold-spiking somatostatin interneurons in adulthood, suggesting a circuit mechanis
151 corticolimbic parvalbumin-positive GABAergic interneurons in Grin1 mutant mice.
152 ngs are the first to suggest a role for NK1R interneurons in itch and extend our understanding of the
153 d that GIN cells account for 44% of the SST+ interneurons in layer II/III and around 35% in layers IV
154  of striatal tyrosine hydroxylase-expressing interneurons in mediating this inhibition.
155                     Chemogenetic blocking PV interneurons in PrL alleviated ACE-enhanced anxiety-like
156 red GABAergic neurotransmitter system and PV interneurons in PrL.
157 wever, little is known about the role of VIP interneurons in Rett Syndrome.
158 ted that alterations in parvalbumin-positive interneurons in schizophrenia are the consequence of a d
159 rt a critical role for both PV(+) and SST(+) interneurons in slow hippocampal gamma oscillations, and
160                       Nonpyramidal GABAergic interneurons in the basolateral nuclear complex (BNC) of
161 nnervating synaptic connections in GABAergic interneurons in the brain.
162 hat KA stimulated the activity of inhibitory interneurons in the CA1 hippocampus (P = 0.04) which fai
163 umulation of phosphorylated tau in GABAergic interneurons in the dentate gyrus (DG) of AD patients an
164 ork are the natural substrates for GABAergic interneurons in the developing mouse forebrain, and prov
165  we identified three categories of potential interneurons in the GAD67-GFP line (GABA+GFP ~45%, GABA+
166 ting different roles for EGCs than analogous interneurons in the MOB.SIGNIFICANCE STATEMENT The mouse
167  inhibitory outputs and excitatory inputs of interneurons in the mouse cerebral cortex, respectively.
168 ap in vivo activity onto multiple classes of interneurons in the mouse hippocampal area CA1 during he
169 cal, and transcriptomic features to classify interneurons in the mouse visual cortex, this work provi
170  approach to determine if inhibition of GABA interneurons in the mPFC of male mice is sufficient to p
171 ow the vHPC engages different populations of interneurons in the PFC.
172 t the visual pathway and in the structure of interneurons in the primary visual cortex.
173                         Stimulation of these interneurons in the rat model rescued turning performanc
174 s (vLGN) or parabigeminal nucleus (PBG), and interneurons in the stratum griseum superficiale (SGS) t
175 h cells (UBCs) are excitatory granular layer interneurons in the vestibulocerebellum.
176 elieved to be mediated by inhibition of GABA interneurons in the VTA that subsequently leads to disin
177 n the present study, we explored the role of interneurons in this circuit.
178 enting a fraction of mainly upper layer SST+ interneurons in various cortical areas, were recently cl
179  changes and abnormal allocation of cortical interneurons in vivo These data suggest that JNK signali
180 population assemblies.SIGNIFICANCE STATEMENT Interneuron (IN) diversity empowers the spinal cord with
181 ecystokinin (CCK), released from dentate CCK interneurons, in regulating neurogenic niche cells and N
182  wiring of specific populations of GABAergic interneurons, in which it paradoxically regulates both t
183 o abundant populations of cortical GABAergic interneurons include the low-threshold, somatostatin (SS
184                                  Many spinal interneurons, including those identified as projecting t
185 ns that synthesize tyramine, the RIM and RIC interneurons, induced intestinal UPR(ER) activation and
186 ynaptic mu-opioid stimulation of local PV(+) interneurons induces a long-lasting suppression of GABAe
187 cuit motifs including reciprocal (inhibitory interneurons inhibiting other interneurons) and feedforw
188 er interneurons) and feedforward (inhibitory interneurons inhibiting principal neurons) connections,
189 d that increased excitability of presynaptic interneurons (INs) and decreased intrinsic excitability
190                                          How interneurons (INs) in the dorsal horn encode these modal
191 as well as inhibitory parvalbumin-expressing interneurons (INs).
192                                   Inhibitory interneurons integrate into developing circuits in speci
193      How a dysfunction of GABAergic cortical interneurons interacts with maturation during adolescenc
194 cation: an initial cardinal step, allocating interneurons into a few major classes, followed by defin
195 ation likely hinder the integration of PV(+) interneurons into cortical neuronal circuits, leading to
196 termination, reflecting the incorporation of interneurons into functional circuit ensembles.
197   Transplantation of human stem cell-derived interneurons is a promising cell-based therapy for treat
198 ng in parvalbumin-expressing (PV) inhibitory interneurons is critical for visual cortical plasticity.
199            The precise migration of cortical interneurons is essential for the formation and function
200 tional connectivity between abDGCs and local interneurons is required to understand their development
201 on factors in fate specification of cortical interneurons is well established, how these interact wit
202 te progenitor cells, excitatory neurons, and interneurons isolated from mid-gestational samples of th
203  Hpse+ layer IV cells targeting parvalbumin+ interneurons, leading to quantitative alterations in the
204 rential deletion of Shank3 in vS1 inhibitory interneurons led to pyramidal neuron hyperactivity and i
205 r neuropils via parallel pathways, and local interneurons (LNs), which provide lateral processing wit
206                                              Interneuron loss correlates with reduced AKT signaling i
207 elay, further implicating mitotic defects in interneuron loss.
208 ate that activation of cortical somatostatin interneurons may constitute a less invasive alternative
209 soactive intestinal peptide-expressing (VIP) interneurons may play a critical role in the proper deve
210  parvalbumin- and cholecystokinin-expressing interneurons mediate distinct features of pyramidal cell
211    LFPI caused a reduction in the numbers of interneurons mediating both perisomatic and dendritic in
212 otor cortex (M1) appear to activate distinct interneuron networks that contribute differently to two
213                                   Inhibitory-interneuron networks, consisting of multiple forms of ci
214  Magoh homozygotes, p53 loss fails to rescue interneuron number and mitotic delay, further implicatin
215 ergic neurons and parvalbumin (PV) GABAergic interneurons of Ahnak KO mice.
216 tor-mediated transmission in molecular layer interneurons of the mouse cerebellum.
217 ls, and impaired fear-induced activity of PV interneurons only in the right BLA.
218             These separate populations of L1 interneurons participate in different inhibitory network
219 tudies found that two most common inhibitory interneurons, parvalbumin- (PV) and somatostatin-(SST) p
220                 Parvalbumin-expressing (PV+) interneurons play a key role in the maturation and synch
221 implicate the minority striatal fast-spiking interneuron population as a key component of compulsive
222 a molecular basis for controlling inhibitory interneuron population size during circuit formation.
223 target neuron is reflected in VIP(+)/ChAT(+) interneuron pre-synaptic terminals, as quantitative mole
224 e xenograft studies, human stem cell-derived-interneuron precursors could differentiate in vivo, but
225 4R/V gliomas are neuronal malignancies where interneuron progenitors are stalled in differentiation b
226 synaptic organization of SST and parvalbumin interneurons provides a potential circuit basis for SST
227 ruption of parvalbumin-expressing inhibitory interneurons (PV) in the auditory cortex.
228                       Parvalbumin-expressing interneurons (PV-INs) are highly vulnerable to stressors
229 ive principal cells and parvalbumin-positive interneurons (PV-INs) was higher in Scn1a+/- relative to
230  and LVb) as well as fast-spiking inhibitory interneurons receive direct excitatory input from the in
231   Chemogenetic activation of DLS parvalbumin interneurons reduces the elevated lever pressing of GEE
232 genetic basis of brain function is shaped by interneuron-related transcripts and may capture individu
233 we demonstrate that reductions of inhibitory interneurons result from elevated apoptosis during the c
234  that Arid1b haploinsufficiency in PV or SST interneurons resulted in distinct features that do not o
235 natal ablation of the NMDAR in corticolimbic interneurons results in an overactive but desynchronized
236 veal, in adult zebrafish, a logic of the V2a interneuron rhythm-generating circuits involving recurre
237                             We show that SST interneuron-selective overexpression of Lypd6, an endoge
238 n in Q175 mice at 18 months, but cholinergic interneurons showed dendrite attenuation by 6 months.
239 BA(B)Rs, while optogenetic activation of the interneurons shows that their inhibitory output is also
240 its that encompass excitatory and inhibitory interneurons, similarly to those driven by sensory exper
241 maintaining this balance is the somatostatin interneuron (SOM-IN) feedback microcircuit.
242 We present our updated three-stage model for interneuron specification: an initial cardinal step, all
243 ons (L5-6_Fezf2 and L2-3_Cux2) and GABAergic interneurons (Sst and Pvalb), whereas other subtypes in
244 rthermore, it is critical to determine which interneuron subtypes contribute to distinct behavioral p
245  and spatial distributions, the influence of interneuron subtypes on brain function, cortical special
246 nnectivity relationships with specific local interneuron subtypes, suggesting that the CSDn influence
247 onal nets surrounding parvalbumin expressing interneurons, suggesting that these plasticity-related m
248         Patch-clamp recordings from cortical interneurons supported these predictions, and further in
249  While clozapine N-oxide (CNO) activation of interneurons suppressed firing of pyramidal cells, unexp
250 ed Protocadherins (cPCDHs) control GABAergic interneuron survival during developmentally-regulated ce
251 genome-wide association study identified the interneuron synaptic gene ELFN1 as conferring significan
252 ndelier cells (ChCs) are a type of GABAergic interneuron that control pyramidal cell output through a
253 usly unidentified group of catecholaminergic interneurons that are apt to sense changes in GH levels
254                              PyrNs are local interneurons that form two stratified dendritic arbors a
255  Amacrine cells (ACs) are a diverse class of interneurons that modulate input from photoreceptors to
256 AT(+) neurons in mice are specialized VIP(+) interneurons that release GABA strongly onto other inhib
257                    These are mostly the same interneurons that were previously shown (using a differe
258  drive from local cholecystokinin-expressing interneurons, the activity of which is required for disc
259  neurons, suggesting that they interact with interneurons to act as excitatory pacemakers for the V1
260 istently constrain the ability of spinal DYN interneurons to limit ascending nociceptive transmission
261 ated parvalbumin (PV) and somatostatin (SST) interneurons to map the timing and strength of inputs to
262 ing cell, which is one of the first types of interneurons to migrate into the cerebral cortex and bec
263       The cell surface molecules that select interneurons to survive or die are unknown.
264 ty preference for cholecystokinin-expressing interneurons to target calbindin-expressing principal ce
265 which together decouple the responses of the interneurons to the training odorants to generate learne
266      A highly connected downregulated set of interneuron transcripts is present in the most significa
267  states, while highlighting the potential of interneuron transplantation as an autism therapy.
268              These findings demonstrate that interneuron transplantation can exert therapeutic behavi
269                                              Interneuron transplantation can thus correct behavioral
270                   Our findings indicate that interneuron transplantation could offer a novel cell-bas
271  the behavioral and physiological effects of interneuron transplantation in a mouse genetic model of
272              It is unknown, however, whether interneuron transplantation may be therapeutically effec
273 subcortical innovation: an abundant striatal interneuron type in primates that had no molecularly hom
274                                     One such interneuron type is the low-threshold, somatostatin (SST
275 ion of the AII depends primarily on a single interneuron type, the NOS-1 AC: a multistratified, axon-
276  in different mammalian species and specific interneuron types is poorly known.
277 ircuits is generated by phylogenetically old interneuron types, complemented by an evolutionary incre
278 vation of associative cortex targets several interneuron types, modulating dynamics and influencing p
279                                   Homologous interneuron types-which were readily identified by their
280 ng the number of synaptic contacts from both interneuron types.
281              During early development, these interneurons undergo long-range migration from germinal
282 from parvalbumin and somatostatin expressing interneurons undergo long-term depression and potentiati
283 )-impermeable AMPARs on parvalbumin-positive interneurons underlying circuit dysfunction in SYNGAP1 h
284 al role of COX6A2 in energy balance of PV(+) interneurons, underscored by a decrease in the ATP-to-AD
285    In the cerebellar cortex, molecular layer interneurons use chemical and electrical synapses to for
286 apitulating this transient activation of SST interneurons using chemogenetics similarly enhanced V1 p
287   We observed that the number of MGE-derived interneurons was preserved in mature hippocampus despite
288 uction in SP+ striatal perikarya or striatal interneurons was seen in Q175 mice at 18 months, but cho
289 lution, vHPC input onto prefrontal GABAergic interneurons was specifically disrupted, whereas input o
290 pressed for most projection neurons, whereas interneurons were strongly activated at a latency preced
291 d hmx3a are coexpressed in spinal dI2 and V1 interneurons, whereas hmx3b, hmx1, and hmx4 are not expr
292                              The PVC command interneurons, which are known to promote forward locomot
293  in vitro These afferents engage cholinergic interneurons, which drive dopamine release from dopamine
294 d that POA(PAG) neurons directly inhibit PAG interneurons, which in turn inhibit PAG-USV neurons, whe
295 ional, innervating thalamocortical and local interneurons while also receiving synapses from the reti
296 e were heterogenous changes in the number of interneurons while motor cortex, showed no obvious loss
297 lassical Golgi staining studies did not find interneurons with locally ramifying axons in the LH [11,
298 and vasoactive intestinal peptide-expressing interneurons with long-range cortical networks.
299  areas comprise multiple types of inhibitory interneurons, with stereotypical connectivity motifs tha
300 ic transmission, especially parvalbumin (PV) interneurons within PrL in the development of ACE-induce

 
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