Department of Neuroscience, Scripps Research Institute Florida, Jupiter, Florida 33458, and Graduate School of Pharmaceutical Sciences, Chiba University, Chuo-ku, Chiba 260-8675, Japan.
Department of Neuroscience, Scripps Research Institute Florida, Jupiter, Florida 33458, and
J Neurosci. 2015 Jan 21;35(3):1173-80. doi: 10.1523/JNEUROSCI.0978-14.2015.
Although aging is known to impair intermediate-term memory in Drosophila, its effect on protein-synthesis-dependent long-term memory (LTM) is unknown. We show here that LTM is impaired with age, not due to functional defects in synaptic output of mushroom body (MB) neurons, but due to connectivity defects of dorsal paired medial (DPM) neurons with their postsynaptic MB neurons. GFP reconstitution across synaptic partners (GRASP) experiments revealed structural connectivity defects in aged animals of DPM neurons with MB axons in the α lobe neuropil. As a consequence, a protein-synthesis-dependent LTM trace in the α/β MB neurons fails to form. Aging thus impairs protein-synthesis-dependent LTM along with the α/β MB neuron LTM trace by lessening the connectivity of DPM and α/β MB neurons.
虽然衰老已知会损害果蝇的中期记忆,但它对蛋白质合成依赖性长时记忆 (LTM) 的影响尚不清楚。我们在这里表明,LTM 会随着年龄的增长而受损,这不是由于蘑菇体 (MB) 神经元突触输出的功能缺陷,而是由于背侧配对内侧 (DPM) 神经元与其 Postsynaptic MB 神经元的连接缺陷。通过 GFP 重组跨越突触伙伴(GRASP)实验发现,在 α 叶神经突中 DPM 神经元与 MB 轴突的老年动物存在结构连接缺陷。因此,α/β MB 神经元中的蛋白质合成依赖性 LTM 痕迹无法形成。因此,衰老通过降低 DPM 和 α/β MB 神经元的连接,损害了蛋白质合成依赖性 LTM 以及 α/β MB 神经元 LTM 痕迹。