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 eceptor, which may function as a presynaptic autoreceptor.

5 lly well as did D2L as an impulse-modulating autoreceptor.

6 ents was further increased after blocking D2-autoreceptors.

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

8 ber excitability through activation of GABAB autoreceptors.

9 neurotransmission by derepression of 5-HT1A autoreceptors.

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

11 tions at pre-synaptic metabotropic glutamate autoreceptors.

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

13 mechanism that required Octbeta2R octopamine autoreceptors.

14 ment of desensitization of presynaptic M2/M4 autoreceptors.

15 les lack presynaptic synthesis modulating D2 autoreceptors.

16 that is significantly regulated by dopamine autoreceptors.

17 stimulating group II metabotropic glutamate autoreceptors.

18 inhibited through activation of metabotropic autoreceptors.

19 tsynaptic receptors and synthesis modulating autoreceptors.

20 from the Starburst cell itself, making them autoreceptors.

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

22 dopamine neurons express D2 and D3 dopamine autoreceptors.

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

24 eurotransmitter, are governed by presynaptic autoreceptors.

25 athways remained normal in the absence of D2 autoreceptors.

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

27 ne neurons through activation of D2 dopamine autoreceptors.

28 d GABA release activated presynaptic GABA(B) autoreceptors.

29 arization frequency, uptake, and presynaptic autoreceptors.

30 y, rather than by blocking presynaptic GABAB autoreceptors.

31 orsal raphe nucleus is controlled by 5-HT(1) autoreceptors.

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

33 tion similar to that exhibited by endogenous autoreceptors.

34 ons is under strict control of inhibitory D2 autoreceptors.

35 anisms underlying drug-induced changes in D2 autoreceptors.

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

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

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

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

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

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

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

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

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

45 Modelling autoreceptor activation during repetitive stimulation re

46 When D2 autoreceptor activation was minimal, the combined effect

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

48 sponse to impaired serotonin release or less autoreceptor activation.

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

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

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

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

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

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

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

56 pressing neurons also exhibited increased D2 autoreceptor activity.

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

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

59 692, consistent with data indicating that D2 autoreceptor agonists increase neurotensin release from

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 erminal dopamine concentrations after global autoreceptor blockade.

100 rease dopamine signaling through presynaptic autoreceptor blockade.

101 rease dopamine signaling through presynaptic autoreceptor blockade.

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

103 5-HT1A autoreceptor BPF in the raphe was reduced 18% on SSRI tr

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

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

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

107 GABA(A) autoreceptor/Cl(-) channel activity in cultured CP/SP ne

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

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

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

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

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

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

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

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

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

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

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

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

120 1A)R internalization might underlie 5-HT(1A) autoreceptor desensitization under SSRI antidepressant t

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

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

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

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

125 5-HT1A autoreceptor downregulation is thought to induce transie

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

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

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

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

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

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

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

133 -1 displays dual activity, repressing 5-HT1A autoreceptor expression in serotonergic raphe cells whil

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

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

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

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

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

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

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

141 Dysfunctional D2 autoreceptors following repeated drug exposure could lea

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

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

144 Reduced D2 autoreceptor function could lead to enhanced DA signalin

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

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

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

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

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

150 role in dopamine release via its recognized autoreceptor function.

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

152 imulants, dopamine neurotransmission, and D2 autoreceptor function.

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

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

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

156 s, and synaptic activation of a facilitatory autoreceptor has not been established.

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

158 5-HT(1B) autoreceptors have been implicated in animal models of s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 As autoreceptors in terminals of Adelta and C afferent fibe

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

178 hat the absence of release-regulating 5-HT1A autoreceptors in the DRN can not account for the anxiety

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

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

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

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

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

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

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

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

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

188 ariety of synapses, as it could occur during autoreceptor inhibition by glutamate or GABA, heterosyna

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

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

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

192 post-synaptic receptor desensitization, and autoreceptor inhibition.

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

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

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

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

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

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

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

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

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

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

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

204 Dopamine D2 autoreceptors located on the midbrain dopaminergic neuro

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

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

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

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

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

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

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

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

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

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

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

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

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

218 Presynaptic autoreceptors modulate transmitter release at many synap

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

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

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

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

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

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

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

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

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

228 (1a) binding in pre-synaptic somatodendritic autoreceptors on dorsal raphe nucleus relative to each o

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

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

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

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

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

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

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

236 GluRs in taste cells might be presynaptic autoreceptors or postsynaptic receptors at afferent or e

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

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

239 The autoreceptor population located on the axon terminals of

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

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

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

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

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

245 D2 autoreceptors regulate dopamine release throughout the b

246 These terminal autoreceptors regulate serotonin release from dorsal rap

247 5-HT(1B) autoreceptors regulate serotonin release from terminals

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

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

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

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

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

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

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

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

256 cholinergic terminals, indicating a possible autoreceptor role.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

281 D2-autoreceptors tune firing rates and dopamine release of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

296 %) but significant occupancy of the 5-HT(1A) autoreceptor, while the regime used in the vast majority

297 opaminergic neurons and therefore are called autoreceptors, while others are on nondopaminergic neuro

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