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1 with hypothalamic Crh expression results in anxiolysis.
2 omotion, and seizure inhibition, but not for anxiolysis.
3 ehavior as well as locomotor stimulation and anxiolysis.
4 ause of negative contrast or novelty-induced anxiolysis.
5 , expensive, and do not consistently provide anxiolysis.
6 role for 5-HT(4) receptors in cognition and anxiolysis.
7 nt differences in the quality of sedation or anxiolysis.
8 eased in the amygdala during ethanol-induced anxiolysis.
9 for chromatin remodeling possibly leading to anxiolysis.
10 underlying the mechanisms of ethanol-induced anxiolysis.
11 s of drug for similar levels of sedation and anxiolysis (14.4 +/- 1.2 mg/8 hrs vs. 1.6 +/- 0.1 mg/8 h
12 of NPS in the basolateral amygdala promotes anxiolysis after chronic ethanol consumption, thereby pr
14 clear complex of the amygdala (BLA) produces anxiolysis and interferes with the generation of conditi
15 al role of treatment expectations in placebo anxiolysis and provide insight into the underlying neura
17 -2 adrenergic receptor agonist that produces anxiolysis and sleep-like sedation without narcosis or r
18 sant agents, including motor incoordination, anxiolysis, and the elicitation of signs of physical dep
20 cebo treatments on fear and anxiety (placebo anxiolysis) are well known from clinical practice, and t
21 ns seem essential for neuropeptide S-induced anxiolysis, as this effect was blocked by pharmacologica
22 e treatment along with verbal suggestions of anxiolysis can attenuate experimentally induced states o
26 Compound 23 induced significantly stronger anxiolysis in mice than piperine and thus may serve as a
27 anol at concentrations relevant to abuse and anxiolysis, in a cAMP-dependent and ERK-dependent manner
32 ced temporal plastic changes in EtOH-induced anxiolysis or withdrawal anxiety, and the presence or ab
33 a-each implemented an independent feature of anxiolysis: reduced risk-avoidance, reduced respiratory
34 cal activities, such as vasoconstriction and anxiolysis, remains to be investigated, adequate tools a
36 expression of the social familiarity-induced anxiolysis (SFiA) appears dependent on the prefrontal co
39 2-GABAARs) are required for diazepam-induced anxiolysis, with no evidence for an involvement of any o
40 g GABAA receptors have been shown to provide anxiolysis without sedation in preclinical models, where
41 e a greater ability to achieve analgesia and anxiolysis without some of the adverse concomitant effec
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