RUI: Circadian Rhythms in NPY and Y5 Receptor Deficient Mice

玛丽E.哈灵顿，0234203，RUI：NPY和Y5受体缺陷小鼠的昼夜节律。生物节律每天通过外部信号重置，以维持24小时的内部循环。 光暗周期是同步这些昼夜节律的一个非常重要的线索。 对光线的反应是通过对昼夜节律钟的直接视网膜输入来介导的，这种输入可以被其他神经输入修改。 一种重要的调节神经化学物质是神经肽Y（NPY）。 神经肽Y和光重置之间的相互作用为光诱导相对于生态或内部因素的调节提供了一个灵活的点。 利用缺失NPY基因或重要NPY受体（NPY Y5受体）基因的小鼠，通过光重置生物钟相位中的NPY。将研究这些小鼠的跑轮活动节律，并且预期NPY和NPY Y5受体缺陷小鼠将显示出降低的稳定性和对光：暗循环的夹带的可靠性。 在持续黑暗下研究的小鼠将揭示这些神经化学物质对昼夜节律产生和表达的影响。 哺乳动物的昼夜节律起搏点位于下丘脑视交叉上核（SCN）。 视交叉上核细胞在培养中保持自我维持的振荡，允许从一个孤立的时钟相移行为的措施。 为了确定Y5受体是否介导NPY对光相移的影响，将具有基因缺失的小鼠与对照比较相移后施加于SCN中的昼夜节律钟的NPY的影响。 预计Y5受体缺陷小鼠将不会显示出NPY阻断光诱导的相移的证据，这提供了明确的证据证明该受体在介导NPY对昼夜节律钟resetting.This工作的影响中的重要性，涉及到与外部24小时光：暗周期保持同步的日常情况。扩大我们对NPY在昼夜节律系统中作用的理解，将使我们更好地了解适应不断变化的环境周期的神经基础。 这项研究将在一所女子本科学院进行，有前途的女本科生和少数民族将在研究中发挥领导作用。

Mary E. Harrington, 0234203, RUI: Circadian rhythms in NPY and Y5 receptor deficient mice. Biological rhythms are reset each day by external signals to maintain a 24 hour internal cycle. The light:dark cycle is one very important cue for synchronizing these circadian rhythms. Responses to light are mediated through a direct retinal input to the circadian clock, an input that can be modified by other neural inputs. One important modulating neurochemical is neuropeptide Y (NPY). Interactions between NPY and light resetting provide a point of flexibility for adjustments of light entrainment relative to ecological or internal factors.The present research will examine the role of NPY in circadian clock phase resetting by light, making use of mice with deletion of either the NPY gene or the gene for an important NPY receptor, the NPY Y5 receptor. Wheel-running activity rhythms of these mice will be studied and it is expected that NPY- and NPY Y5 receptor-deficient mice will show decreased stability and reliability of entrainment to a light:dark cycle. Mice studied under constant darkness will reveal effects these neurochemicals have on circadian rhythm generation and expression. The mammalian circadian pacemaker is located in the hypothalamic suprachiasmatic nuclei (SCN). Suprachiasmatic nucleus cells maintain a self-sustained oscillation in culture, allowing measures of phase-shifting behavior from an isolated clock. To determine if the Y5 receptor mediates the effects of NPY on light phase shifts, mice with gene deletions will be compared with controls for the effect of NPY applied to the circadian clock in the SCN after a phase shift. It is expected that the Y5 receptor deficient mouse will not show evidence for NPY blocking light-induced phase shifts, providing definitive proof of the importance of this receptor in mediating the effect of NPY on circadian clock resetting.This work relates to the everyday situation of maintaining synchronization with the external 24 h light:dark cycle. Expanding our understanding of the role of NPY in the circadian system will allow better knowledge of the neural basis of flexibility as we adapt to changing environmental cycles. This research will be conducted at an undergraduate college for women, with promising undergraduate women and minorities taking leadership roles in conducting the studies.