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Authors & Affiliations
Dylan Myers-Joseph,Adil Khan
Abstract
When animals attend to visual stimuli, neural responses in visual cortex show increased stimulus selectivity compared to viewing the same stimuli without attending. This increased stimulus selectivity is believed to underlie the improved behavioural detection and discrimination of attended stimuli and is a key neural cor-relate of cognitive control. However, the neural circuit mechanisms of attentional modulation are poorly understood. While GABAergic inhibitory circuits can strongly modulate cortical neural activity, it is un-known whether these circuits implement the attentional modulation observed in visual cortex. Vasoactive intestinal peptide (VIP) expressing interneurons in primary visual cortex (V1) receive top-down inputs from prefrontal cortex and exert disinhibitory control over pyramidal neurons by inhibiting somatostatin (SOM) expressing interneurons. We hypothesised that VIP expressing interneurons are involved in the endoge-nous attentional modulation of V1 stimulus responses.
We performed chronic in vivo two-photon calcium imaging of neurons in layer 2/3 of V1 in mice performing an attention switching task. VIP cells in V1 were either optogenetically activated or inhibited, while simul-taneously imaging the calcium activity of the network. Attention produced a robust increase in neural re-sponse selectivity, through a combination of boosting and suppression of responses. Activation of VIP cells produced a strong additive modulation of pyramidal neurons both during passive viewing of visual stimuli, and during active visual discrimination. However, the VIP-induced modulation did not interact with the at-tentional modulation of firing rates. Similarly, inhibition of VIP cells during the task did not affect the atten-tional modulation of pyramidal neuron responses. These results show that VIP interneurons play a minor role, if any, in producing attentional modulation, and suggest a re-evaluation of existing models of top-down response modulation in visual cortex.