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Effects of Visual Deprivation on the Visual System

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Our research continues to be directed at an understanding of thalamic relays, with emphasis on the visual thalamus (LGN & LP-Pul), using the in vitro slice preparation in mice and cats. Techniques include the use of simple thalamic slices to study LGN and LP-Pul in cats and the use of thalamocortical slices to study VPM and POre (somatosensory thalamus) in mice. We shall also use photostimulation with caged glutamate, partly in order to identify presynaptic units in a search for synaptically coupled pairs for corticothalamic, TRN to relay cell, and relay cell to TRN synapses. A general hypothesis is that LGN and VPM are first order relays, being the first relay of peripheral information (e.g., retinal or lemniscal) to cortex, whereas LP-Pul and POm are higher order relays, relaying information between cortical areas. In particular, we have defined 3 Aims: In Aim 1, we shall study corticothalamic inputs and how they differ between LGN (or VPM) and LP-Pul (or POm). The hypothesis is that LGN (or VPM), being a first order relay, receives only layer 6 input from cortex, and that this is modulatory, whereas LP-Pul (or POm), being mostly a higher order relay, receives cortical input from layer 5 and 6. We shall determine if the layer 6 input to LP-Pul (or POm), like that to LGN (or VPM), is modulatory, whereas the layer 5 input is driver, functioning like the retinal input to LGN. This would implicate the LP-Pul (and POm) as playing a heretofore ignored, key role in corticocortical communication and would challenge the conventional hypothesis of how visual and somatosensory cortical areas are functionally connected. Finally, we will study the efficacy of layer 6 corticothalamic inputs in controlling an important voltage gated current in relay cells, known as Iv. Aim 2 will broadly test the function of the TRN in modulating thalamic relays, and in particular will test details of TRN circuitry, challenging the conventional views that relay cell to TRN connections represent feedback inhibition and that layer 6 cortical input to TRN connections represent feedforward inhibition. We will also test hypotheses regarding the different synaptic properties of relay cell and cortical layer 6 inputs to TRN cells. As above, we will study the efficacy of TRN inputs in controlling It. Finally, Aim 3 will test the hypothesis that different cell classes can be recognized in LP-Pul on the same basis that distinguishes X and Y cells in LGN.

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