Donald Hebb chose visual learning in main visual cortex (V1) of
March 28, 2017
Donald Hebb chose visual learning in main visual cortex (V1) of the rodent to exemplify his theories of how the mind stores info through long-lasting homosynaptic plasticity. viewed through the deprived attention. Second we describe a less analyzed but no less interesting form of plasticity in the visual cortex known as stimulus-selective response potentiation (SRP). SRP results in raises in the response of V1 to a visual stimulus through repeated looking at and bears all the hallmarks of perceptual learning. We describe evidence implicating an important part for potentiation of thalamo-cortical synapses in SRP. In addition we present fresh data indicating that there are some features of this form of plasticity that cannot be fully accounted for by such feed-forward Hebbian plasticity suggesting contributions from intra-cortical circuit parts. requires activation of cortical NMDAR [23 44 and the LTD model suggests how NMDAR might result in the loss of visual responsiveness . This ‘LTD hypothesis’ is Adamts4 now very well supported by experimental findings. Over the past decade extensive study has shown (we) that MD in visual cortex causes LTD-like synaptic modifications and (ii) the molecular mechanisms of LTD are required for the effects of MD. Mimicry and occlusion are the two main criteria used to assess whether two different causes of synaptic plasticity converge onto a common set of mechanisms . This approach has been taken to establish for example that one-trial learning in the hippocampus [48 49 induces plasticity akin to LTP. A biochemical signature of LTD is the loss of surface indicated AMPAR CUDC-907 and concomitant changes in AMPAR subunit phosphorylation at specific residues and these same changes have been observed in visual cortex following brief MD . Furthermore the induction of LTD using electrical stimulation of the dLGN causes major depression of VEP amplitude related to that observed after MD. Therefore deprivation-induced major depression and LTD mimic one another. In addition the induction of synaptic major depression by MD reduces the amount of LTD that can be accomplished [15 50 (number 1pharmacological approach applies medicines locally round the VEP recording site in V1 in awake animals. Phasic inhibition can be blocked by applying the GABAA receptor antagonist bicuculline … Actually if the cause of the OD shift is a modification of excitatory synaptic transmission the question remains as CUDC-907 to which excitatory synapses are primarily responsible. It is known from your pioneering work of Hubel and Wiesel that long-term MD enduring weeks or weeks can shrink dLGN axon arbours but it has been less clear the extent to which modification of thalamocortical (TC) synaptic CUDC-907 transmission is responsible for the rapid loss of visual responsiveness during MD . This question was addressed recently in the mouse using an pharmacological strategy to isolate purely TC synaptic VEPs . By co-applying a cocktail of CUDC-907 the GABAA receptor agonist muscimol with the GABAB receptor blocker “type”:”entrez-protein” attrs :”text”:”SCH50911″ term_id :”1052743264″ term_text :”SCH50911″SCH50911 it was possible to prevent all unit firing in an area of cortex while preserving TC input . Under these circumstances purely synaptic TC VEPs can be recorded in awake animals before or after deprived vision depressive disorder induced by three days of MD. Prior to any OD shift the TC VEP shows a normal 2 : 1 contralateral:ipsilateral vision response ratio indicating that TC input from your contralateral eye is usually twice as strong overall as input from your ipsilateral vision . Deprived vision depressive disorder pushes the OD ratio to 1 1 : 1 and this ratio is retained in the presence of the inhibitory cocktail indicating that OD shifts can be fully accounted for through TC plasticity (physique 2and synaptic scaling (but not LTP) are both absent in juvenile mice lacking TNFα  all support the scaling model. We note that evidence supporting scaling is not inconsistent with metaplasticity. Because interocular correlations are still possible during MD for visual stimuli with low spatial frequencies upward drift of deprived-eye responses could reflect an associative LTP-like process during open-eye.