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The control of multi-neuron temporal encoding in the LGN by striate feedback

Subject Area Experimental and Theoretical Network Neuroscience
Cognitive, Systems and Behavioural Neurobiology
Term since 2023
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 520285844
 
The main source of visual information into the primary visual cortex is provided by the LGN (Lateral Geniculate Nucleus), which in turn receives information from the retinal ganglion cells (RGCs). The existence of major differences in temporal response properties between LGN neurons and the RGCs, as well as the fact that the LGN integrates retinal and cortical input, suggest that the LGN is not a simple relay nucleus. Rather, LGN likely performs complex computations on the RGC input. Here, we focus on the importance of multi-neuron temporal coding in the LGN. LGN neurons have highly precise stimulus responses and that they encode stimulus information not only by firing rates but also spike timing patterns, which may play an important role in temporal coding. Furthermore, LGN is a prominent source of rhythmic patterns of activity that can entrain the cortex. The synchrony among LGN neurons is thought to be critical for cortico-thalamic transmission. Evidence from previous studies suggests that multi-neuron temporal encoding in the LGN depends on striate feedback. In this project, we will test the following hypotheses in awake, head-fixed mice: (1) that the multi-neuron temporal encoding of naturalistic stimuli (movies) depends critically on the interaction between feedforward inputs from RGCs and feedback inputs from striate cortex; (2) that cortico-thalamic feedback has distinct effects on neural activity for predictable and unpredictable natural visual inputs; (3) that silencing cortico-thalamic feedback alters multi-neuron LGN representations, making them more dissimilar to V1 and more similar to representations closer to the image input level; (4) that cortico-thalamic feedback enhances the encoding of naturalistic stimuli within V1 itself. We will investigate these questions using a combination of multi-areal electrophysiology as well as optogenetics perturbations, including: (i) suppression of cortico-thalamic neurons (Objective 1), and (ii) suppression of neurotransmitter release from cortico-thalamic synaptic terminals (Objective 2). The latter manipulation allows us to distinguish effects of feedback mediated by the visTRN and the dLGN, and examine the functional impact of cortico-thalamic activity on V1 activity itself. The project will involve a tight cooperation between computational and experimental neuroscientists. The results of the project will inform the general function of feedback processing in the central nervous system.
DFG Programme Priority Programmes
 
 

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