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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.
3 by activating PV interneurons and by a TAAR1/5-HT(1A) agonist.
4 serotonergic agonist LSD and clinically used 5-HT(1A) agonists.
6 se in the oxytocin and ACTH responses to the 5-HT(1A) agonist 8-hydroxy-dipropylamino-tetralin (8-OH-
7 injections were duplicated by injection of a 5-HT(1A) agonist 8-hydroxy-dipropylaminotetralin (8-OH-D
8 se it was blocked by coadministration of the 5-HT(1A) agonist 8-OH-DPAT [((+/-)-8-hydroxy-2-(di-n-pro
12 t serotonergic neurotransmission such as the 5-HT1A agonist 8-hydroxy-2-(di-n-propyl-amino)tetralin (
13 cal microdialysis perfusion of the selective 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetralin (
14 ctions of AVP in combination with either the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetraline
15 [WAY100635] 0.5 mg/kg, intravenous) and the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin) [
20 pharmacological approach, we found that the 5-HT1A agonist 8-OH-DPAT also potentiated the antidepres
21 Administration of low doses of the selective 5-HT1A agonists 8-OH-DPAT (5-20 micrograms/kg) and ipsap
22 ts (CP-93,129 and anpirtoline), but not by a 5-HT1A agonist (8-OH-DPAT), indicating that 5-HT1B recep
23 before and after unilaterally dialyzing the 5-HT1A agonist (+/-)-8-hydroxy-2-(dipropylamino)-tetrali
24 +/- 13 % of control (P < 0.001), as did the 5-HT1A agonist, 8-OH-DPAT (52.5 +/- 17 %, P < 0.001) and
25 complex (MS/DB) following injections of the 5-HT1A agonist, 8-OH-DPAT, into the median raphe nucleus
27 rats (N = 10) received either saline or the 5-HT1A agonist, 8-OHDPAT (0.05 mg/kg) 20 min prior to a
30 behavioral assays for hallucinogen-like and 5-HT(1A) agonist activity and in vitro radioligand compe
31 Both compounds also demonstrated partial 5-HT(1A) agonist activity in vivo in rat serotonin syndr
32 , 4-fluoro-5-methoxy-DMT (6), displayed high 5-HT(1A) agonist activity, with potency greater than tha
33 The combined treatment with FGF-2 and the 5-HT1A agonist also synergistically increased FGFR1 and
34 ood volume changes in the rat in response to 5-HT(1A) agonist and antagonist administration were meas
35 se autoreceptor preferring treatments with a 5-HT1A agonist and antagonist can strongly modify the be
37 with fibroblast growth factor 2 (FGF2) and a 5-HT1A agonist, and dependent on the heteroreceptor inte
38 nding autoradiography using [3H]8-OH-DPAT, a 5-HT1A agonist, and in situ hybridization using radiolab
42 ult indicates that this novel, high affinity 5-HT(1A) agonist, BAY X3702, is neuroprotective in this
43 effect of a novel, high affinity serotonin (5-HT1A) agonist, BAY X3702, in a rat model of acute subd
45 Systemic application of the somatodendritic 5-HT1A agonist BMY 7378 had a significantly greater supp
49 udies, we present an argument for the use of 5-HT(1A) agonists in the treatment of Dup15q epilepsy.
50 -2-di-(n-propylamino) tetralin hydrobromide; 5-HT(1A) agonist; in vivo] reduced respiratory instabili
51 mic administration of either full or partial 5-HT1A agonists increases neuroendocrine responses and t
52 In vitro and in vivo studies also revealed a 5-HT1A agonist induced phosphorylation of FGFR1 and extr
53 induced prolactin response, but also blunted 5-HT(1A) agonist-induced hypothermia and increased 5-HT(
54 adigm using rats trained to discriminate the 5-HT(1A) agonist LY293284 was 0.17 micromol/kg, and the
55 However, 3a and 3b fully substituted for the 5-HT1A agonist LY293284 ((-)-(4R)-6-acetyl-4-(di-n-propy
56 as suggested experimentally, that effects of 5-HT(1A) agonists on the respiratory neural circuit suff
57 effect of a serotonin (5-hydroxytryptamine, 5-HT(1A)) agonist on these processes was investigated.
58 s of 50mM ethanol and 100nM of ipsapirone, a 5-HT(1A) agonist, on the expression of several NF-kappaB
61 he [35S]GTPgammaS labeling stimulated by the 5-HT1A agonist (R)-8-hydroxy-2-dipropylaminotetralin [(R
62 ed when the 5-hydroxytryptamine 1A receptor (5-HT1A) agonist (R)-(+)-8-hydroxy-2(di-n-propylamino)tet
64 78 alone and in combination with these other 5-HT1A agonists reduced copulatory behavior, though not
65 sion of Rh-CT(5-HT1A), but not Rh, decreases 5-HT(1A) agonist sensitivity, suggesting that Rh-CT(5-HT
67 which is released from astrocytes following 5-HT(1A) agonist stimulation, can reduce apoptosis in et
69 tration of either azapirone or aminotetralin 5-HT1A agonists, such as 8-hydroxy-2-dipropylaminotetral
71 fects are mediated in part by the ability of 5-HT(1A) agonists to activate the phosphatidyl 3'-kinase
74 r disruption compromises the ability of this 5-HT1A agonist to antagonize the feeding suppressant act