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”)
Summary
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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