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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Bioactive lipids in excitatory neurotransmission and neuronal plasticity.
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Bioactive lipids in excitatory neurotransmission and neuronal plasticity.

机译：兴奋性神经传递和神经元可塑性中的生物活性脂质。

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摘要

Long-term potentiation (LTP), a model of activity-dependent synaptic plasticity and of certain forms of memory, comprises the persistent enhancement of excitatory neurotransmission that results from high-frequency activation. A presynaptic component of LTP is thought to be modulated by a retrograde messenger generated by the postsynaptic neuron. Arachidonic acid, nitric oxide, carbon monoxide and PAF have each been proposed as retrograde messengers in LTP, but arachidonic acid, unlike PAF, requires NMDA receptor activation. A PAF antagonist (BN 52021) that provides neuroprotection in ischemia-reperfusion displaces [3H] PAF bound to presynaptic membranes, blocks PAF-induced glutamate exocytosis and inhibits LTP. An antagonist selective for the intracellular PAF binding site (BN 50730) did not affect LTP, nor did BN 52021 modify NMDA currents. LTP was induced with weak synaptic stimulation coupled with postsynaptically administered enzyme resistant mcPAF. Theta-burst stimulation (10 min) after bath applications of mcPAF (1 microM) induced APV-independent LTP that was blocked by 5 microM BN 52021. When this antagonist was infused into the hippocampus before or immediately after training, it impaired memory of inhibitory avoidance training in the rat. Memory was not altered if the antagonist is infused 30 or 60 min after training. Moreover, mcPAF enhances memory on retention test performance of step-down inhibitory avoidance habituation and learning in rats. Also, memory was studied using a caudate nucleus-dependent cued water maze task. Rats received an 8 trial (30 s intertrial interval) training session in which a visible cued escape platform was located in a different quadrant of the maze of each trial. Following trial 8, the rats received a unilateral post-training intra-caudate injection of mcPAF (1 microgram/0.5 microliter), BN 52021 (0.5 microgram/0.5 microliter) or vehicle. On a retention test session 24 h later, latency to mount the escape platform was used as a measure of memory. The retention test escape latencies of rats given mcPAF were significantly lower than those of the vehicle-injected controls, indicating a memory enhancing effect of mcPAF. Injection of mcPAF did not affect retention when administered 2 h post-training, indicating a time-dependent effect of mcPAF on memory. The latencies for animals injected with BN 52021 were significantly higher than those of the controls, indicating that antagonism of endogenous PAF impairs memory. The findings show that PAF plays a role in memory formation in a caudate-mediated cued discrimination task. Administration of BN 52021 2 h post-training had no affect on retention, indicating a time-dependent effect of endogenous PAF on memory formation. PAF, the most potent bioactive lipid known, modulates excitatory synaptic transmission, neuronal plasticity and memory. When PAF production is overstimulated as in seizures or ischemia, it becomes neurotoxic.
机译：长期增强（LTP）是一种依赖于活动的突触可塑性和某些形式的记忆的模型，它包括由高频激活引起的兴奋性神经传递的持续增强。 LTP的突触前组件被认为是由突触后神经元产生的逆行信使调节的。花生四烯酸，一氧化氮，一氧化碳和PAF均已被提议作为LTP中的逆行信使，但是花生四烯酸与PAF不同，它需要NMDA受体活化。在缺血再灌注中提供神经保护作用的PAF拮抗剂（BN 52021）取代了[3H]与突触前膜结合的PAF，阻断了PAF诱导的谷氨酸胞吐作用并抑制LTP。对细胞内PAF结合位点有选择性的拮抗剂（BN 50730）不影响LTP，BN 52021也不改变NMDA电流。 LTP是由弱突触刺激与突触后施用的酶抗性mcPAF结合诱导的。洗澡后应用mcPAF（1 microM）的Theta爆发刺激（10分钟）诱导了独立于APV的LTP，被5 microM BN 52021阻断。将这种拮抗剂在训练前或训练后立即注入海马体，会削弱抑制性记忆在大鼠中进行回避训练。如果在训练后30或60分钟注入拮抗剂，记忆不会改变。此外，mcPAF增强了大鼠降压回避习惯和学习的记忆力。此外，使用尾状核依赖性暗示水迷宫任务研究记忆。大鼠接受了8次试验（间隔30 s），其中在每个试验迷宫的不同象限中都有一个可见的提示逃生平台。在试验8之后，大鼠接受了单侧训练后尾状注射mcPAF（1微克/0.5微升），BN 52021（0.5微克/0.5微升）或赋形剂。在24小时后的保留测试会话中，将安装逃生平台的等待时间用作内存的度量。给予mcPAF的大鼠的保留测试逃逸潜伏期显着低于溶媒注射的对照组，表明mcPAF具有增强记忆力的作用。训练后2 h注射mcPAF不会影响记忆力，这表明mcPAF对记忆力具有时间依赖性。注射BN 52021的动物的潜伏期显着高于对照组，表明内源性PAF的拮抗作用会损害记忆。研究结果表明，PAF在尾状介导的提示歧视任务中在记忆形成中起作用。训练后2 h服用BN 52021对保留没有影响，表明内源性PAF对记忆形成具有时间依赖性。 PAF是已知的最有效的生物活性脂质，可调节兴奋性突触传递，神经元可塑性和记忆力。当癫痫发作或局部缺血时过度刺激PAF产生时，它会产生神经毒性。

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