School of Psychology/Centre for Robotics and Neural Systems, University of Plymouth, Plymouth, United Kingdom.
PLoS Comput Biol. 2011 Aug;7(8):e1002117. doi: 10.1371/journal.pcbi.1002117. Epub 2011 Aug 18.
Stimulus-specific adaptation (SSA) occurs when the spike rate of a neuron decreases with repetitions of the same stimulus, but recovers when a different stimulus is presented. It has been suggested that SSA in single auditory neurons may provide information to change detection mechanisms evident at other scales (e.g., mismatch negativity in the event related potential), and participate in the control of attention and the formation of auditory streams. This article presents a spiking-neuron model that accounts for SSA in terms of the convergence of depressing synapses that convey feature-specific inputs. The model is anatomically plausible, comprising just a few homogeneously connected populations, and does not require organised feature maps. The model is calibrated to match the SSA measured in the cortex of the awake rat, as reported in one study. The effect of frequency separation, deviant probability, repetition rate and duration upon SSA are investigated. With the same parameter set, the model generates responses consistent with a wide range of published data obtained in other auditory regions using other stimulus configurations, such as block, sequential and random stimuli. A new stimulus paradigm is introduced, which generalises the oddball concept to Markov chains, allowing the experimenter to vary the tone probabilities and the rate of switching independently. The model predicts greater SSA for higher rates of switching. Finally, the issue of whether rarity or novelty elicits SSA is addressed by comparing the responses of the model to deviants in the context of a sequence of a single standard or many standards. The results support the view that synaptic adaptation alone can explain almost all aspects of SSA reported to date, including its purported novelty component, and that non-trivial networks of depressing synapses can intensify this novelty response.
当神经元的尖峰率随着相同刺激的重复而降低,但当呈现不同的刺激时又恢复时,就会发生刺激特异性适应(SSA)。有人认为,单个听觉神经元中的 SSA 可能为在其他尺度上明显的变化检测机制提供信息(例如,事件相关电位中的失匹配负波),并参与注意力的控制和听觉流的形成。本文提出了一个尖峰神经元模型,该模型根据传递特征特定输入的压抑性突触的收敛来解释 SSA。该模型在解剖学上是合理的,仅由几个均匀连接的群体组成,并且不需要有组织的特征图。该模型经过校准,以匹配一项研究中在清醒大鼠皮层中测量的 SSA。研究了频率分离、偏差概率、重复率和持续时间对 SSA 的影响。使用相同的参数集,该模型生成的响应与其他听觉区域使用其他刺激模式(如块、顺序和随机刺激)获得的广泛发表数据一致。引入了一种新的刺激范式,将异类概念推广到马尔可夫链,允许实验者独立地改变音调概率和切换速率。该模型预测,切换速率越高,SSA 越大。最后,通过比较模型对序列中单一标准或多个标准背景下偏差的响应,解决了稀有或新颖性引发 SSA 的问题。结果支持了这样一种观点,即单独的突触适应可以解释迄今为止报告的 SSA 的几乎所有方面,包括其所谓的新颖性成分,并且具有压抑性突触的非平凡网络可以增强这种新颖性反应。