ライフサイエンスコーパス: autoreceptor

1 pporting the role of mGluR8 as a presynaptic autoreceptor.

2 icating DOR may act in part as a presynaptic autoreceptor.

3 e M2 receptor is an inhibitory prejunctional autoreceptor.

4 stream 5-HT(1a) heteroreceptors from that of autoreceptors.

5 ulates raphe 5-hydroxytryptamine 1A (5-HT1A) autoreceptors.

6 ber excitability through activation of GABAB autoreceptors.

7 neurotransmission by derepression of 5-HT1A autoreceptors.

8 ents was further increased after blocking D2-autoreceptors.

9 produced by desensitization of DRN 5-HT(1A) autoreceptors.

10 tions at pre-synaptic metabotropic glutamate autoreceptors.

11 s, and the expression of the Htr1a and Htr1b autoreceptors.

12 mechanism that required Octbeta2R octopamine autoreceptors.

13 ment of desensitization of presynaptic M2/M4 autoreceptors.

14 les lack presynaptic synthesis modulating D2 autoreceptors.

15 that is significantly regulated by dopamine autoreceptors.

16 stimulating group II metabotropic glutamate autoreceptors.

17 inhibited through activation of metabotropic autoreceptors.

18 tsynaptic receptors and synthesis modulating autoreceptors.

19 from the Starburst cell itself, making them autoreceptors.

20 tic inhibition via the activation of GABA(B) autoreceptors.

21 dopamine neurons express D2 and D3 dopamine autoreceptors.

22 y 20 ms) that was mediated by dendritic AMPA autoreceptors.

23 eurotransmitter, are governed by presynaptic autoreceptors.

24 athways remained normal in the absence of D2 autoreceptors.

25 ne neurons through activation of D2 dopamine autoreceptors.

26 that allows for selective ablation of 5-HT1B autoreceptors.

27 al role for the co-expression of D2S and D2L autoreceptors.

28 tion similar to that exhibited by endogenous autoreceptors.

29 ons is under strict control of inhibitory D2 autoreceptors.

30 anisms underlying drug-induced changes in D2 autoreceptors.

31 of the neuronal calcium sensor NCS-1 with D2-autoreceptors.

32 Moreover, they confer midbrain dopamine autoreceptors a hitherto neglected role in the therapeut

33 Loss of D2 autoreceptors abolishes D2-mediated control of DA synthe

34 Mice lacking D2 autoreceptors acquire a cued-operant self-administration

35 Here we report that D2 autoreceptors act chronically to produce an opposite act

36 We show that 5-HT(1A) autoreceptors act to affect anxiety-like behavior.

37 Thus, autoreceptor action on the synaptic response is masked b

38 on-dependent release may occur because of D2 autoreceptor activation by DA that is released via rever

39 Modelling autoreceptor activation during repetitive stimulation re

40 When D2 autoreceptor activation was minimal, the combined effect

41 ame overall time course as in the absence of autoreceptor activation.

42 sponse to impaired serotonin release or less autoreceptor activation.

43 r DA concentrations than are required for D2 autoreceptor activation.

44 To elucidate the long-term effects of D2 autoreceptor activity on dopamine signaling, dopamine ov

45 tion between ethanol and presynaptic GABA(B) autoreceptor activity regulates the ethanol sensitivity

46 n previously possible to manipulate 5-HT(1B) autoreceptor activity selectively without also changing

47 a mixture to reinstate neonatal levels of LC autoreceptor activity to assess the source of NE.

48 viously been possible to manipulate 5-HT(1B) autoreceptor activity without also changing 5-HT(1B) het

49 etween Cav1.3- L-type-Ca(2+) channels and D2-autoreceptor activity, controlled by NCS-1, and indicate

50 pressing neurons also exhibited increased D2 autoreceptor activity.

51 It was further assessed if the alpha2-autoreceptor agonist clonidine (which decreases norepine

52 ed that treatment with a 5-hydroxytryptamine autoreceptor agonist, CGS 12066A, can lower TPH mRNA lev

53 692, consistent with data indicating that D2 autoreceptor agonists increase neurotensin release from

54 The alpha2A-adrenergic autoreceptor (alpha2A-AR) expression was assessed by aut

55 system to independently manipulate 5-HT(1A) autoreceptor and heteroreceptor populations.

56 itionally, it exhibits dual functionality as autoreceptor and heteroreceptor, and this enables H3Rs t

57 ere it functions as a presynaptic inhibitory autoreceptor and heteroreceptor.

58 s linked to cooperative interactions with D2 autoreceptors and associated downstream molecular target

59 D2-autoreceptors and Cav1.3-containing L-type Ca(2+) channe

60 l mutant mice support the suggestion that D2 autoreceptors and dopamine transporters interact to regu

61 ptic mechanisms-such as presynaptic dopamine autoreceptors and dopamine transporters-as well as heter

62 detected elevated messenger RNA levels of D2-autoreceptors and GIRK2 in Parkinson's disease.

63 ovided increased tone on GABA(B) presynaptic autoreceptors and heteroreceptors because blocking GABA(

64 HDPAT (8OH) in a low dose range to stimulate autoreceptors and in this way assess the separate and co

65 etralin) hydrobromide] (DPAT), which acts on autoreceptors and inhibits 5-HT neural activity.

66 cal neuron development that involves GABA(A) autoreceptors and L-type Ca(2+) channels.

67 ing and concurrent activation of presynaptic autoreceptors and postsynaptic targets.

68 xyindoleacetic acid (5-HIAA), fewer 5-HT(1A) autoreceptors and reduced cortical serotonin transporter

69 simultaneous activation of presynaptic NMDA autoreceptors and retrograde signalling by endocannabino

70 rs produce a desensitization of DRN 5-HT(1A) autoreceptors and that this desensitization is responsib

71 functional emergence of LC alpha2 inhibitory autoreceptors and the downregulation of LC alpha1 excita

72 in highly aggressive animals via feedback to autoreceptors and via GABAergic and glutamatergic inputs

73 Dopamine release is regulated by D2 dopamine autoreceptors, and D2 receptor ligands are used to treat

74 tent antagonist of central 2alpha-adrenergic autoreceptors, and heteroreceptors and is an antagonist

75 rs, including voltage-gated ion channels, D2-autoreceptors, and nAChRs.

76 indings suggest an important role for 5-HT1A autoreceptors, and thus DRNshort right arrowNAc 5-HT neu

77 g results in graded inhibition of muscarinic autoreceptor- and glial cell line-derived neurotrophic f

78 ist, yohimbine, or the more selective alpha2-autoreceptor antagonist, idazoxan (Smith et al., 2012).

79 e effect of yohimbine, an alpha-2 adrenergic autoreceptor antagonist, on the extinction of conditione

80 The alpha(2)-adrenergic autoreceptor antagonist, yohimbine (1.0 microM), caused

81 the stria terminalis (BSTv) with the alpha2-autoreceptor antagonist, yohimbine, or the more selectiv

82 ermine whether synthesis modulating dopamine autoreceptors are also affected in an adult atypical man

83 s indicate that synthesis modulating D2-like autoreceptors are functional during the late preweanling

84 pression in mice, we demonstrate that 5-HT1A autoreceptors are necessary for cocaine conditioned plac

85 Differential roles of these isoforms as autoreceptors are poorly understood.

86 ther SSRIs also cause desensitization of the autoreceptor as reported by some rodent studies and whet

87 ors are located on serotonin (5-HT) neurons (autoreceptors) as well as neurons of the respiratory net

88 attributable to the upregulation of RGS4-an autoreceptor-associated, GTPase-accelerating protein.

89 found that inhibition of dorsal raphe 5-HT1A autoreceptors attenuates cocaine self-administration in

90 that the impact of decreased midbrain D2/D3 autoreceptor availability on trait impulsivity is mediat

91 were predicted by diminished midbrain D2/D3 autoreceptor binding and greater amphetamine-induced DA

92 Downregulation of 5-HT1A autoreceptor binding by SSRI treatment of major depressi

93 on of increased dopamine signaling evoked by autoreceptor blockade and cocaine administration allowed

94 erminal dopamine concentrations after global autoreceptor blockade.

95 rease dopamine signaling through presynaptic autoreceptor blockade.

96 rease dopamine signaling through presynaptic autoreceptor blockade.

97 In addition to their roles as autoreceptors, BNST alpha(2A)-ARs suppress glutamatergic

98 5-HT1A autoreceptor BPF in the raphe was reduced 18% on SSRI tr

99 However, the degree of reduction in 5-HT1A autoreceptor BPF was unrelated to improvement in depress

100 gether, the results indicate that the 5-HT1A autoreceptors by being part of a FGFR1-5-HT1A receptor h

101 Under this mechanism, activation of Octss2R autoreceptors by octopamine at octopaminergic neurons in

102 We conclude that presynaptic DA autoreceptors concurrently downregulate release and upre

103 n evoked DA levels were measured to evaluate autoreceptor control mechanisms.

104 ing adaptation extended to a broader loss of autoreceptor control of interneuron spiking.

105 ding is associated with decreased inhibitory autoreceptor control of midbrain dopamine neurons.

106 erneurons was unchanged, but M(4) muscarinic autoreceptor coupling to these same channels was markedl

107 aint stress, animals with increased 5-HT(1B) autoreceptors demonstrated restoration of robust FPS res

108 An increase in somatodendritic 5-HT(1A) autoreceptor density in the dorsal raphe (DR) attenuates

109 nificant inverse relationship wherein 5-HT1A autoreceptor density predicted a notable 30-44% of the v

110 nction in terminal dopamine release and D(2) autoreceptor-dependent currents in dopamine neurons from

111 hways of calcium signaling that regulated D2 autoreceptor-dependent GIRK signaling were identified, w

112 ocaine exposure removed calcium-dependent D2 autoreceptor desensitization in wild type, but not D2S-o

113 n in vitro brain-slices, we observed that D2-autoreceptor desensitization is reduced with postnatal m

114 1A)R internalization might underlie 5-HT(1A) autoreceptor desensitization under SSRI antidepressant t

115 as a possible mechanism underlying 5-HT(1A) autoreceptor desensitization, we examined whether this r

116 After chronic SSRI treatment, 5-HT(1A) autoreceptors desensitize, which allows 5-HT tone elevat

117 Mice lacking 5-HT1B autoreceptors displayed the expected increases in extrac

118 tory and contralateral PDFMEs inhibitory PDF autoreceptors, diurnal PDF release keeps both PDF-depend

119 educes 5-HT release by acting on presynaptic autoreceptors, dose-dependently increased consumption of

120 5-HT1A autoreceptor downregulation is thought to induce transie

121 the hypothesis that stimulation of serotonin autoreceptors during development contributes to the adul

122 tamate activates presynaptic group I mGluRs (autoreceptors) during the repetitive activation of gluta

123 We conclude that low levels of D2 autoreceptors enhance the salience of cocaine-paired cue

124 expressed by midbrain DA neurons function as autoreceptors, exerting inhibitory feedback on DA synthe

125 cells prior to hearing onset requires P2RY1 autoreceptors expressed by inner supporting cells.

126 s suggest that effects of increased 5-HT(1B) autoreceptor expression are dependent on stress context.

127 an inescapable stressor, increased 5-HT(1B) autoreceptor expression attenuated FPS response compared

128 Five-HT1a autoreceptor expression depended transiently on Pet-1, t

129 -1 displays dual activity, repressing 5-HT1A autoreceptor expression in serotonergic raphe cells whil

130 An increase in 5-HT1A inhibitory autoreceptor expression may contribute to the attenuatio

131 We have shown that increased 5-HT(1B) autoreceptor expression reduced anxiety in unstressed an

132 the behavioral effects of increased 5-HT(1B) autoreceptor expression through blockade of transgenic r

133 or the complex relationship between 5-HT(1B) autoreceptor expression, stress, and anxiety behavior.

134 ng blocked the effects of increased 5-HT(1B) autoreceptor expression.

135 Together these data imply a loss of autoreceptor feedback control.

136 nces in DA release arise from differences in autoreceptor feedback.

137 Dysfunctional D2 autoreceptors following repeated drug exposure could lea

138 s support a strategy for antagonizing 5-HT1A autoreceptors for treating cocaine addiction.

139 campus, ethanol enhances presynaptic GABA(B) autoreceptor function and that this interaction reduces

140 Reduced D2 autoreceptor function could lead to enhanced DA signalin

141 ently inhibit transmitter release, but their autoreceptor function has been questioned because endoge

142 WKY rats exhibited changes in anxiety and autoreceptor function only following morphine dependence

143 e differences in dopamine release, reuptake, autoreceptor function or the tissue levels of dopamine a

144 y slowed norepinephrine clearance, decreased autoreceptor function, and elevated anxiety.

145 increases activity by decreasing D2 dopamine autoreceptor function, yet little is known about the mec

146 release probability deviates from canonical autoreceptor function.

147 effects of calcium signaling on D2S and D2L autoreceptor function.

148 role in dopamine release via its recognized autoreceptor function.

149 reuptake inhibitor nomifensine, and elevated autoreceptor function.

150 imulants, dopamine neurotransmission, and D2 autoreceptor function.

151 dulation of the EPSC and suggests that mGluR autoreceptors function to change the synaptic state and

152 These results suggest that LC autoreceptor functional changes rather than olfactory bu

153 otor symptoms of DA loss by suppressing M(4)-autoreceptor-Galpha (i/o) signaling in striatal choliner

154 ing 5-HT neuron-specific reduction of 5-HT1A autoreceptor gene expression in mice, we demonstrate tha

155 x (mPFC), as opposed to the somatic 5-HT(1A) autoreceptor, has been shown to play a critical role in

156 (mf-CA3) synapse, two types of glutamatergic autoreceptors have been identified: transmitter release

157 5-HT(1B) autoreceptors have been implicated in animal models of s

158 cy agonists at D2 postsynaptic receptors and autoreceptors (i.e., terguride increases locomotor activ

159 Here, we show that selective loss of D2 autoreceptors impairs the feedback inhibition of DA rele

160 was performed to determine whether M2R is an autoreceptor in cholinergic axons innervating the BLa.

161 ccupancy of the serotonin type 1A (5-HT(1A)) autoreceptor in depressed patients receiving medication.

162 een identified functionally as a presynaptic autoreceptor in rod photoreceptors.

163 but it is known to function as a presynaptic autoreceptor in rod photoreceptors.

164 ion includes higher binding of serotonin(1A) autoreceptor in the brainstem raphe of individuals who d

165 e histamine 3 (H3) receptor is a presynaptic autoreceptor in the central nervous system that regulate

166 cortical, and striatal inhibitory muscarinic autoreceptors in a more direct manner, we used genetical

167 within 100 ms of the first pulse, whereas D2 autoreceptors in DAN terminals are engaged in a slower i

168 stent with a presynaptic role for muscarinic autoreceptors in decreasing ACh release from olivocochle

169 eport the effect of SSRI treatment on 5-HT1A autoreceptors in depressed patients.

170 esults suggest that overactivity of 5-HT(1B) autoreceptors in DRN neurons may be an important mediato

171 lutinin-tagged 5-HT(1B) and manipulate these autoreceptors in DRN.

172 Here, we find that ATP stimulates purinergic autoreceptors in ISCs, triggering Cl(-) efflux and osmot

173 e with targeted ablation of dopamine (DA) D2 autoreceptors in mesencephalic dopaminergic neurons.

174 evelop a new strategy to manipulate 5-HT(1A) autoreceptors in raphe nuclei without affecting 5-HT(1A)

175 As autoreceptors in terminals of Adelta and C afferent fibe

176 e, we further investigate the role of 5-HT1A autoreceptors in the acute and chronic stimulant effects

177 t there was no change in binding at 5-HT(1A) autoreceptors in the DRN.

178 from activation of somatodendritic 5-HT(1A) autoreceptors in the DRN.

179 tization of 5-HT type 1A (5-HT1A) inhibitory autoreceptors in the DRN.

180 We conclude that neurons expressing 5-HT1A autoreceptors in the juxtafacial PGCL are involved in re

181 Because dopamine D2-type autoreceptors in the midbrain influence striatal dopamin

182 We conclude that D2 autoreceptors, in addition to mediating acute negative f

183 difference in how midbrain dopamine D2-type autoreceptors influence nicotine dependence.

184 hether mGluRs function as activity-dependent autoreceptors inhibiting pain transmission to the rat CN

185 tors (mGluRs) function as activity-dependent autoreceptors, inhibiting transmission in supraspinal si

186 utamate transmission combined with decreased autoreceptor inhibition could work in concert to enhance

187 , and delayed inhibition of breathing due to autoreceptor inhibition of 5-HT neurons.

188 NE release and decreases alpha(2)-adrenergic autoreceptor inhibition of NE release, an effect not obs

189 ell as activation of the alpha(2)-adrenergic autoreceptor inhibits stimulation-evoked norepinephrine

190 tivation of D2Rs on dopaminergic neurons (D2 autoreceptors); instead, using site-specific D2R knock-o

191 The serotonin 1A (5-HT(1A)) autoreceptor is known to play a role in mood disorders a

192 ynamic range of the presynaptic metabotropic autoreceptor is similar to that of the postsynaptic iono

193 e that signaling through endogenous 5-HT(1A) autoreceptors is necessary and sufficient for the establ

194 ly, the activation of metabotropic glutamate autoreceptors is necessary to maintain rhythmic motor ou

195 Although guanfacine engages alpha(2a)-AR autoreceptors, it also activates excitatory G(i)-coupled

196 ISCs), resulting in activation of purinergic autoreceptors, K(+) efflux, and subsequent depolarizatio

197 In addition, post-natal knockdown of autoreceptors leads to long-term increases in the excita

198 Furthermore, reducing 5-HT(1A) autoreceptor levels prior to antidepressant treatment is

199 blish a causal relationship between 5-HT(1A) autoreceptor levels, resilience under stress, and respon

200 mice with higher (1A-High) or lower (1A-Low) autoreceptor levels.

201 otonin release activates metabotropic 5-HT1A autoreceptors located on serotonin neurons that leads to

202 Dopamine D2 autoreceptors located on the midbrain dopaminergic neuro

203 fects of cocaine and suggest that the 5-HT1A autoreceptor may be an important pharmacological target

204 est that strategies aimed at blocking 5-HT1B autoreceptors may be useful for the treatment of anxiety

205 aphe nucleus mediated by metabotropic 5-HT1A autoreceptors may occur via point-to-point synapses rath

206 ts suggest a novel mechanism by which D(2S)R autoreceptors may regulate DAT in the central nervous sy

207 y evoked AMPAR/NMDAR ratios and increased D2 autoreceptor-mediated desensitization in dopamine neuron

208 The 5-HT1A autoreceptor-mediated inhibition did not develop until P

209 sponses to AMPA were enhanced and the 5-HT1A autoreceptor-mediated inhibitory response to 5-HT was at

210 amines the release and resulting dopamine D2-autoreceptor-mediated IPSCs (D2-IPSCs) in the VTA of mou

211 nce in the regulation of these neurons by D2 autoreceptor-mediated mechanisms.

212 nt because of initial activation of 5-HT(1A) autoreceptor-mediated negative feedback of 5-HT release.

213 s to determine the effects of NT on dopamine autoreceptor-mediated neurotransmission.

214 ed by the activity of presynaptic muscarinic autoreceptors mediating inhibition of ACh release.

215 ctivating presynaptic metabotropic glutamate autoreceptors (mGluRs) on the baroreceptor central termi

216 Presynaptic autoreceptors modulate transmitter release at many synap

217 rease in dams' anxiety, and that BSTv alpha2-autoreceptor modulation alone has little influence on an

218 ted alterations in 5-HT clearance, in 5-HT1A autoreceptor modulation of raphe neuron firing, and in b

219 passive equilibration between N and P masks autoreceptor modulation of the EPSC and suggests that mG

220 ted in a basal increase in 5-HT1A inhibitory autoreceptor mRNA in the rostral-mid DRN.

221 neurons, and basal expression of DRN 5-HT1A autoreceptor mRNA.

222 f regulating 5-HT neuron firing through 5-HT autoreceptors, neurotransmitter release, enzymatic degra

223 rt the presence of an alternative octopamine autoreceptor, Octss1R, with antagonistic functions on sy

224 is work indicates that the effects of 5-HT1A autoreceptors on anxiety and social behaviors are develo

225 terminals enhance DA release, whereas M2/M4 autoreceptors on cholinergic terminals inhibit ACh relea

226 (1a) binding in pre-synaptic somatodendritic autoreceptors on dorsal raphe nucleus relative to each o

227 However, NMDAr are also present as autoreceptors on glutamate terminals, where they act to

228 utamate receptors 2 and 3 (mGluR2/3) are key autoreceptors on glutamatergic terminals that maintain g

229 y, we suggest that GABA may act through GABA autoreceptors on HCs, thereby possibly modulating hemich

230 Activation of D2 autoreceptors on midbrain dopamine neurons has been show

231 ng that kainate receptors act as presynaptic autoreceptors on mossy fiber terminals to facilitate syn

232 sorin released during LTF appears to bind to autoreceptors on the sensory neuron, thereby activating

233 presynaptic active zone and typically act as autoreceptors or heteroceptors to depress synaptic relea

234 tors in either the dorsal raphe (presynaptic autoreceptors) or the hippocampus (a brain area with hig

235 ed that the expression of this sensitized D2-autoreceptor phenotype required Cav1.3 L-type Ca(2+) cha

236 The autoreceptor population located on the axon terminals of

237 hown that the combined pretreatment with low autoreceptor preferring dose levels of apomorphine (0.05

238 of cocaine using 5-HT1A receptor ligands in autoreceptor preferring doses.

239 These findings demonstrate that low dose autoreceptor preferring treatments with a 5-HT1A agonist

240 back activation by Galphai/o -coupled 5-HT1A autoreceptors reduces the excitability of serotoninergic

241 oal of this study was to investigate whether autoreceptors regulate both mechanisms concurrently.

242 Serotonin 1A (5-HT(1A)) autoreceptors regulate brain-wide serotonin neuron firin

243 D2 autoreceptors regulate dopamine release throughout the b

244 These terminal autoreceptors regulate serotonin release from dorsal rap

245 5-HT(1B) autoreceptors regulate serotonin release from terminals

246 -HT system compensate for the lack of 5-HT1A autoreceptor regulation of DRN.

247 This was the first examination of autoreceptor regulation of naturally occurring phasic do

248 tance, increased firing rate, lack of 5-HT1A autoreceptor response, and lack of GABA synaptic activit

249 minent, non-desensitizing somatodendritic D2-autoreceptor responses that show pronounced desensitizat

250 ne, induced adult-like, non-desensitizing D2-autoreceptor responses, selectively in juvenile SN DA ne

251 urons for homeostatic modulation of their D2-autoreceptor responses.

252 apse, mGlu7 is thought to be the predominant autoreceptor responsible for regulating glutamate releas

253 The transient activation of 5-HT1A autoreceptors resulted in brief pauses in neuron firing

254 cholinergic terminals, indicating a possible autoreceptor role.

255 esulting in a divergence from the canonical "autoreceptor" role of Type III mGluRs, and substantially

256 diated by activation of presynaptic mGluR2/3 autoreceptors secondary to AM251-induced increase (disin

257 ivation of presynaptic inhibitory adrenergic autoreceptors selectively potentiated the magnitude of K

258 istration of the SSRI fluoxetine on 5-HT(1A) autoreceptor sensitivity in mice administered with corti

259 ted dopamine metabolism, uptake, release, D2 autoreceptor sensitivity, and tyrosine hydroxylase expre

260 ork highlights the key role of noradrenergic autoreceptor signaling in the persistent modifications i

261 RGS4-dependent attenuation of interneuronal autoreceptor signaling is a major factor in the elevatio

262 eprogramming in response to dysfunctional D2 autoreceptor signaling leading to altered DA levels, a p

263 Sustained depression of D2 autoreceptor signaling required activation of the type 2

264 ss sensitive to the inhibitory effects of D2 autoreceptor stimulation.

265 ct effects on serotonergic signaling: (1) an autoreceptor that limits 5-HT release throughout the bra

266 izing putative presynaptic inhibitory opioid autoreceptors that "gate" the release of endogenous opio

267 ted by a number of 5-HT receptors, including autoreceptors that act to inhibit 5-HT release.

268 released during bursts feeds back onto D(2) autoreceptors that depress neuronal activity.

269 ude that sympathetic neurons possess beta(1)-autoreceptors that negatively regulate axon outgrowth.

270 tropic glutamate receptors (mGluRs) serve as autoreceptors throughout the CNS to inhibit glutamate re

271 a suggest that the DOR may act in part as an autoreceptor to regulate synaptic input to GABAergic as

272 calizes near active zones and operates as an autoreceptor to tune baseline transmission and enhance p

273 -specific neuropeptide sensorin, which binds autoreceptors to activate MAPK.

274 In order to study the contribution of 5-HT1B autoreceptors to anxiety and depression-related behavior

275 TP release from ISCs and activation of P2RY1 autoreceptors to elicit coordinated excitation of neuron

276 ing group II metabotropic glutamate receptor autoreceptors to inhibit cue-induced synaptic glutamate

277 elf-administration reduced the ability of D2 autoreceptors to inhibit DA release in the NAcc as deter

278 amine neuron activity through action on D(2) autoreceptors to produce an overexcitation-induced cessa

279 N cell firing through activation of 5-HT(1A) autoreceptors to reduce 5-HT levels in postsynaptic regi

280 n dopamine neurons, both variants can act as autoreceptors to regulate neuronal excitability and dopa

281 e concentration, which activates dopamine D2 autoreceptors to stimulate cAMP-dependent protein kinase

282 niques to examine the contribution of 5-HT1A autoreceptors to these effects.

283 D2-autoreceptors tune firing rates and dopamine release of

284 d the downregulation of LC alpha1 excitatory autoreceptors underlie the dramatic reduction in NE rele

285 ic effects, at least at synthesis modulating autoreceptors, until long after conclusion of reserpine

286 Lmx1b(f/f/p) neonatal mice to differentiate autoreceptor versus heteroreceptor effects of 8-OH-DPAT

287 Thus, expression of D2S as the exclusive autoreceptor was insufficient for cocaine-induced plasti

288 rrent induced by activation of D(2) dopamine autoreceptors was significantly less in Mecp2(-) neurons

289 Furthermore, although mice lacking D2 autoreceptors were able to extinguish self-administratio

290 A uptake was inhibited by GBR-12909 and D(2) autoreceptors were blocked by sulpiride, although these

291 However, the net effect of these autoreceptors when activated by endogenous glutamate is

292 The presynaptic facilitatory autoreceptor, which modulates glutamate release from mos

293 ic release of dopamine activates dopamine D2 autoreceptors, which are inhibitory G protein-coupled re

294 ly impairs desensitization of presynaptic M2 autoreceptors, which causes presynaptic M2 hyperactivity

295 Serotonin 1A autoreceptors, which inhibit serotonin synthesis and rel

296 lective desensitization of 5-HT1A inhibitory autoreceptors, which resembles the effect of sustained a

297 sts the hypothesis that activation of 5-HT1A autoreceptors, which would lessen 5-HT neuron firing, co

298 nerated by glutamate activation of dendritic autoreceptors, while the slow frequency was determined p

299 We examined the contribution of 5-HT1A autoreceptors (with [11C]WAY100635 positron emission tom

300 y and is an antagonist for the dopamine D(2) autoreceptors, with some evidence of a weak affinity to