1 to contribute to the pro-survival effects of ipsapirone.

2 uggest that their survival is not reduced by ipsapirone.

3 nd Bcl-xl was prevented by co-treatment with ipsapirone.

4  agonists 8-OH-DPAT (5-20 micrograms/kg) and ipsapirone (20-100 micrograms/kg) produced rhythmic slow

5 ine the effects of 50mM ethanol and 100nM of ipsapirone, a 5-HT(1A) agonist, on the expression of sev

6 d the effect of clinically available agents, ipsapirone, a 5-HT(1A) receptor partial agonist, and the

7 ite to what has previously been reported for ipsapirone, a 5-HT1A agonist.

8                                     However, ipsapirone, at all doses (0.3, 1, 3, but not 0.1 mg/kg)

9                  Importantly, treatment with ipsapirone augmented the activity of catalase and the ex

10 to the serotonin 1A receptor partial agonist ipsapirone hydrochloride in patients with seasonal affec

11 ys later for the first of 2 drug challenges (ipsapirone hydrochloride, 0.3 mg/kg, or placebo), each s

12          Moreover, the protective effects of ipsapirone on ethanol-treated neurons might involve thei

13 the other hand, the effect of higher dose of ipsapirone on striatal DA release may be due to 5-HT(1A)

14 also investigated the effects of ethanol and ipsapirone on the expression of the gene encoding the 5-

15 ted the temporal effects of both ethanol and ipsapirone on the expression of three NF-kappaB dependen

16                     The serotonin-1A agonist ipsapirone prevented ethanol-associated apoptosis; it al

17                                              Ipsapirone produced a biphasic effect; low dose (0.1 mg/

18 ts suggest that the ability of lower dose of ipsapirone to decrease DA release in the NAC is more lik

19 eased expression of the 5-HT(1A) receptor in ipsapirone-treated control neurons.

20                                     Although ipsapirone treatment decreased the expression of cIAP1,

21 nitudes of the core hypothermic responses to ipsapirone were (1) not different between groups and (2)