Abstract
Synchronous neural activity occurs throughout the brain in association with normal and pathological brain functions. Despite theoretical work exploring how such neural coordination might facilitate neural computation and be corrupted in disease states, it has proven difficult to test experimentally the causal role of synchrony in such phenomena. Attempts to manipulate neural synchrony often alter other features of neural activity such as firing rate. Here we evaluate a single gene which encodes for the blue-light gated cation channel channelrhodopsin-2 and the yellow-light driven chloride pump halorhodopsin from Natronobacterium pharaonis, linked by a ‘self-cleaving’ 2A peptide. This fusion enables proportional expression of both opsins, sensitizing neurons to being bi-directionally controlled with blue and yellow light, facilitating proportional optical spike insertion and deletion upon delivery of trains of precisely-timed blue and yellow light pulses. Such approaches may enable more detailed explorations of the causal role of specific features of the neural code.
Highlights
It has long been debated to what extent synchronous or preciselytimed neural activity contributes to neural computation and behavior
We illuminated the neuron with the Poisson train of alternating yellow and blue light pulses shown in Figure 1D
When an optically-sensitized neuron was driven by the Poisson train of yellow and blue light pulses, the neuron fired spikes with different timings than occurred in darkness, but the resultant spikes were still similar across repeated trials of current injection + light illumination
Summary
It has long been debated to what extent synchronous or preciselytimed neural activity contributes to neural computation and behavior. Synchronous neural activity within or between brain regions has been observed during, or associated with, many brain functions including timing-dependent plasticity, global stimulus feature processing, visuomotor integration, emotion, working memory, motor planning, and attention (e.g., Gray et al, 1989; Roelfsema et al, 1997; Brivanlou et al, 1998; Donoghue et al, 1998; Steinmetz et al, 2000; Fries et al, 2001; Tallon-Baudry et al, 2001; Froemke and Dan, 2002; Perez-Orive et al, 2002; Seidenbecher et al, 2003; Courtemanche and Lamarre, 2004; Buschman and Miller, 2007), as measured with multielectrode recording, electroencephalography (EEG), magnetoencephalography (MEG), and local field potential (LFP) analysis. In which pharmacological or genetic strategies for selectively disrupting synchrony happened to be compatible with local cellular and network properties, pioneering attempts have been made to perturb spike timing without altering other aspects of neural coding such as spike rate (MacLeod and Laurent, 1996; Bao et al, 2002; Robbe et al, 2006), but no generalized method for doing so exists
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