Environmental enrichment and visual system: thalamocortical and crossmodal plasticity

It has been demonstrated that the complex sensorimotor and social stimulation achieved by rearing animals in an enriched environment (EE) can reinstate juvenile-like plasticity in the adult cortex. However, it is not known whether EE can affect thalamocortical transmission. In the first part of this work, I investigated this problem by recording in vivo field potentials from the visual cortex evoked by electrical stimulation of the dorsal lateral geniculate nucleus (dLGN) in anaesthetized rats. I found that a period of EE during adulthood shifted the input-output curves and increased paired-pulse depression, suggesting an enhanced synaptic strength at thalamocortical terminals. Accordingly, EE animals showed an increased expression of the vesicular glutamate transporter 2 (vGluT-2) in geniculocortical afferents to layer IV. Rats reared in EE also showed an enhancement of thalamocortical long-term potentiation (LTP) triggered by theta-burst stimulation (TBS) of the dLGN. To monitor the functional consequences of increased LTP in EE rats, I recorded visual evoked potentials (VEPs) before and after application of TBS to the geniculocortical pathway. I found that responses to visual stimulation were enhanced across a range of contrasts in EE animals. This was accompanied by an upregulation of the intracortical excitatory synaptic marker vGluT-1 and a decrease in the expression of the vesicular GABA transporter (vGAT), indicating a shift in the excitation/inhibition ratio. Thus, in the adult rat, EE enhances synaptic strength and plasticity of the thalamocortical pathway associated with specific changes in glutamatergic and GABAergic neurotransmission. Another interesting problem connected to EE, is the possibility that the multimodal sensory stimulation provided by this rearing protocol can affect functional relationships among different cortical areas, thus contributing to the effect observed on visual cortical plasticity. In the second part of my work, I explored this problem by looking for cortical areas monosynaptically connected with primary visual cortex (V1), using stererotaxic injections of cholera toxin β subunit. I found that primary visual cortex is connected with secondary motor cortex (M2, also known as frontal eye field), primary somatosensory cortex (S1) and primary auditory cortex (A1). These connections could explain how the sensorimotor stimulation provided by EE, which does not have a specific “visual” component, can affect visual function. Functional interactions between V1 and M2 or A1 were investigated using multichannel local field potential recordings in awake, freely moving mice, subjected to EE since birth. Quantitative analysis of LFP signals revealed that EE has opposite effects on V1-M2 and V1-A1 activity correlation, resulting in a decrease of functional coupling in the first case and in an increase in the second case. These data provide novel insights into the mechanisms by which EE shapes the adult brain.