ライフサイエンスコーパス: DPAT

1 DPAT (30 mM) changed room air breathing pattern by incre

2 DPAT also induced phase shifts when applied during mid-s

3 DPAT, at doses of 1-8 mg/kg, reduced these three indices

4 whether neonatal exposure to a 5-HT(1A) (8OH-DPAT) or a 5-HT(1B) (CGS 12066B) receptor agonist can mi

5 v infusion of the 5HT1A receptor agonist 8OH-DPAT, but it did not alter their anxiety-related behavio

6 e-effect relationship (assessed 45 min after DPAT injection) is bell-shaped with an ED50 approximatel

7 s and flips, were inhibited by these agents: DPAT>buspirone>gepirone (inactive at 2 mg/kg).

8 first confirm that the 5HT1A/5HT7 agonist (+)DPAT maximally advances the SCN clock when applied at ze

9 bited phase advances by the 5-HT agonist, (+)DPAT, and this inhibition was decreased by co-applicatio

10 ist 8-hydroxy-N, N-dipropyl-2-aminotetralin (DPAT; 0.1 mg/kg and 0.3 mg/kg) or 5-HT3 receptor antagon

11 s indicate that the effects of buspirone and DPAT on sexual behavior in the male rat may be possible

12 For the pulse-chase assay, DPAT promoted a significant loss of radiolabel almost eq

13 For the incorporation assay, DPAT elicited an approximate doubling in labeling at the

14 NPY appears to block (+)DPAT-induced phase shifts by preventing increases in cyc

15 again acting through Y2 receptors, blocks (+)DPAT-induced phase shifts at ZT 6, while neither (+)DPAT

16 y period to erection was at least doubled by DPAT (2 mg/kg).

17 If a tentative shared target site by DPAT and buspirone is the 5-HT1A receptor, than the same

18 st effects in L-Agg animals; while high-dose DPAT effects were confounded by side effects on locomoti

19 Low-dose DPAT treatment inhibited both behaviors in H-Agg animals

20 1,2,3, 4-tetrahydronaphthalene hydrobromide (DPAT), with an EC(50) of approximately 10 nm.

21 2-(di-n-propylamino)tetralin) hydrobromide] (DPAT), which acts on autoreceptors and inhibits 5-HT neu

22 alysis decreased body temperature, and 30 mM DPAT increased the percentage of experimental time in wa

23 e during hypercapnia, microdialysis of 30 mM DPAT into the MRR did not change the ventilatory respons

24 Microdialysis of 1, 10 and 30 mM DPAT into the MRR significantly decreased absolute venti

25 Additionally, 10 and 30 mM DPAT MRR microdialysis decreased body temperature, and 3

26 duced phase shifts at ZT 6, while neither (+)DPAT nor 5-HT affect NPY-induced phase shifts at ZT 10.

27 due to differences in tissue distribution of DPAT.

28 e D3 receptor (apomorphine, quinpirole, 7-OH DPAT and PD 128907) triggered the response.

29 s treated with AL-8309A (0.1-30 mg/kg), 8-OH DPAT (0.1-1 mg/kg), buspirone (5-20 mg/kg) or topical oc

30 ide (3 mg/kg, i.p.) given 20 min before 8-OH DPAT negated the effect of 8-OH DPAT.

31 ion provided by dosing with AL-8309B or 8-OH DPAT was inhibited in rats predosed with WAY-100635.

32 response after single administration of 8-OH DPAT were dose dependent and lasted for approximately 4

33 8-hydroxy-2-(di-n-propylmino)tetralin (8-OH DPAT) (250 microg/kg, i.p.) restored hypercapnic Ve at 2

34 e dosed (subcutaneously) with AL-8309A, 8-OH DPAT, or buspirone once or three times before 6-hour exp

35 Retinas from AL-8309A and 8-OH DPAT-treated rats were devoid of histologic lesions.

36 before 8-OH DPAT negated the effect of 8-OH DPAT.

37 cts of the dopamine D3 receptor agonist 7-OH-DPAT (7-hydroxy-N,N-di-n-propyl-2-aminotetralin) in a 6-

38 ja (IC; 44%), without affecting [3H](+)-7-OH-DPAT (D3); N-chloroethyl-7-OH-DPATs blocked both radioli

39 Local perfusion with quinpirole, 7-OH-DPAT and BHT-920 into the globus pallidus/putamen also p

40 These doses of 7-OH-DPAT and l-nafadotride are behaviorally active and are 1

41 7-OH-DPAT in the mumolar range increased cAMP formation in gr

42 7-OH-DPAT produced a significant increase in LCGU in the subs

43 gonist 7-hydroxy-diphenylaminotetralin (7-OH-DPAT) (0.1 mg/kg), or antagonist l-nafadotride (1 mg/kg)

44 7-hydroxy-N,N-dipropyl-2-aminotetralin (7-OH-DPAT) than with the antagonist radioligand [(3)H]N-methy

45 -hydroxy-1,2,3,4-tetrahydronaphthalene (7-OH-DPAT), 1-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (E

46 (+/-)-7-hydroxy-dipropylamino-tetralin (7-OH-DPAT), [DA D3/D2 preferring], Antagonists: R(+)-SCH 2339

47 st, U99194, or the D3 receptor agonist, 7-OH-DPAT, did not alter choice behavior.

48 ces in D3 binding, measured using [(3)H]7-OH-DPAT, in DLB compared with controls.

49 low doses of the D3-preferring agonist 7-OH-DPAT, increased the numbers of Fos-like-immunoreactive n

50 ptors, significantly (P < 0.01) blocked 7-OH-DPAT- and quinpirole-induced increases in ACh.

51 dopamine antagonist, completely blocked 7-OH-DPAT-induced elevations in ACh.

52 the dopamine agonists, apomorphine and 7-OH-DPAT.

53 -methoxy-dimethyl-tryptamine (5.4)> or =8-OH-DPAT (<5.0)=alpha-methyl-5-HT (<5.0).

54 g/kg) and the 5-HT(1A) receptor agonist 8-OH-DPAT (0.003 and 0.01 mg/kg) also increased social intera

55 ats showed that acute administration of 8-OH-DPAT (0.01-0.3 mg/kg, subcutaneous [s.c.]) dose dependen

56 ns of the 5-HT receptor-selective drugs 8-OH-DPAT (0.025 or 0.1mug), WAY 100635 (0.01 or 0.04mug), DO

57 single intra-DRN infusion of HSV-LacZ, 8-OH-DPAT (0.03 mg/kg, s.c.) decreased 5-HT levels to an exte

58 wed a blunted neurochemical response to 8-OH-DPAT (0.03 mg/kg, s.c.); however, increasing the dose to

59 er, both amphetamine (1 mg/kg) and R(+)-8-OH-DPAT (0.05 mg/kg) decreased cortical DOPA accumulation;

60 mg/kg) decreased basal DA release; R(+)-8-OH-DPAT (0.05 mg/kg) inhibited DA release produced by the 5

61 Neither amphetamine (1 mg/kg), R(+)-8-OH-DPAT (0.05 mg/kg), or the combination, significantly aff

62 umulation, an effect attenuated by R(+)-8-OH-DPAT (0.05 mg/kg).

63 R(+)-8-OH-DPAT (0.05, but not 0.025, 0.1, 1 mg/kg), a 5-HT(1A) rec

64 le (dH(2)O) or the 5-HT(1A)R agonist +/-8-OH-DPAT (0.1 or 1.0 mg/kg, i.p.), followed by a second inje

65 In both STR and NAC, R(+)-8-OH-DPAT (0.2 mg/kg) decreased basal DA release; R(+)-8-OH-D

66 In Experiment 1, systemically injected 8-OH-DPAT (0.4 mg/kg) decreased extracellular 5-HT levels in

67 roM) and mimicked by the 5-HT1A agonist 8-OH-DPAT (1 microM).

68 T treated rats, however, the ability of 8-OH-DPAT (125 microg/kg) to block FEN and FLU induced anorex

69 ase in relative theta power produced by 8-OH-DPAT (20 micrograms/kg) was greatly attenuated by spiper

70 ats received a systemic injection of (+)8-OH-DPAT (200 microg/kg, s.c.).

71 ifts induced by local administration of 8-OH-DPAT (30 microM, i.e., 1.97 ng) or 5-carboxamidotryptami

72 ivity evoked by the I.V. application of 8-OH-DPAT (42 microg kg(-1)).

73 doses of the selective 5-HT1A agonists 8-OH-DPAT (5-20 micrograms/kg) and ipsapirone (20-100 microgr

74 8-OH-DPAT (50, 100 or 200 ng per bilateral site) infused into

75 In Experiment 2, 8-OH-DPAT (500 microM) administered directly into the MPOA vi

76 In Experiment 2, 8-OH-DPAT (500 microM), retrodialyzed into the MPOA through a

77 (P < 0.001), as did the 5-HT1A agonist, 8-OH-DPAT (52.5 +/- 17 %, P < 0.001) and the 5-HT1B agonist,

78 Experiment 1 co-administered 8-OH-DPAT (6 microgram) with either the 5-HT1A antagonist 4-i

79 cimol (87.6 pmol) or vehicle before DRN 8-OH-DPAT (6 pmol) microinjections at ZT6.

80 8-OH-DPAT (62.5-250 microg/kg) pretreatment reversed the anor

81 8-OH-DPAT (62.5-250 microg/kg) was administered 5 min prior t

82 In Experiment 3, 8-OH-DPAT (8 microg) co-injected with 5,7-dihydroxytryptamine

83 Application of 5-HT or 8-OH-DPAT (a mixed 5-HT1A/5-HT7 agonist) reversed mGluR-LTD i

84 The ionophoretic application of 8-OH-DPAT (a selective 5-HT(1A) receptor agonist) influenced

85 epirone were compared to the effects of 8-OH-DPAT (or DPAT, a selective 5-HT1A reference agonist), an

86 ssion treatment with the 5-HT1A agonist 8-OH-DPAT (subcutaneous injections at a dose of 0.15 mg/kg) r

87 In contrast, the prolactin response to 8-OH-DPAT (which cannot be blocked by 5-HT(1A) antagonists) w

88 oadministration of the 5-HT(1A) agonist 8-OH-DPAT [((+/-)-8-hydroxy-2-(di-n-propylamino)tetralin) hyd

89 th application of 5-HT and injection of 8-OH-DPAT [(+/-)-8-hydroxy-2-di-(n-propylamino) tetralin hydr

90 elective 5-HT(1A) receptor agonist R(+)-8-OH-DPAT [R(+)-8-hydroxy-2-(di-n-propylamino)tetralin] was i

91 clusion, these results demonstrate that 8-OH-DPAT activation of MAP kinase signaling in vivo is a tra

92 Forty-five minutes after 8-OH-DPAT administration (0.5 mg/kg), body temperatures dropp

93 Acute 8-OH-DPAT administration, under conditions known to suppress

94 8-OH-DPAT also altered the temporal characteristics of spike

95 DRN at the time of tail-flick testing, 8-OH-DPAT also effectively prevented this effect.

96 8-OH-DPAT also increased latencies to chase.

97 roach, we found that the 5-HT1A agonist 8-OH-DPAT also potentiated the antidepressant-like effects of

98 no) tetralin-HBr (8-OH-DPAT), or 200 ng 8-OH-DPAT and 1000 or 2000 ng of N-(3-trifluoro-methylphenyl)

99 Rats receiving 8-OH-DPAT and 1000 or 2000 ng quipazine or TFMPP were protect

100 s matched the known distribution of [3H]8-OH-DPAT and [3H]WAY-100635.

101 8-OH-DPAT and CP 93129 increased the paired pulse ratio (1.38

102 8-OH-DPAT and eticlopride significantly reduced the proportio

103 ratio declined following infusion with 8-OH-DPAT and the decline was dose-dependently reduced by coi

104 rogesterone also reduced the effects of 8-OH-DPAT and this effect was also seen in females primed onl

105 rious doses of the serotonin-1A agonist 8-OH-DPAT at training on 72-hr retention of passive avoidance

106 t with NMDA (20 pmol) or vehicle before 8-OH-DPAT at ZT 6.

107 In rostral sections, [3H]8-OH-DPAT binding (fmol/mg protein) in the dorsal subnucleus

108 or the inhibition by GTPgammaS of [(3)H]8-OH-DPAT binding in the hypothalamus.

109 The distribution of [3H]8-OH-DPAT binding sites was identical to that of the [35S]GTP

110 sites, autoradiographic analyses of [3H]8-OH-DPAT binding to 5-HT1A receptors in brains of these rats

111 /5 microliter, i.c.v.; 48 hr before the 8-OH-DPAT challenge) did not inhibit the ACTH response, poten

112 f the ACTH and oxytocin responses to an 8-OH-DPAT challenge.

113 reduce the effects of VMN infusion with 8-OH-DPAT contrasts with prior studies in which estrogen's pr

114 Consistently, 8-OH-DPAT decreased mGluR-mediated reduction of AMPA glutamat

115 e in a brief access test confirmed that 8-OH-DPAT decreased preference for saline by both increasing

116 nd eliminated the effects of subsequent 8-OH-DPAT dialysis on REM but not the effects on body tempera

117 8-OH-DPAT dialysis resulted in fragmented sleep with an incre

118 After 8-OH-DPAT dialysis, there were decreases in body movements, i

119 ceptor internalization process, because 8-OH-DPAT did not inhibit the internalization induced by incu

120 Animals receiving 200 ng 8-OH-DPAT exhibited a decline in lordosis behavior following

121 ite as a potential locus for short-term 8-OH-DPAT feeding effects.

122 cal homogenate 5-HT2A receptors and [3H]8-OH-DPAT from rat hippocampal homogenate 5-HT1A receptors.

123 iven 20 min before 8-OH-DPAT, prevented 8-OH-DPAT from restoring respiration to normal.

124 At 50 ng, 8-OH-DPAT had a selective action on anxiety, while at 200 ng

125 on potential firing whereas the agonist 8-OH-DPAT had the opposite effect.

126 While 8-OH-DPAT has been characterized as an agonist at the 5-HT1A

127 the exaggerated hypothermic response to 8-OH-DPAT in HDS rats.

128 HT1A receptor, by competition with [3H]-8-OH-DPAT in rat hippocampal homogenates, and for affinity at

129 Instead, the facilitative effects of 8-OH-DPAT in the MPOA on male copulatory behavior may result,

130 ent studies suggest that the effects of 8-OH-DPAT in the MPOA on male rat copulatory behavior may be

131 Phase advances to 8-OH-DPAT in the slice were attenuated by pretreatment with M

132 eceptor subtype play important roles in 8-OH-DPAT induction of circadian phase shifts in vivo and tha

133 PFC increased impulsive choice, whereas 8-OH-DPAT infused into OFC decreased impulsive choice.

134 8-OH-DPAT inhibited lordosis behavior within 15 min of the in

135 urrent experiments investigated whether 8-OH-DPAT injected into the MPOA facilitates male sexual beha

136 15 min before microinjection of 5-CT or 8-OH-DPAT into the dorsal raphe of young hamsters, significan

137 s induced by administration of 5-CT and 8-OH-DPAT into the dorsal raphe.

138 ling model, bilateral microperfusion of 8-OH-DPAT into the PPTn (n = 23 rats) significantly increased

139 the effects of bilateral infusion with 8-OH-DPAT into the ventromedial nucleus of the hypothalamus (

140 ons might alter feeding after injecting 8-OH-DPAT into this midbrain region.

141 gestion that systemic administration of 8-OH-DPAT is especially effective in disrupting learning task

142 the reversal of FEN and FLU anorexia by 8-OH-DPAT is partially dependent on the integrity of brain 5-

143 cal application of the 5-HT1A/7 agonist 8-OH-DPAT lowered movement thresholds in vivo and increased m

144 ative effects of systemic injections of 8-OH-DPAT may result from decreased 5-HT release in several s

145 Comparison of the effect of 8-OH-DPAT microdialysed into a more rostral portion of the MR

146 ces in running-wheel rhythms induced by 8-OH-DPAT microinjected during the midsubjective day.

147 circadian phase resetting responses to 8-OH-DPAT microinjection.

148 s were conducted to test the effects of 8-OH-DPAT on 5-HT and dopamine (DA) neurotransmission in the

149 etic application of the 5-HT 1A agonist 8-OH-DPAT on auditory responses were compared with the charac

150 st in part, from stimulatory effects of 8-OH-DPAT on DA transmission.

151 ceptor versus heteroreceptor effects of 8-OH-DPAT on hypoglossal nerve respiratory output.

152 compounds as the inhibitory activity of 8-OH-DPAT on light-induced phase advances is not apparent whe

153 nt study investigated the effects of +/-8-OH-DPAT on pERK density in rats treated with l-DOPA or the

154 e present study examined the effects of 8-OH-DPAT on the feeding suppressant action of the indirect 5

155 ifferent sensitivities to midazolam and 8-OH-DPAT or more intriguingly, the tests are evoking fundame

156 DOI did not alter the binding of [(3)H]8-OH-DPAT or the inhibition by GTPgammaS of [(3)H]8-OH-DPAT b

157 OI), clorgyline, and then injected with 8-OH-DPAT or vehicle (VEH) either 4 h before or after the ons

158 mg/kg) did not alter the effect of R(+)-8-OH-DPAT or WAY100635 alone on basal DA release in either re

159 Concurrent exposure to light during the 8-OH-DPAT perfusion abolished the phase advances.

160 Phase advances induced by SCN 8-OH-DPAT perfusion were significantly inhibited by the 5-HT(

161 Reversal of mGluR-LTD by 8-OH-DPAT persisted in the presence of the 5-HT1A receptor an

162 opylamino) tetralin (8-OH-DPAT) or with 8-OH-DPAT plus varying concentrations (200 to 2000 ng) of the

163 ingly, in the ventromedial striatum, +/-8-OH-DPAT potentiated l-DOPA-induced pERK; in the motor corte

164 A-induced pERK; in the motor cortex, +/-8-OH-DPAT potentiated pERK with l-DOPA or SKF81297.

165 That is, 8-OH-DPAT pretreatment did not reverse the feeding inhibitory

166 (+)8-OH-DPAT produced a rapid increase (at 5 min) and transient

167 mice in vivo, subcutaneous injection of 8-OH-DPAT produced similar biphasic respiratory effects as in

168 onses correlated significantly with [3H]8-OH-DPAT receptor binding in only a few areas of frontal cor

169 As expected, 8-OH-DPAT reduced lordosis behavior and muscimol attenuated t

170 s, the serotonin 1A receptor agonist +/-8-OH-DPAT reduces dyskinesia, suggesting it may exhibit effic

171 Preadministration of WAY100635 and 8-OH-DPAT resulted in 87% and 76% average reductions in BPF v

172 Administration of the 5-HT(1A) agonist 8-OH-DPAT resulted in decreases in fractional brain blood vol

173 tagonist WAY-100635 following a dose of 8-OH-DPAT resulted in increases in fractional blood volumes g

174 Because systemic and MPOA injections of 8-OH-DPAT resulted in opposite effects on extracellular 5-HT

175 mally enhanced; similarly to wild-type, 8-OH-DPAT reversed mGluR-LTD and decreased mGluR-induced redu

176 made after 0 vs. 250 microg (760 nmol) 8-OH-DPAT s.c.

177 se-dependently reduced 2 h food intake, 8-OH-DPAT stimulated eating behavior.

178 characterized by loss of sensitivity to 8-OH-DPAT suggests that this region and this receptor subtype

179 8-OH-DPAT tended to cause inhibition at low currents (40 nA)

180 Retrodialyzing 8-OH-DPAT through a microdialysis probe in the MPOA had been

181 mster exhibited specific binding of [3H]8-OH-DPAT to both the 5-HT7 and 5-HT1A receptors, and that th

182 ion of MAP kinase in hypothalamus by (+)8-OH-DPAT to determine the regional differences and receptor

183 ol benzoate (EB) reduced the ability of 8-OH-DPAT to inhibit lordosis behavior, rats were preprimed w

184 ion, the increase in the binding of [3H]8-OH-DPAT to serotonin-1A receptors was detected in the entir

185 The binding of [3H]8-OH-DPAT to serotonin-1A receptors was increased significant

186 The specific binding of [3H]8-OH-DPAT to serotonin7 (5-HT7) and serotonin1A (5-HT1A) rece

187 ytocin and ACTH dose-response curves of 8-OH-DPAT to the right (increased ED(50)) with no change in t

188 8-OH-DPAT transiently increased respiratory burst frequency i

189 Especially after combined FGF-2 and 8-OH-DPAT treatment, a marked and significant increase in PLA

190 CVPNs tested, this excitatory action of 8-OH-DPAT was attenuated by co-application of the selective 5

191 The effect of 8-OH-DPAT was attributed to inhibition of opioid release and

192 The effect of 8-OH-DPAT was eliminated by pre-treatment with a selective au

193 ebroventricular treatment with FGF2 and 8-OH-DPAT was found to produce evidence of highly significant

194 SSRI fluvoxamine and 5-HT(1A)R agonist 8-OH-DPAT were also potentiated in RGS6(+/-) mice.

195 The effects of 8-OH-DPAT were blocked by local pretreatment with N-[2-[4-(2-

196 Phase shifts induced by 8-OH-DPAT were enhanced more than threefold by pretreatment w

197 f MRN 5-HT neurons by MRN injections of 8-OH-DPAT would disinhibit MS/DB neurons, allowing them to bu

198 y at D2 receptors or indirectly through 8-OH-DPAT's ability to increase extracellular dopamine.

199 least in part, either directly through 8-OH-DPAT's activity at D2 receptors or indirectly through 8-

200 Raclopride blocked 8-OH-DPAT's facilitative effects on ejaculation frequency and

201 ydrochloride (p-MPPI) failed to prevent 8-OH-DPAT's stimulatory effects on DA and 5-HT levels in the

202 oxy-2-(di-n-propylamino)-tetralin (R(+)-8-OH-DPAT) and n-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]

203 hydroxy-1,2,3,4-tetrahydro-naphthalene (8-OH-DPAT) at midday advanced the phase of the free-running c

204 -hydroxy-2-(dipropylamino)tetralin ([3H]8-OH-DPAT) in the absence or presence of guanylylimidodiphosp

205 nist 8-hydroxy-2-dipropylaminotetralin (8-OH-DPAT) inhibited the evoked mu-opioid receptor internaliz

206 )-8-hydroxy-2-(dipropylamino)-tetralin (8-OH-DPAT) into the juxtafacial PGCL in conscious newborn pig

207 gonist 8-hydroxy-dipropylaminotetralin (8-OH-DPAT) into the NRM.

208 not (+)-8-hydroxydipropylaminotetralin (8-OH-DPAT) or cyanopindolol.

209 -hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) or with 8-OH-DPAT plus varying concentrations (200

210 -hydroxy-2-(di-n-propyl-amino)tetralin (8-OH-DPAT) stimulate food intake.

211 ific binding to 5-HT(1A) receptors ([3H]8-OH-DPAT) was significantly increased in the dorsal and medi

212 8-hydroxy-N,N-dipropyl-2-aminotetralin (8-OH-DPAT) was similar in each strain.

213 8-hydroxy 2-(di-n-propylamino)tetralin (8-OH-DPAT), 25 ng (5-aminomethyl-3-hydroxyisoxazole)hydrobrom

214 -hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), a 5-HT1A receptor agonist, into the lateral cereb

215 8-hydroxy-2-di-n-propylamino-tetralin (8-OH-DPAT), a drug that reduces 5-HT release by acting on pre

216 -hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), although this agonist had minimal or no effect on

217 8-hydroxy-2-(di-n-propyl)aminotetralin (8-OH-DPAT), an agonist at serotonin-1A receptors, is altered

218 droxy-2-[di-N-propylamine] tetralin (3H-8-OH-DPAT), and 125I-RTI-55 was used to map the distribution

219 -hydroxy-2-(di-N-propylamino) tetralin (8-OH-DPAT), could either be due to decreased firing of 5-HT n

220 8-hydroxy-2(di-n-propylamino)tetralin, (8-OH-DPAT), either systemically or into the midbrain raphe nu

221 irtoline), but not by a 5-HT1A agonist (8-OH-DPAT), indicating that 5-HT1B receptors mediate the inhi

222 -hydroxy-2-(di-N-propylamino) tetralin (8-OH-DPAT), inhibits cyclic AMP (cAMP) accumulation in the me

223 onist 8-hydroxy-di-propylaminotetralin (8-OH-DPAT), injected either systemically or into the medial p

224 onist 8-hydroxy-di-propylaminotetralin (8-OH-DPAT), injected systemically or directly into the medial

225 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), on female rat lordosis behavior.

226 roxy 2-(di-n-propylamino) tetralin-HBr (8-OH-DPAT), or 200 ng 8-OH-DPAT and 1000 or 2000 ng of N-(3-t

227 his impairment is acute and reversible (8-OH-DPAT), or chronic and irreversible (5,7-DHT).

228 t, 8-hydroxy-2-(dipropylamino)tetralin (8-OH-DPAT), to cause a phase advance in the firing pattern of

229 -hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), were examined in ovariectomized rats, hormone pri

230 -8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT), with simultaneous dialysis of ACSF in or near to

231 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT).

232 onist 8-hydroxy-dipropylamino-tetralin (8-OH-DPAT).

233 agonist 8-hydroxydipropylaminotetralin (8-OH-DPAT).

234 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT).

235 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT).

236 h as 8-hydroxy-2-dipropylaminotetralin (8-OH-DPAT).

237 -8-hydroxy-2-dipropylaminotetralin [(R)-8-OH-DPAT)].

238 (R)-8-OH-DPAT, (S)-8-OH-DPAT, and buspirone stimulated [35S]GTPga

239 d (+)-8-hydroxy-dipropylaminotetraline (8-OH-DPAT, 1-30 microM) dose-dependently activated an outward

240 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, 10 mum) into the PPTn; this tool has been shown to

241 igand-binding autoradiography using [3H]8-OH-DPAT, a 5-HT1A agonist, and in situ hybridization using

242 inding in primate brain, in contrast to 8-OH-DPAT, a potent 5-HT1A receptor agonist.

243 from the lordosis-inhibiting effects of 8-OH-DPAT, alone.

244 (R)-8-OH-DPAT, (S)-8-OH-DPAT, and buspirone stimulated [35S]GTPgammaS binding in

245 tested with ionophoretic application of 8-OH-DPAT, excitation was observed that was attenuated by WAY

246 Three 5-HT1A receptor agonists (8-OH-DPAT, F13714 and F15599) and one 5-HT1A receptor antagon

247 receptor subtypes that is activated by 8-OH-DPAT, in the dorsal raphe nucleus.

248 mg/kg, i.p.; n = 3) given 20 min before 8-OH-DPAT, prevented 8-OH-DPAT from restoring respiration to

249 The 5-HT(1A) receptor agonist, 8-OH-DPAT, reduced cAMP accumulation after stimulation by iso

250 ere given two injections: first with +/-8-OH-DPAT, the D1 receptor antagonist SCH23390 or their vehic

251 tration of the 5-HT1A receptor agonist, 8-OH-DPAT, the D2 receptor antagonist, eticlopride, and the D

252 educe the lordosis-inhibiting effect of 8-OH-DPAT, the mechanisms responsible for the effects of the

253 tryptamine, but not the partial agonist 8-OH-DPAT, triggered internalization of tagged 5-HT(1A)R in s

254 Next, a 5-HT1A agonist, 8-OH-DPAT, was coadministered with CP-154,526 into the DRN to

255 eatment decreased the magnitude of both 8-OH-DPAT- and VEH-induced phase advances, but not the magnit

256 The 8-OH-DPAT-evoked change in response did not correlate with CF

257 The 8-OH-DPAT-evoked change in response significantly correlated

258 Overall, the results suggest that 8-OH-DPAT-induced 5-HT hypofunction increases thirst without

259 No significant (+)8-OH-DPAT-induced changes in pERK were observed in dorsal rap

260 8-OH-DPAT-induced hypothermia was absent in female 5-HTT -/-

261 This R(+)-8-OH-DPAT-induced inhibition of the effects of clozapine, ris

262 Bicuculline also potentiated 8-OH-DPAT-induced phase advances (P<0.05).

263 -HT release, did not suppress intra-SCN 8-OH-DPAT-induced phase advances.

264 The results indicate that 8-OH-DPAT-induced phase-advances and delays are functionally

265 hase advances, but not the magnitude of 8-OH-DPAT-induced phase-delays.

266 showed significantly lower levels of 3H-8-OH-DPAT-labeled 5-HT(1a) binding in post-synaptic areas (fr

267 Group Random showed higher levels of 3H-8-OH-DPAT-labeled 5-HT(1a) binding in pre-synaptic somatodend

268 0.17 micromol/kg, and the K(i) at [(3)H]8-OH-DPAT-labeled 5-HT(1A) receptors was 0.23 nM.

269 study examined the distribution of [3H]8-OH-DPAT-labeled 5-HT1A receptors and their degree of coupli

270 [3H]ketanserin-labeled 5-HT2A and [3H]-8-OH-DPAT-labeled 5-HT1A sites.

271 tioned response (CR) performance and 3H-8-OH-DPAT-labeled binding of 5-HT(1a) receptors as well as 12

272 e (WAY100635) completely blocked the (+)8-OH-DPAT-mediated changes in pERK levels in PVN, medial basa

273 rs (1.34 +/- 0.30), while those in NMDA/8-OH-DPAT-microinjected hamsters (0.67 +/- 0.17) were smaller

274 smaller (P<0.05) than those in vehicle/8-OH-DPAT-microinjected hamsters (0.97 +/- 0.10).

275 shifts (mean +/- S.E.M., h) in muscimol/8-OH-DPAT-microinjected hamsters (1.02 +/- 0.30) were not dif

276 ifferent (P=0.11) from those in vehicle/8-OH-DPAT-microinjected hamsters (1.34 +/- 0.30), while those

277 tagonist by dose-dependently inhibiting 8-OH-DPAT-stimulated (35)S-GTPgammaS binding.

278 In a two-bottle test, however, 8-OH-DPAT-treated animals (30 microg/kg/ml) demonstrated decr

279 ting effects of systemic treatment with 8-OH-DPAT.

280 to an injection of the 5-HT(1A) agonist 8-OH-DPAT.

281 eased in response to the application of 8-OH-DPAT.

282 r 0, 0.4, 0.8 or 1.6 nmol injections of 8-OH-DPAT.

283 nd eliminated the prolactin response to 8-OH-DPAT.

284 eater than that of the 5-HT(1A) agonist 8-OH-DPAT.

285 to the specific 5-HT1A receptor agonist 8-OH-DPAT.

286 ked the inhibition produced by 1 microM 8-OH-DPAT.

287 e reduced at both 5 and 15 min after (+)8-OH-DPAT.

288 [(11)C]10 was blocked by WAY100635 and 8-OH-DPAT.

289 -hydroxy-2-(di-n-propylamine)-tetralin (8-OH-DPAT; 1 microgram) microinjected into the dorsal raphe n

290 -hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT; 200 ng), or were coinfused with the 5-HT1A recepto

291 8-hydroxy-2-(di-n-propylmino)tetralin (8-OH-DPAT; 250 microg/kg, i.p.) at 24 hr (n = 5) or 7 d (n =

292 -hydroxy-2-(di-n-propylamino)tetralin) [8-OH-DPAT] 2 mg/kg, intravenous).

293 ere compared to the effects of 8-OH-DPAT (or DPAT, a selective 5-HT1A reference agonist), and BMY-737

294 )-(+)-8-hydroxy-2(di-n-propylamino)tetralin (DPAT) is microdialysed into the MRR of the unanaesthetiz

295 , (+)8-hydroxy-2-(di-n-propylamino)tetralin (DPAT), when applied to mouse SCN brain slices.

296 st 8-hydroxy-2-(di-n-propylamino) tetraline (DPAT) or the 5-HT1B agonist CGS-12066A (CGS) directly wi

297 Furthermore, in combination with DPAT (2 mg/kg, 45 min), the effects were synergistic suc

298 ered alone and even more in combination with DPAT or buspirone.

299 were also tested for their interaction with DPAT.

300 Though treatment with DPAT resulted in a dose-dependent inhibition of AVP-faci