ライフサイエンスコーパス: PFC

1 PFC activation suppressed social behavior and modulated

2 PFC spontaneous default activity is altered in neuropsyc

3 PFC-thalamic anatomical connectivity may be an important

4 we address three common misconceptions: (1) PFC lesions do not affect subjective perception; (2) PFC

5 ons do not affect subjective perception; (2) PFC activity does not reflect specific perceptual conten

6 reflect specific perceptual content; and (3) PFC involvement in studies of perceptual awareness is so

7 model mice display substantial deficits in a PFC-dependent task.

8 ity were attenuated in patients, revealing a PFC-independent, alpha-beta system.

9 Accuracy, PFC low-theta activity, and PFC --> parieto-occipital co

10 We then assessed how altering adolescent PFC dopamine axon growth changes the structural and func

11 ore, focal knockdown of cacna1c in the adult PFC recapitulated the social deficit and elevated anxiet

12 etary methyl donor supplementation can alter PFC-dependent cognitive behaviors.

13 These indicate abnormalities in amygdala-PFC FC and further support the importance of the interac

14 Additionally, the alterations in amygdala-PFC FC may underlie the initial similarities observed be

15 Accuracy, PFC low-theta activity, and PFC --> parieto-occipital connectivity were attenuated i

16 of the interaction between the amygdala and PFC in adolescents and young adults with these disorders

17 rdings shows that, during DMC tasks, LIP and PFC neurons demonstrate mixed, time-varying, and heterog

18 art preferred similar spatial locations, and PFC neurons up to approximately 700 mum apart preferred

19 ference between mnemonic encoding in PPC and PFC is associated with the presence of functional cluste

20 e presence of functional clustering: PPC and PFC neurons up to approximately 700 mum apart preferred

21 (15-30 Hz) activity decreased in the STN and PFC, and this decrease was progressively enhanced as mor

22 ctivity, dopaminergic inputs to striatum and PFC can elicit divergent behavioral effects.

23 Information transfer between V1 and PFC was reduced bidirectionally, but with a stronger dec

24 ealed negative coupling between the anterior PFC and the VS in the treatment context, suggesting that

25 (NR3C2) genes in the prefrontal cortex area (PFC) and central nucleus of the amygdala (CeA) in monkey

26 ned this principle in the association areas, PFC, and ventral intraparietal area of rhesus monkeys an

27 wise approaches, and the association between PFC-thalamic anatomical connectivity and severity of exe

28 f erosion during pulsed heat loading between PFC candidate materials will ensure that future fusion d

29 n can prevent the social deficits induced by PFC activation.

30 CA1-PFC synchronization was stronger during awake SWRs, and

31 Finally, awake CA1-PFC reactivation was enhanced most prominently during in

32 s accumbens to the PFC and profoundly change PFC structural and functional development.

33 upon other protein fragment complementation (PFC) approaches by offering both multidimensionality and

34 to the surrounding plasma-facing components (PFCs).

35 ocused on the key role of prefrontal cortex (PFC) [1-8].

36 c profiling approaches on prefrontal cortex (PFC) and hippocampal (HPC) tissue from Df(16)A(+/-) mice

37 holine is released in the prefrontal cortex (PFC) and is a key modulator of cognitive performance in

38 on processing between the prefrontal cortex (PFC) and thalamus, particularly the mediodorsal nucleus.

39 The amygdala and prefrontal cortex (PFC) appear to have critical roles in these disorders; h

40 urenic acid (KYNA) in the prefrontal cortex (PFC) are thought to contribute to the development of cog

41 2 receptors (D2Rs) in the prefrontal cortex (PFC) are thought to play important roles in behaviors, i

42 DAR GluN2D subunit in the prefrontal cortex (PFC) as compared to ANAs while the two phenotypes expres

43 cleus accumbens (NAc) and prefrontal cortex (PFC) associated with time-dependent increases in food cr

44 howed reduced GBCr in the prefrontal cortex (PFC) but increased GBCr in the posterior cingulate, prec

45 4 receptor upregulated in prefrontal cortex (PFC) but not striatum or hippocampus where CK2alpha is a

46 Is activity in prefrontal cortex (PFC) critical for conscious perception?

47 ychopathologies involving prefrontal cortex (PFC) dysfunction.

48 ally been associated with prefrontal cortex (PFC) dysfunction.

49 ng intraoperative STN and prefrontal cortex (PFC) electrophysiology as participants perform a novel t

50 wever, whereas descending prefrontal cortex (PFC) fibers in primates form a well defined and topograp

51 are observed in the mouse prefrontal cortex (PFC) following chronic exposure to stress.

52 Dopaminergic input to the prefrontal cortex (PFC) increases throughout adolescence and, by establishi

53 The prefrontal cortex (PFC) is a crucial hub for the flexible modulation of rec

54 The prefrontal cortex (PFC) is crucial for accurate memory performance when pri

55 neuron maturation in the prefrontal cortex (PFC) is crucial for cognitive development.

56 The prefrontal cortex (PFC) is thought to flexibly regulate sensorimotor respon

57 abnormal elevation in the prefrontal cortex (PFC) is thought to impair cognitive functions in individ

58 The prefrontal cortex (PFC) is thought to play a critical role in behavioral fl

59 opaminergic modulation of prefrontal cortex (PFC) is thought to play key roles in many cognitive func

60 t microstimulation in the prefrontal cortex (PFC) modulates the gain of the PLR, changing how a simpl

61 DA and AMPA) responses in prefrontal cortex (PFC) neurons and used pharmacological and genetic interv

62 allopregnanolone, in the prefrontal cortex (PFC) of D1CT-7 mice.

63 pathway analysis from the prefrontal cortex (PFC) of male rats revealed changes in several genes asso

64 n of cacna1c in the adult prefrontal cortex (PFC) of mice recapitulates the antidepressant-like effec

65 rea (VIP) and the lateral prefrontal cortex (PFC) of rhesus monkeys.

66 , but not the infralimbic prefrontal cortex (PFC) or dorsal raphe nucleus (DRN), prevented disruption

67 er dopaminergic inputs to prefrontal cortex (PFC) play similar or distinct roles.

68 ch is that neurons in the prefrontal cortex (PFC) retain stimulus-specific information when vibrotact

69 optogenetic activation of prefrontal cortex (PFC) terminals in the NAc are similarly modulated by act

70 gnals in the ventromedial prefrontal cortex (PFC) tracked the latent growth of cumulative economic ou

71 The prefrontal cortex (PFC) underlies higher cognitive processes that are modul

72 n in pyramidal neurons of prefrontal cortex (PFC) was diminished in SHR, which was correlated with th

73 cal connectivity with the prefrontal cortex (PFC), and decreased MD-PFC connectivity is observed in s

74 the mTORC1 pathway in the prefrontal cortex (PFC), and that infusion of the selective mTORC1 inhibito

75 ic deficits in the medial prefrontal cortex (PFC), contributing to development of anxiety- and depres

76 Perturbations in the prefrontal cortex (PFC), hippocampus, and amygdala are implicated in the de

77 se and nonresponse in the prefrontal cortex (PFC), nucleus accumbens, hippocampus, and amygdala.

78 In the prefrontal cortex (PFC), PV(+) neuron activity is involved in cognitive fun

79 de attention in the mouse prefrontal cortex (PFC), that the mediodorsal thalamus sustains these repre

80 two receptors within the prefrontal cortex (PFC), with D2 receptors enabling flexible decision makin

81 lurane in area V1 and the prefrontal cortex (PFC)-as predicted by our alternative hypothesis.

82 ht to be supported by the prefrontal cortex (PFC).

83 proved by nicotine is the prefrontal cortex (PFC).

84 bout their projections to prefrontal cortex (PFC).

85 f the dorsal premotor and prefrontal cortex (PFC).

86 e brain, particularly the prefrontal cortex (PFC).

87 or processing through the prefrontal cortex (PFC).

88 tric disorders, including prefrontal cortex (PFC).

89 ergic function within the prefrontal cortex (PFC).

90 imbic circuits, including prefrontal cortex (PFC).

91 processing and altered prefrontal cortical (PFC) structure and activity.

92 ay represent an important part of descending PFC pathways that control social behavior.

93 Our results show that the descending PFC fibers in the rat form WM fascicles embedded within

94 nce from neurological patients with discrete PFC damage that challenges the dominant models attributi

95 consistent with models implicating disrupted PFC-thalamic connectivity in the pathophysiology of schi

96 r findings reveal neurologically dissociable PFC and parieto-occipital systems and suggest that paral

97 tive control network [e.g., dorsolateral (dl)PFC], and a salience network (e.g., insula).

98 onist carbachol onto neurons in dorsolateral PFC (DLPFC) of male rhesus macaques performing rule-guid

99 also detected in the postmortem dorsolateral PFC of individuals with depression.

100 mygdala and ventral PFC (VPFC), dorsolateral PFC (DLPFC), and dorsal anterior cingulated cortex (dACC

101 ior cingulate cortex, precuneus, dorsomedial PFC, and amygdala.

102 nd local field potentials in the dorsomedial PFC (dmPFC) of male rats during a set-shifting task that

103 philic triblock copolymer which can emulsify PFCs and be cross-linked.

104 he PFC during a Go/No-Go task, which engages PFC-mediated executive control.

105 ral deficits in adolescent SHR and enhancing PFC activity could be a treatment strategy for ADHD.

106 nsistent with this notion, broadly enhancing PFC excitability diminishes rule specificity and behavio

107 ice with altered nAChR gene function exhibit PFC-dependent behavioral deficits, but it is unknown how

108 oscillations, which provide a mechanism for PFC to communicate with posterior cortical regions [13],

109 Fourteen PFC patients and 20 healthy, age-matched controls perfor

110 tly subserve communications both to and from PFC-uncovering parallel oscillatory mechanisms for worki

111 e over PFC and directional connectivity from PFC to parieto-occipital regions commensurate with execu

112 ctionally, but with a stronger decrease from PFC to V1.

113 Furthermore, PFC-associated deficits are rescued by initiating produc

114 most promising candidate material for future PFCs, concerns over the thermal shock performance during

115 The literature highlights PFC's essential role in enabling the subjective experien

116 a PKA-dependent manner, whereas hippocampal-PFC projections involved in SWM were not affected in Oph

117 How PFC ensembles represent shifts in behavior in response t

118 ors in the infralimbic prefrontal cortex (IL-PFC) facilitates learning during extinction of cue-condi

119 Systemic and intra-IL-PFC treatment with apamin (KCa2 channel allosteric inhib

120 Positive modulation of IL-PFC KCa2 channels significantly attenuated mGlu5-depende

121 n learning and synaptic plasticity in the IL-PFC involves functional inhibition of KCa2 channels.

122 litation of long-term potentiation in the IL-PFC.

123 reduced KCa2 channel currents in layer V IL-PFC pyramidal neurons, confirming functional downregulat

124 iatric-related disease symptoms via impaired PFC function.

125 est that the disrupted function of AMPARs in PFC may underlie the behavioral deficits in adolescent S

126 a shift to excitatory-inhibitory balance in PFC neural activity.

127 valuated the consequences for E/I balance in PFC pyramidal neurons as well as cognition, social inter

128 hibitory interneurons and pyramidal cells in PFC and VIP.

129 hiatric diseases that involve impairments in PFC-dependent behaviors.

130 ted by postsynaptic AMPAR internalization in PFC pyramidal cells, and we observed a profound impairme

131 ty for motion direction was only observed in PFC.

132 try and cellular actions for D3 receptors in PFC.SIGNIFICANCE STATEMENT The D3 dopamine receptor, a m

133 tigated the contribution of KOR signaling in PFC-driven heterosynaptic suppression of HP inputs onto

134 e decrease in source entropy was stronger in PFC compared to V1.

135 vity between six cortical regions, including PFC, and the thalamus.

136 ory recall in COMT-Val-tg mice and increased PFC dopamine levels.

137 d that nicotine can differentially influence PFC pyramidal cell activity by nAChR modulation of layer

138 pathways was achieved using unilateral intra-PFC infusions of DA antagonists combined with contralate

139 Crucially, the STN and lateral PFC beta decrease was significantly attenuated during th

140 hanges were associated with increase lateral PFC-STN coherence and altered STN neuronal spiking.

141 etamine showed increased GBCr in the lateral PFC, caudate, and insula.

142 he mediodorsal thalamus connected to lateral PFC.

143 altered connectivity to the ventral lateral PFC (vlPFC) and local circuitry in MDD.

144 h spinal (LC(:SC)) or prefrontal cortex (LC(:PFC)) projections.

145 By contrast, activation of LC(:PFC) exacerbated spontaneous pain, produced aversion and

146 sed anti-nociception while activation of LC(:PFC) produced aversion.

147 a short latency (50 ms) following burst-like PFC electrical stimulation, and the magnitude of this su

148 cifically, mediodorsal input amplifies local PFC connectivity, enabling rule-specific neural sequence

149 ate mouse lines, we found that in the mature PFC, both ChCs and BCs are abundant in superficial layer

150 Since the causal relationships between MD-PFC abnormalities and cognitive impairment, as well as t

151 he prefrontal cortex (PFC), and decreased MD-PFC connectivity is observed in schizophrenia patients.

152 s that provide a new understanding on how MD-PFC circuits support higher-order cognitive function.

153 nal interactions between mouse MD and medial PFC (mPFC), with MD-to-mPFC supporting working memory ma

154 the prelimbic (PLmPFC) or infralimbic medial PFC (ILmPFC).

155 e these, we assessed the influence of medial PFC (mPFC) activity on spatial learning and hippocampal

156 e mTORC1 inhibitor rapamycin into the medial PFC (mPFC) blocks the antidepressant behavioral actions

157 ted knockdown of neuronal CSF1 in the medial PFC attenuated microglia-mediated neuronal remodeling an

158 neuron-microglia interactions in the medial PFC during development of anxiety- and depressive-like b

159 a-mediated neuronal remodeling in the medial PFC, contributing to synaptic deficits and development o

160 n pyramidal neurons in layer 1 of the medial PFC.

161 ng and dendritic spine density in the medial PFC.

162 nce imaging was combined with hM3Dq-mediated PFC activation to identify novel nodes in the "social br

163 We show here that in mouse models PFC dysfunction in Fragile X Syndrome (FX) can be attrib

164 KORDi were used to bidirectionally modulate PFC activity and measure social behavior and global func

165 TG2 levels are increased in the post-mortem PFC of depressed suicide subjects relative to matched co

166 -218 in pyramidal neurons of human and mouse PFC.

167 ayer 5 glutamatergic pyramidal cell in mouse PFC (either sex).

168 Remarkably, upregulation of Dcc in mouse PFC pyramidal neurons causes vulnerability to stress-ind

169 on of glutamatergic principal cells in mouse PFC that largely lack expression of D1 or D2 receptors.

170 ver, the overexpression of TrkB in the mouse PFC ameliorated the depressive-like phenotype of TG2-ove

171 hCs and BCs in different layers of the mouse PFC, and found that, from early postnatal age, ChCs and

172 plicated in successful execution of multiple PFC-dependent behaviors in both animal research and the

173 self-stimulation sustained by activation of PFC afferents in the NAc.

174 Activation of PFC pyramidal neurons with a CaMKII-driven Gq-coupled de

175 Rs and KORs resulted in complete blockade of PFC-induced heterosynaptic suppression of less salient H

176 KYNA attenuated the inhibitory component of PFC LFP responses, a disruption that resulted from local

177 ophrenia because proper GABAergic control of PFC output is one key mechanism for supporting such cort

178 Bidirectional modulation of PFC activity further refined this subset of brain region

179 Disrupting D2 (but not D1) modulation of PFC-->BLA circuitry impaired adjustments in decision bia

180 In contrast, disrupting D1 modulation of PFC-->NAc networks reduced risky choice, attenuating rew

181 lity that DA may act on separate networks of PFC neurons that are modulated by D1 or D2 receptors and

182 y acting on different functional networks of PFC neurons that can be distinguished by the subcortical

183 MR to quantitatively measure the presence of PFC-labeled CAR T cells, followed by histological valida

184 activity within the amygdala and regions of PFC known a priori to be involved in the cognitive contr

185 make distinct predictions about the role of PFC, providing an opportunity to arbitrate between these

186 hypothesized that cholinergic stimulation of PFC during performance of a cognitive task would augment

187 As behavior was updated, a subset of PFC ensembles encoded the current trial outcome before t

188 ed the hypothesis that cortical thickness of PFC regions and gray matter volume of the hippocampus an

189 Erosion and splashing of PFCs can contaminate the plasma and shorten material lif

190 These results establish local eCB actions on PFC terminals within the NAc that inhibit mesolimbic DA

191 llatory activity in the low-theta range over PFC and directional connectivity from PFC to parieto-occ

192 ansgene were labeled with a perfluorocarbon (PFC) emulsion ex vivo and infused into immunocompromised

193 low-boiling point (low-bp) perfluorocarbons (PFCs) at physiological temperatures by an amphiphilic tr

194 re of hippocampal (area CA1) and prefrontal (PFC) activity recorded across behavior and sleep stages

195 rom posterior parietal (PPC) and prefrontal (PFC) cortices in two male monkeys that performed spatial

196 ter apamin microinfusions into the prelimbic PFC.

197 ckness was evaluated both within an a priori PFC mask (small-volume corrected) and using an explorato

198 narily subthreshold relapse trigger in a PrL-PFC CB1R activation-dependent manner.

199 within the prelimbic prefrontal cortex (PrL-PFC) to potentiate reinstatement.

200 inoid mobilization, which can disinhibit PrL-PFC projection neurons, we investigated whether cannabin

201 Finally, PrL-PFC AM251 microinfusions (300 ng/side, 15-min pretreatme

202 Reduced PFC-thalamic connectivity in schizophrenia correlated wi

203 In contrast to reduced PFC-thalamic connectivity, thalamic connectivity with so

204 lular actions for D3 receptors in regulating PFC networks.

205 ction in the PFC of adult FX animals rescues PFC function.

206 proteomic brain profiling analysis revealed PFC and HPC changes in various molecular pathways associ

207 isruption of D1 or D2 modulation of separate PFC output pathways was achieved using unilateral intra-

208 n from developmental dysregulation, and that PFC function can be restored in the adult FX brain.SIGNI

209 These results demonstrate that PFC neurons support flexible rule-based action selection

210 ere rewarded pseudorandomly, indicating that PFC neurons are not merely providing an expectancy signa

211 We show that PFC cells recorded from male and female rhesus macaques

212 onditional restoration mice, suggesting that PFC dysfunction may persist as long as FMRP is absent an

213 ior cortical regions [9-12], suggesting that PFC engagement during working memory is dependent on the

214 The PFC patients still demonstrated task proficiency, which

215 operant testing, progressive ratio, and the PFC-dependent 5-choice serial reaction timed task (5-CSR

216 tonic GlyR currents in the striatum and the PFC.

217 suggest that control structures such as the PFC can add complexity and flexibility to even a basic b

218 ity that anatomical connectivity between the PFC and mediodorsal thalamus may be 1) reduced in schizo

219 ted a pattern of dysconnectivity between the PFC/subcortex and the rest of the brain in MDD, which ap

220 egulation of a basic brainstem reflex by the PFC.SIGNIFICANCE STATEMENT The pupil light reflex (PLR)

221 ce for glutamatergic inputs arising from the PFC and limbic regions, such as the hippocampus (HP).

222 LHb) receives direct synaptic input from the PFC and that activation of LHb neurons or the PFC inputs

223 ed to the continued absence of FMRP from the PFC, independent of FMRP status during development.

224 Furthermore, the PFC E/I balance has been implicated in successful execut

225 Our analyses highlight the PFC as a key site of common transcriptional regulation b

226 ts (1) are due to the absence of FMRP in the PFC alone and (2) are not the result of developmental dy

227 knock-out mice to eliminate FMRP only in the PFC alone of adult mice.

228 tudy 2, we measured Nr3c2 mRNA levels in the PFC and CeA of dependent and nondependent rats and the c

229 nd may contribute to GABA dysfunction in the PFC and hippocampus of patients with schizophrenia.

230 Ketamine significantly increased GBCr in the PFC and reduced GBCr in the cerebellum.

231 of rapamycin signalling were detected in the PFC and with glutamatergic signalling in the hippocampus

232 of neurons and reduced levels of TrkB in the PFC as well as a depressive-like phenotype.

233 ption reduced dendritic spine density in the PFC at both time points.

234 sion (LTD) of excitatory transmission in the PFC at inputs from the basolateral amygdala.

235 the degree of GABAergic dysregulation in the PFC could be a clinically relevant contributing factor f

236 nal magnetic resonance imaging signal in the PFC during a Go/No-Go task, which engages PFC-mediated e

237 Dopamine in the PFC is implicated in both these processes and genetic va

238 DCC and whether changes in DCC levels in the PFC lead to vulnerability to depression-like behaviors.

239 Neural activity in the PFC must thus be specialized to specific tasks while ret

240 the inhibitory action exerted by KYNA in the PFC occurred primarily at local GABAergic synapses throu

241 mbining localized excitotoxic lesions in the PFC of a nonhuman primate and functional neuroimaging ([

242 ermore, initiation of FMRP production in the PFC of adult FX animals rescues PFC function.

243 nd local field potential oscillations in the PFC of behaving rats.

244 rophysiological and molecular studies in the PFC of cacna1c fbKO mice revealed higher E/I ratio in la

245 y Akt, revealed higher nuclear levels in the PFC of cacna1c HET mice that was further increased follo

246 tive to the inverse agonist, GR113808 in the PFC of CK2alpha KO mice.

247 s of KYNA alter synaptic transmission in the PFC of male adult rats.

248 n was attributable to cAMP elevations in the PFC secondary to reduced phosphodiesterase 4 activity pr

249 ith AAV-mediated deletion of CK2alpha in the PFC show a robust 'anti-depressed-like' phenotype and di

250 gional specificity to ubiquitous Arf6 in the PFC to modulate human alcohol-drinking behaviors.

251 Concomitantly, microglia in the PFC undergo morphological and functional changes followi

252 promoting allopregnanolone synthesis in the PFC, and corroborate previous clinical results pointing

253 ess-induced anhedonia through actions in the PFC, but the mechanisms by which these receptors act are

254 two major PV(+) neuron subtypes found in the PFC, chandelier cells (ChCs) and basket cells (BCs), are

255 pe and synchronize neuronal ensembles in the PFC, these alterations could contribute to deficits in b

256 rvations may be particularly relevant in the PFC, where D-serine and its converting enzyme are highly

257 ulation of the endocannabinoid system in the PFC.

258 a function thought to occur primarily in the PFC.

259 in a different catabolism of dopamine in the PFC.

260 d resilience-associated transcription in the PFC.

261 ectively overexpressed Sox10 and BRG1 in the PFC.

262 rotein synthesis and higher E/I ratio in the PFC.

263 the excitability of pyramidal neurons in the PFC.

264 ncreased messenger RNA levels of CSF1 in the PFC.

265 reatment responders were most similar in the PFC.

266 sed structure-to-function correlation in the PFC/ACC in the MDD group.

267 is methods and modalities alterations in the PFC/ACC were a common finding, each modality and method

268 structural and functional development of the PFC by quantifying pyramidal neuron morphology and cogni

269 ced thiol-ene cross-linking, the core of the PFC emulsion remains in liquid form even at temperatures

270 n humans and emphasize the importance of the PFC for information maintenance during WM also in humans

271 right inferior frontal gyrus as part of the PFC.

272 ting (SC) pyramidal neurons within L5 of the PFC.

273 FC and that activation of LHb neurons or the PFC inputs to the LHb suppresses social preference.

274 n the treatment context, suggesting that the PFC can suppress the expression of prediction errors in

275 wever, there is increasing evidence that the PFC cannot be dissociated from its main thalamic counter

276 ctopically from the nucleus accumbens to the PFC and profoundly change PFC structural and functional

277 ns continue to grow from the striatum to the PFC during adolescence.

278 ains unknown: it remains unclear whether the PFC can modulate basic reflexes.

279 e we investigate (1) the extent to which the PFC exhibits computationally relevant properties, such a

280 ive of the endocannabinoid system within the PFC, but not in the striatum and hippocampus, which was

281 Thus, PFC projections to the LHb may represent an important pa

282 ominant models attributing working memory to PFC-dependent systems.

283 nnectivity from parieto-occipital regions to PFC, regardless of processing demands.

284 y, with increasing heterogeneity from VIP to PFC.

285 light a mechanism by which strong, transient PFC activity can take precedence over other excitatory i

286 re observed between the amygdala and ventral PFC (VPFC), dorsolateral PFC (DLPFC), and dorsal anterio

287 , the hippocampus, amygdala and ventromedial PFC during conditioning.

288 ited thicker cortex in the left ventromedial PFC (vmPFC) and left precentral gyrus.

289 hippocampus, amygdala, and the ventromedial PFC.

290 Rather, dopaminergic VTA-PFC activity can control whether mice maintain or deviat

291 ncreases in the activity of dopaminergic VTA-PFC fibers.

292 ic nor tonic stimulation of dopaminergic VTA-PFC projections elicited place preference.

293 mary, despite the fact that dopaminergic VTA-PFC projections exhibit phasic increases in activity tha

294 ed these projections and observed phasic VTA-PFC fiber photometry signals after the delivery of rewar

295 Furthermore, substituting phasic VTA-PFC stimulation for food rewards was not sufficient to r

296 habenula as a node robustly correlated with PFC activity.

297 about their distribution or function within PFC.

298 ong an anterior-to-posterior gradient within PFC.

299 ong an anterior-to-posterior gradient within PFC.

300 for a lesser degree of specialization within PFC.