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Thalamic Activity that Drives Visual Cortical Plasticity

Thalamic Activity that Drives Visual Cortical Plasticity. Linden, Heynan, Haslinger & Bear 2009 Laura Pynn 21/04/09. Readings for the week focus on sprouting, changing receptive fields and cortical remapping What patterns of neuronal activity follow a lesion?

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Thalamic Activity that Drives Visual Cortical Plasticity

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  1. Thalamic Activity that Drives Visual Cortical Plasticity Linden, Heynan, Haslinger & Bear 2009 Laura Pynn 21/04/09

  2. Readings for the week focus on sprouting, changing receptive fields and cortical remapping What patterns of neuronal activity follow a lesion? How do these changing patterns of activity play a role in plasticity? Specifically, what are the effects of depriving visual input from one eye on the LGN activity?

  3. Monocular lid closure known to result in LTD in visual cortex Results of this study support homosynaptic depression as the mechanism that triggers LTD in the visual cortex

  4. Monocular Lid Closure vs Retinal Inactivation Monocular Lid Closure - responsiveness of deprived eye causes LTD in visual cortex Retinal Inactivation - no effect on responsiveness on deprive eye - increased responsiveness in contralateral eye

  5. Methods • Recorded from the dLGN in awake mice, comparison between • Normal visual experience (NVE) • Monocular Lid Closure • Retinal inactivation (tetrodotoxin - TTX) • ~ postnatal day 28 • sensitive period for monocular deprivation • Baseline recordings taken approximate NVE (ipsilateral eye occluded) • Monocular lid closure/inactivation carried out on anaesthetized mice

  6. Methods • Experimental Set-up • Head restrained mice • Viewing grating stimuli/natural scene stimuli

  7. Firing Rate for Inactivation and Lid Closure • A: Arrows - phase reversal • B: Black line - median values, no differences between groups Both inactivation and lid closure - no effect on spontaneous activity O = open,C = closed I = inactivated • Visual cortex still receives input Eye manipulation Firing Rate Average Baseline

  8. Temporal Pattern of Spikes ISI analysis • Lid Closure: no effect on ISI distribution • Retinal Inactivation: shift to the left in ISI distribution; increased probability of ISI’s 2-4ms • dLGN firing in bursts

  9. Retinal Inactivation • Retinal inactivation resulted in an increase in thalamic bursts • Bursts persisted throughout monocular inactivation

  10. Retinal Inactivation • Recording from the contralateral eye changes the firing patterns of the dLGN ipsilateral core

  11. Lid Closure • Leads to a decrease in correlated firing between active dLGN neurons (compared to NVE) • Decorrelated input to visual cortex leads to LTD • Conversely, the synchronous dLGN bursts that follow retinal inactivation increases correlative firing

  12. Lid Closure • Ratio of contralateral:ipsilateral VEP amplitude shows significant decrease following lid closure vs inactivation Black - eye contralateral to recording electrode White - eye ipsilateral to recording electrode

  13. Lid Closure • A: Cross-correlogram for pairs of simultaneously recorded neurons, grey line represents unity • Points indicating correlation for lid closure show the opposite pattern from retinal inactivation

  14. Bursts in Retinal Inactivation • Thalamic bursts from retinal inactivation resembles thalamic activity during sleep • Corticothalamic inputs • Increased response of the ipsilateral eye? • intrathalamic circuitry (inhibitory TRN) • Corticothalamic feedback • Altered activity of local dLGN circuitry

  15. Summary • Total dLGN activity the same for retinal inactivation and monocular lid closure • Neither caused decreased total amount of firing, therefore lack of retinal input does not eliminate input to visual cortex • Retinal inactivation leads to synchronous bursts from dLGN which increases correlative firing • Monocular lid closure leads to a decrease in correlative firing of dLGN neurons -- LTD

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