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1 s previously been reported for ipsapirone, a 5-HT1A agonist.
2 , but blunted by 10 microM buspirone, a weak 5-HT1A agonist.
4 se in the oxytocin and ACTH responses to the 5-HT(1A) agonist 8-hydroxy-dipropylamino-tetralin (8-OH-
5 injections were duplicated by injection of a 5-HT(1A) agonist 8-hydroxy-dipropylaminotetralin (8-OH-D
6 se it was blocked by coadministration of the 5-HT(1A) agonist 8-OH-DPAT [((+/-)-8-hydroxy-2-(di-n-pro
10 t serotonergic neurotransmission such as the 5-HT1A agonist 8-hydroxy-2-(di-n-propyl-amino)tetralin (
11 cal microdialysis perfusion of the selective 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetralin (
12 ctions of AVP in combination with either the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetraline
13 [WAY100635] 0.5 mg/kg, intravenous) and the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin) [
18 pharmacological approach, we found that the 5-HT1A agonist 8-OH-DPAT also potentiated the antidepres
19 Administration of low doses of the selective 5-HT1A agonists 8-OH-DPAT (5-20 micrograms/kg) and ipsap
20 ts (CP-93,129 and anpirtoline), but not by a 5-HT1A agonist (8-OH-DPAT), indicating that 5-HT1B recep
21 before and after unilaterally dialyzing the 5-HT1A agonist (+/-)-8-hydroxy-2-(dipropylamino)-tetrali
22 +/- 13 % of control (P < 0.001), as did the 5-HT1A agonist, 8-OH-DPAT (52.5 +/- 17 %, P < 0.001) and
23 complex (MS/DB) following injections of the 5-HT1A agonist, 8-OH-DPAT, into the median raphe nucleus
25 rats (N = 10) received either saline or the 5-HT1A agonist, 8-OHDPAT (0.05 mg/kg) 20 min prior to a
28 behavioral assays for hallucinogen-like and 5-HT(1A) agonist activity and in vitro radioligand compe
29 Both compounds also demonstrated partial 5-HT(1A) agonist activity in vivo in rat serotonin syndr
30 , 4-fluoro-5-methoxy-DMT (6), displayed high 5-HT(1A) agonist activity, with potency greater than tha
31 The combined treatment with FGF-2 and the 5-HT1A agonist also synergistically increased FGFR1 and
32 ood volume changes in the rat in response to 5-HT(1A) agonist and antagonist administration were meas
33 se autoreceptor preferring treatments with a 5-HT1A agonist and antagonist can strongly modify the be
35 with fibroblast growth factor 2 (FGF2) and a 5-HT1A agonist, and dependent on the heteroreceptor inte
36 nding autoradiography using [3H]8-OH-DPAT, a 5-HT1A agonist, and in situ hybridization using radiolab
40 ult indicates that this novel, high affinity 5-HT(1A) agonist, BAY X3702, is neuroprotective in this
41 effect of a novel, high affinity serotonin (5-HT1A) agonist, BAY X3702, in a rat model of acute subd
43 Systemic application of the somatodendritic 5-HT1A agonist BMY 7378 had a significantly greater supp
46 -2-di-(n-propylamino) tetralin hydrobromide; 5-HT(1A) agonist; in vivo] reduced respiratory instabili
47 mic administration of either full or partial 5-HT1A agonists increases neuroendocrine responses and t
48 In vitro and in vivo studies also revealed a 5-HT1A agonist induced phosphorylation of FGFR1 and extr
49 induced prolactin response, but also blunted 5-HT(1A) agonist-induced hypothermia and increased 5-HT(
50 adigm using rats trained to discriminate the 5-HT(1A) agonist LY293284 was 0.17 micromol/kg, and the
51 However, 3a and 3b fully substituted for the 5-HT1A agonist LY293284 ((-)-(4R)-6-acetyl-4-(di-n-propy
52 effect of a serotonin (5-hydroxytryptamine, 5-HT(1A)) agonist on these processes was investigated.
53 s of 50mM ethanol and 100nM of ipsapirone, a 5-HT(1A) agonist, on the expression of several NF-kappaB
56 he [35S]GTPgammaS labeling stimulated by the 5-HT1A agonist (R)-8-hydroxy-2-dipropylaminotetralin [(R
57 ed when the 5-hydroxytryptamine 1A receptor (5-HT1A) agonist (R)-(+)-8-hydroxy-2(di-n-propylamino)tet
59 78 alone and in combination with these other 5-HT1A agonists reduced copulatory behavior, though not
60 sion of Rh-CT(5-HT1A), but not Rh, decreases 5-HT(1A) agonist sensitivity, suggesting that Rh-CT(5-HT
62 which is released from astrocytes following 5-HT(1A) agonist stimulation, can reduce apoptosis in et
64 tration of either azapirone or aminotetralin 5-HT1A agonists, such as 8-hydroxy-2-dipropylaminotetral
66 fects are mediated in part by the ability of 5-HT(1A) agonists to activate the phosphatidyl 3'-kinase
69 r disruption compromises the ability of this 5-HT1A agonist to antagonize the feeding suppressant act
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