Centre for Integrative Physiology, University of Edinburgh, Edinburgh, United Kingdom.
PLoS Comput Biol. 2012;8(10):e1002740. doi: 10.1371/journal.pcbi.1002740. Epub 2012 Oct 18.
Vasopressin neurons, responding to input generated by osmotic pressure, use an intrinsic mechanism to shift from slow irregular firing to a distinct phasic pattern, consisting of long bursts and silences lasting tens of seconds. With increased input, bursts lengthen, eventually shifting to continuous firing. The phasic activity remains asynchronous across the cells and is not reflected in the population output signal. Here we have used a computational vasopressin neuron model to investigate the functional significance of the phasic firing pattern. We generated a concise model of the synaptic input driven spike firing mechanism that gives a close quantitative match to vasopressin neuron spike activity recorded in vivo, tested against endogenous activity and experimental interventions. The integrate-and-fire based model provides a simple physiological explanation of the phasic firing mechanism involving an activity-dependent slow depolarising afterpotential (DAP) generated by a calcium-inactivated potassium leak current. This is modulated by the slower, opposing, action of activity-dependent dendritic dynorphin release, which inactivates the DAP, the opposing effects generating successive periods of bursting and silence. Model cells are not spontaneously active, but fire when perturbed by random perturbations mimicking synaptic input. We constructed one population of such phasic neurons, and another population of similar cells but which lacked the ability to fire phasically. We then studied how these two populations differed in the way that they encoded changes in afferent inputs. By comparison with the non-phasic population, the phasic population responds linearly to increases in tonic synaptic input. Non-phasic cells respond to transient elevations in synaptic input in a way that strongly depends on background activity levels, phasic cells in a way that is independent of background levels, and show a similar strong linearization of the response. These findings show large differences in information coding between the populations, and apparent functional advantages of asynchronous phasic firing.
加压素神经元对渗透压产生的输入做出反应,利用内在机制从缓慢不规则的放电转变为明显的相位模式,由持续数十秒的长爆发和沉默组成。随着输入的增加,爆发持续时间延长,最终转变为连续放电。相位活动在细胞之间仍然是异步的,不会反映在群体输出信号中。在这里,我们使用计算加压素神经元模型来研究相位放电模式的功能意义。我们生成了一个简洁的突触输入驱动尖峰放电机制模型,该模型与体内记录的加压素神经元尖峰活动非常吻合,针对内源性活动和实验干预进行了测试。基于积分和放电的模型为涉及由钙失活钾泄漏电流产生的活动依赖性慢去极化后电位 (DAP) 的相位放电机制提供了一个简单的生理解释。这是由活动依赖性树突内 dynorphin 释放的较慢、相反的作用来调节的,该释放会使 DAP 失活,相反的效应产生连续的爆发和沉默期。模型细胞本身没有自发性活动,但当受到模拟突触输入的随机扰动时会放电。我们构建了一个这样的相位神经元群体,以及另一个具有相似细胞但缺乏相位放电能力的群体。然后,我们研究了这两个群体在编码传入输入变化的方式上有何不同。与非相位群体相比,相位群体对持续的突触输入增加呈线性响应。非相位细胞对突触输入的短暂升高的反应强烈依赖于背景活动水平,而相位细胞的反应则独立于背景水平,并且反应也具有类似的强线性化。这些发现表明群体之间的信息编码存在很大差异,并且异步相位放电具有明显的功能优势。