Lashgari Reza, Khakpour-Taleghani Behrooz, Motamedi Fereshteh, Shahidi Siamak
Neuroscience Research Center and Department of Physiology, Shaheed Beheshti Medical University, Tehran, Iran.
Neurobiol Learn Mem. 2008 Sep;90(2):309-16. doi: 10.1016/j.nlm.2008.05.012. Epub 2008 Jul 10.
The locus coeruleus (LC) is the main source of noradrenergic innervations to the forebrain and the hippocampal formation but does not receive noradrenergic projections itself. Previous studies have suggested that hippocampal neural response is modulated by the noradrenergic pathway and that the experimental activation of the LC can potentiate hippocampal responses. Most studies have suggested that the noradrenergic system has controversial effects on long-term potentiation (LTP) in hippocampal neurons, because its influence on synaptic plasticity in perforant path-DG synapses is ambiguous. The aim of this article was to study the LC's role in baseline activity and LTP in perforant path-DG cells of hippocampus by in vivo LC inactivation. Rats were anesthetized with urethane, and LC was temporarily suppressed by intra-LC injection of lidocaine. Population spike (PS) amplitude and excitatory postsynaptic potential (EPSP) slope in DG were recorded 10 min before and 5, 10, 20, 40, 60, and 120 min after tetanization (400 Hz). Saline or lidocaine was injected during the baseline recording (experiment 1), 5 min before tetanus (experiment 2), and 5 min after tetanus (experiment 3). The results from this study indicated that the LC inactivation has no effect on baseline activity of granular cells or maintenance of LTP after tetanization. Moreover, LC inactivation before tetanus had no effect on LTP induction but decreased PS-LTP amplitude 60 and 120 min after tetanization. Taken together, the LC noradrenergic system likely influences LTP induction in later time periods while it has no effect on LTP in earlier time periods.
蓝斑(LC)是去甲肾上腺素能神经支配前脑和海马结构的主要来源,但其本身并不接受去甲肾上腺素能投射。先前的研究表明,海马神经反应受去甲肾上腺素能通路调节,并且LC的实验性激活可增强海马反应。大多数研究表明,去甲肾上腺素能系统对海马神经元的长时程增强(LTP)具有争议性影响,因为其对穿通通路-齿状回(DG)突触的突触可塑性的影响尚不明确。本文的目的是通过体内LC失活来研究LC在海马穿通通路-DG细胞的基线活动和LTP中的作用。用乌拉坦麻醉大鼠,并通过向LC内注射利多卡因来暂时抑制LC。在强直刺激(400Hz)前10分钟以及强直刺激后5、10、20、40、60和120分钟记录DG中的群体峰电位(PS)幅度和兴奋性突触后电位(EPSP)斜率。在基线记录期间(实验1)、强直刺激前5分钟(实验2)和强直刺激后5分钟(实验3)注射生理盐水或利多卡因。本研究结果表明,LC失活对颗粒细胞的基线活动或强直刺激后LTP的维持没有影响。此外,强直刺激前LC失活对LTP诱导没有影响,但在强直刺激后60和120分钟降低了PS-LTP幅度。综上所述,LC去甲肾上腺素能系统可能在后期影响LTP诱导,而在早期对LTP没有影响。