Download 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?
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?
Monocular lid closure known
to result in LTD in visual
cortex
2 Possible Mechanisms
Heterosynaptic Depression
Homosynaptic Depression
result of decreased input from deprived eye
relative to the seeing eye
result of decorrelation of input from
deprive eye relative to seeing eye
Results of this study support homosynaptic depression as the
mechanism that triggers LTD in the visual cortex
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
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
Methods
• Experimental Set-up
– Head restrained
mice
– Viewing grating
stimuli/natural scene
stimuli
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
Baseline
Eye
manipulation
Firing Rate
Average
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
Retinal Inactivation
• Retinal inactivation resulted in an increase in
thalamic bursts
• Bursts persisted throughout monocular
inactivation
Retinal Inactivation
• Recording from the contralateral eye changes
the firing patterns of the dLGN ipsilateral core
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
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
Lid Closure
• A: Crosscorrelogram for pairs
of simultaneously
recorded neurons,
grey line represents
unity
– Points indicating
correlation for lid
closure show the
opposite pattern from
retinal inactivation
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
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