Postsynaptic calcium, but not cumulative depolarization, is necessary for the induction of associative plasticity in Hermissenda
Postsynaptic calcium, but not cumulative depolarization, is necessary for the induction of associative plasticity in Hermissenda
复制标题
突触后钙，但不是累积去极化，对于 Hermissenda 联想可塑性的诱导是必要的
作者：
L. Matzel;R. Rogers
Hermissenda中的关联记忆的神经元修饰起源于视觉和前庭系统之间的突触相互作用，并且可以通过这些会聚通路的连续体外刺激来模仿。在前庭刺激的偏移处（即，毛细胞活性）时，B光感受器短暂地从突触抑制中释放，导致轻微的去极化（2-4 mV）。如果光诱导的去极化和突触前前庭活动的连续配对在时间上连续发生，则这种去极化“积累”并被假设以细胞内Ca 2+的持续升高和由此产生的Ca（2+）介导的K+通道磷酸化以及相关的输入电阻增加而达到高潮。在这里，我们证明，这种累积的去极化是既不必要，也不足以为生物物理修改的B细胞膜指示记忆的形成。与最近的几个报告一致的一次试验学习Hermissenda，一个配对的光与机械刺激的前庭毛细胞导致神经元输入电阻的上升，在整个B细胞膜衰减的prepairing离子电渗注射的Ca 2+螯合剂EGTA（25 mM），表明这种增效作用是Ca 2+依赖。然而，使用单个配对否定了跨试验去极化累积的可能性。在随后的实验中，B光感受器经历了累积的去极化，并在输入电阻的一致上升，在多个配对的光和毛细胞刺激。然而，如果B光感受器在每次配对之前和之后被电压钳位在其初始静息电位，从而消除累积的去极化，则电阻的上升不仅持续，而且增强。此外，如果不成对的光呈现之后是电流诱导的去极化（模拟累积去极化），则未检测到输入电阻的增加。为了直接评估累积去极化对电压依赖性Ca 2+电流的影响，对B细胞索马膜上的内向电流进行了分析。确定了（1）内向电流在持续去极化期间可能经历部分失活，（2）峰电流在重复去极化期间被抑制，以及（3）峰电流经历稳态失活，使得当从比-60 mV更正的保持电位引起时，峰电流降低。对该电流的分析表明，当这些配对在去极化膜电位下进行时，例如在累积去极化期间，光和突触前活动的配对将减少电压依赖性Ca 2+内流。（400字处截断摘要）
The neuronal modifications that underlie associative memory in Hermissenda have their origins in a synaptic interaction between the visual and vestibular systems, and can be mimicked by contiguous in vitro stimulation of these converging pathways. At the offset of vestibular stimulation (i.e., hair cell activity), the B photoreceptors are briefly released from synaptic inhibition resulting in a slight depolarization (2–4 mV). If contiguous pairings of light-induced depolarization and presynaptic vestibular activity occur in close temporal succession, this depolarization “accumulates” and has been hypothesized to culminate in a sustained rise in intracellular Ca2+ and a resultant Ca(2+)-mediated phosphorylation of K+ channels as well as an associated increase in input resistance. Here we demonstrate that this cumulative depolarization is neither necessary nor sufficient for the biophysical modifications of the B cell membrane indicative of memory formation. Consistent with several recent reports of one-trial learning in Hermissenda, one pairing of light with mechanical stimulation of the vestibular hair cells resulted in a rise in neuronal input resistance across the B cell membrane that was attenuated by a prepairing iontophoretic injection of the Ca2+ chelator EGTA (25 mM), indicating that this potentiation was Ca2+ dependent. However, the use of a single pairing negates the possibility of an accumulation of depolarization across trials. In a subsequent experiment, B photoreceptors underwent a cumulative depolarization, and a coincident rise in input resistance, during multiple pairings of light and hair cell stimulation. However, if the B photoreceptor was voltage clamped at its initial resting potential before and after each pairing, thus eliminating the cumulative depolarization, the rise in resistance not only persisted, but was enhanced. Moreover, if unpaired light presentations were followed by a current-induced depolarization (to mimic cumulative depolarization), no increase in input resistance was detected. To assess directly the effect of a cumulative depolarization on the voltage-dependent Ca2+ current, an analysis of the inward current on the B cell soma membrane was conducted. It was determined that (1) the inward current may undergo a partial inactivation during sustained depolarization, (2) the peak current was depressed during repetitive depolarizations, and (3) the peak current underwent a steady- state inactivation, such that it was reduced when elicited from holding potentials more positive than -60 mV. The analysis of this current suggests that pairings of light and presynaptic activity would reduce voltage-dependent Ca2+ influx when those pairings are conducted at depolarized membrane potentials, such as during cumulative depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)