Abstract

NMDA-dependent Hebbian learning drives neuronal plasticity in different cortical areas, and across species. In the primary somatosensory cortex (S-I), Hebbian learning is induced via the persistent low-rate afferent stimulation of a small area of skin. In particular, plasticity is induced in superficial cortical layers II/III of the S-I cortex that represents the stimulated area of skin. Here, we used the model system of NMDA-dependent Hebbian learning to investigate the influence of non-afferent (visual) input on Hebbian plasticity in S-I. We induced Hebbian learning in 48 participants by applying 3 hours of tactile coactivation to the right index fingertip via small loudspeaker membranes. During coactivation, different groups viewed either touches to individual fingers, which is known to activate S-I receptive fields, touches to an object, which should not activate S-I receptive fields, or no touch at all. Our results show that coactivation significantly lowers tactile spatial discrimination thresholds at the stimulated finger post- versus pre-training across groups. However, we did not find evidence for a significant modulatory effect of visual condition on tactile spatial discrimination performance. This suggests that non-afferent (visual) signals do not interact with Hebbian learning in superficial cortical layers of S-I, but may integrate into deeper cortical layers instead.

Highlights

  • In the primary somatosensory cortex (S-I), NMDA (N-methyl-D-aspartate)-dependent Hebbian learning is induced by constant low-rate stimulation from the thalamus

  • We induced Hebbian learning in three groups of participants by applying weak tactile stimuli to a confined area at the tip of the index finger

  • One group observed touches applied to the tip of the index finger (“social group”), one group observed touches applied to an object (“object group”), and a third group looked at a fixation cross (“no-vision group”)

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Summary

Introduction

In the primary somatosensory cortex (S-I), NMDA (N-methyl-D-aspartate)-dependent Hebbian learning is induced by constant low-rate stimulation from the thalamus. We argue that investigating the specific influence of visual signals on NMDA-dependent Hebbian learning that in animals is confined to superficial cortical layers in S-I provides a valuable first step to target these questions. To this end, we induced Hebbian learning in S-I using an established tactile coactivation protocol[14]. Coactivation does not lead to improved tactile spatial discrimination thresholds when NMDA-receptors are blocked using a NMDA-receptor blocker, but effects are doubled by amphetamine, as one would expect for NMDA-dependent learning[14] This provides additional evidence for a similar role of NMDA in human S-I Hebbian learning as has been reported in rodents

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