Vega-Zuniga, T. | bioRxiv Science

bioRxiv2023

A thalamic hub of action cues coordinates early visual processing and perception

Distinguishing between sensory experiences elicited by external stimuli and an animals own actions is critical for accurate perception and motor control. However, the diversity of behaviors and their complex influences on the senses make this distinction challenging. Here, we uncover an action cue hub that coordinates both visual processing in the brains first visual relay and motor commands. We show that the ventral lateral geniculate nucleus (vLGN) acts as a corollary discharge (CD) center, integrating visual translational optic flow signals and motor copies from saccades, locomotion, and pupil dynamics. The vLGN relays these signals to correct action-specific visual distortions and refine perception, as shown for the superior colliculus and a depth estimation task. Simultaneously, brain-wide vLGN projections drive corrective actions necessary for accurate visuomotor control. Our results reveal an extended CD architecture that refines early visual transformations and coordinates actions via a distributed hub-and-spoke network enabling visual perception during action.

neuroscience↗

bioRxiv2022

Subcortical circuit dysfunctions delay perceptual decision-making in autism models

Despite the diverse genetic origins of autism spectrum disorders (ASDs), affected individuals share strikingly similar and correlated behavioural traits that include perceptual and sensory processing challenges. Notably, the severity of these sensory symptoms is often predictive of the expression of other autistic traits. However, the origin of these perceptual deficits remains largely elusive. Here, we show a recurrent impairment in visual threat perception that is similarly impaired in three independent models of ASD with different molecular aetiologies. Interestingly, this deficit is associated with reduced avoidance of threatening environments - a non-perceptual trait. Focusing on a common cause of ASDs, the Setd5 gene mutation, we define the molecular mechanism. We show that the perceptual impairment is caused by a potassium channel (Kv1) mediated hypoexcitability in a subcortical node essential for the initiation of escape responses, the dorsal periaqueductal grey (dPAG). Targeted pharmacological Kv1 blockade rescued both perceptual and place avoidance deficits, causally linking seemingly unrelated trait deficits to the dPAG. Our findings reveal a link between rapid perception controlled by subcortical pathways and appropriate learned interactions with the environment, and define a non-developmental source of such deficits in ASD.

neuroscience↗