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Orexin‐A increases the activity of globus pallidus neurons in both normal and parkinsonian rats
Author(s) -
Xue Yan,
Yang YuTing,
Liu HongYun,
Chen WenFang,
Chen AnQi,
Sheng Qing,
Chen XinYi,
Wang Ying,
Chen Hua,
Liu HongXia,
Pang YaYan,
Chen Lei
Publication year - 2016
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13323
Subject(s) - globus pallidus , orexin , orexin a , neuroscience , basal ganglia , medicine , endocrinology , orexin receptor , neuropeptide , psychology , receptor , central nervous system
Orexin is a member of neuropeptides which was first identified in the hypothalamus. The globus pallidus is a key structure in the basal ganglia, which is involved in both normal motor function and movement disorders. Morphological studies have shown the expression of both OX 1 and OX 2 receptors in the globus pallidus. Employing single unit extracellular recordings and behavioural tests, the direct in vivo electrophysiological and behavioural effects of orexin‐A in the globus pallidus were studied. Micro‐pressure administration of orexin‐A significantly increased the spontaneous firing rate of pallidal neurons. Correlation analysis revealed a negative correlation between orexin‐A induced excitation and the basal firing rate. Furthermore, application of the specific OX 1 receptor antagonist, SB ‐334867, decreased the firing rate of pallidal neurons, suggesting that endogenous orexinergic systems modulate the firing activity of pallidal neurons. Orexin‐A increased the excitability of pallidal neurons through both OX 1 and OX 2 receptors. In 6‐hydroxydopamine parkinsonian rats, orexin‐A‐induced increase in firing rate of pallidal neurons was stronger than that in normal rats. Immunostaining revealed positive OX 1 receptor expression in the globus pallidus of both normal and parkinsonian rats. Finally, postural test showed that unilateral microinjection of orexin‐A led to contralateral deflection in the presence of systemic haloperidol administration. Further elevated body swing test revealed that pallidal orexin‐A and SB ‐334867 induced contralateral‐biased swing and ipsilateral‐biased swing respectively. Based on the electrophysiological and behavioural findings of orexin‐A in the globus pallidus, the present findings may provide a rationale for the pathogenesis and treatment of Parkinson's disease.