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- W1984400009 abstract "The α-adrenoceptor agonist clonidine (12.5–50.0 μg/kg) produced a dose dependent increase in the latency to initiate lateral hypothalamic stimulation. The insurmountable postsynaptic α-adrenoceptor antagonist phenoxybenzamine (0.2–0.8 mg/kg) had no effect on self-stimulation by itself, but potentiated the inbibitory effects of clonidine. The fact that the concurrent escape behavior to thr intracranial stimulation was unchanged by either clonidine or the phenoxybenzamine-clonidine combination suggests that the inhibition is specific to the rewarding component of hypothalamic stimulation. Yohimbine (0.5–2.0 mg/kg) produced a dose-dependent increase in both response latencies. This lack of behavioral specificity may reflect yohimbine's wide range of pharmacological activity. Dexamphetamine (0.25–0.50 mg/kg) reversed clonidine's inhibition of self-stimulation reward in a specific and dose-dependent fashion. This reversal could be blocked by previous inhibition of catecholamine synthesis with α-methyl-p-tyrosine. These data support the concept that the α-adrenoceptors play a critical role in the modulation of hypothalamic self-stimulation reward. They further suggest that the inhibitory effects of clonidinen self-stimulation reward represent an agonist effect on presynaptic α-adrenoceptors." @default.
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- W1984400009 title "α-Adrenergic modulation of hypothalamic self-stimulation: Effects of phenoxybenzamine, yohimbine, dexamphetamine and their interactions with clonidine" @default.
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- W1984400009 doi "https://doi.org/10.1016/0014-2999(78)90261-3" @default.
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