Season primes the brain in an arctic hibernator to facilitate entrance into torpor mediated by adenosine A(1) receptors.
Season primes the brain in an arctic hibernator to facilitate entrance into torpor mediated by adenosine A(1) receptors.
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DOI：
10.1523/jneurosci.1240-11.2011
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发表时间：
2011-07-27
期刊：
影响因子：
--
通讯作者：
Drew KL
中科院分区：
文献类型：
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作者：
Jinka TR;Tøien Ø;Drew KL
冬眠哺乳动物的冬眠定义了哺乳动物代谢需求和体温的最低点，以适应能量供应减少的季节性时期。尽管中枢神经系统（CNS）是冬眠的关键调控者，但在冬眠开始时代谢抑制的机制尚不清楚。季节性冬眠动物，如北极地松鼠（AGS）只在冬季冬眠季节表现出冬眠。因此，冬眠的季节性特征为其调节提供了线索。在本研究中，我们在一年中的不同时间将腺苷受体激动剂和拮抗剂注入AGS的侧脑室，同时监测氧气消耗率和核心体温作为冬眠指标。A1拮抗剂环戊基茶碱（cyclopentyltheophylline， CPT）可逆转自发性进入休眠状态。腺苷A1受体激动剂n6 -环hexyladenosine （CHA）在冬眠季中期有6只，在冬眠季早期有2只，在夏季和淡季无6只。冬眠季节ha引起的冬眠与A1AR激活有关；A3AR激动剂2-Cl-IB MECA未能诱导麻木，A2aR拮抗剂MSX-3未能逆转自发发作的麻木。cha诱导的昏睡与自发进入昏睡相似。这些结果表明，嗜睡发作时的代谢抑制是通过A1AR激活在中枢神经系统内调节的，并且需要嘌呤能信号敏感性的季节性转换。
Torpor in hibernating mammals defines the nadir in mammalian metabolic demand and body temperature that accommodates seasonal periods of reduced energy availability. The mechanism of metabolic suppression during torpor onset is unknown although the central nervous system (CNS) is a key regulator of torpor. Seasonal hibernators such as the arctic ground squirrel (AGS) display torpor only during the winter, hibernation season. The seasonal character of hibernation thus provides a clue to its regulation. In the present study we delivered adenosine receptor agonists and antagonists into the lateral ventricle of AGS at different times of the year while monitoring the rate of O2 consumption and core body temperature as indicators of torpor. The A1 antagonist, cyclopentyltheophylline (CPT) reversed spontaneous entrance into torpor. The adenosine A1 receptor agonist, N6-cyclohexyladenosine (CHA) induced torpor in 6 out of 6 AGS tested during the mid-hibernation season, 2 out of 6 AGS tested early in the hibernation season and none of the 6 AGS tested during the summer, off-season. CHA-induced torpor within the hibernation season was specific to A1AR activation; the A3AR agonist 2-Cl-IB MECA failed to induce torpor and the A2aR antagonist MSX-3, failed to reverse spontaneous onset of torpor. CHA-induced torpor was similar to spontaneous entrance into torpor. These results show that metabolic suppression during torpor onset is regulated within the CNS via A1AR activation and requires a seasonal switch in the sensitivity of purinergic signaling.