Sarda N, Cespuglio R, Gharib A, Reynaud D
I.N.S.E.R.M., U. n 205, Villeurbanne.
C R Acad Sci III. 1989;308(17):473-8.
Immunohistochemical localization of adenosine deaminase (ADA), marker for the putative neurotransmitter/neuromodulator adenosine, has revealed a population of ADA-positive neurons in the ventrolateral hypothalamus in the rat brain. These posterior neurons possess adenosine uptake sites. We have studied the effects of local injections of adenosinergic drugs on the sleep-wake cycle in the rat. Microinjection of erythro-9-(hydroxy-2, nonyl-3) adenine (EHNA), a specific inhibitor of adenosine deaminase, resulted in a significant decrease in wakefulness (W) and an increase in deep slow wave sleep (SWS, or S2) and paradoxical sleep (SP). On the other hand, microinjections of soluflazine, a nucleoside transport inhibitor, increased W and decreased total sleep. These opposite modifications may reflect opposite variations in the extracellular concentrations of Ado and consequently different responses of A1/A2 adenosine receptors.
腺苷脱氨酶（ADA）是假定神经递质/神经调质腺苷的标志物，免疫组织化学定位显示，大鼠脑海马腹外侧存在一群ADA阳性神经元。这些后部神经元具有腺苷摄取位点。我们研究了局部注射腺苷能药物对大鼠睡眠-觉醒周期的影响。微量注射腺苷脱氨酶特异性抑制剂erythro-9-(hydroxy-2, nonyl-3) adenine（EHNA）可导致觉醒（W）显著减少，深度慢波睡眠（SWS，或S2）和异相睡眠（SP）增加。另一方面，微量注射核苷转运抑制剂soluflazine可增加W并减少总睡眠时间。这些相反的改变可能反映了细胞外腺苷浓度的相反变化，从而导致A1/A2腺苷受体的不同反应。
