Abstract
Disorders involving dysfunctional sensory processing are characterized by an inability to filter sensory information, particularly simultaneously arriving multimodal inputs. We examined the effects of prenatal exposure to valproic acid (VPA), a teratogen linked to sensory dysfunction, on the behavior of juvenile and adult rats, and on the anatomy of the superior colliculus, a critical multisensory integration center in the brain. VPA-exposed rats showed deficits in colliculus-dependent behaviors including startle response, prepulse inhibition, and nociceptive responses. Some deficits reversed with age. Stereological analyses revealed that colliculi of VPA-treated rats had significantly fewer parvalbumin-positive neurons, a subset of GABAergic cells. These results suggest that prenatal VPA treatment affects the development of the superior colliculus and leads to persistent anatomical changes evidenced by aberrant behavior in tasks that require sensory processing.
Highlights
Several neurocognitive disorders in humans involve dysfunctional sensory processing
BEHAVIOR Previous studies have shown that the effects of prenatal exposure to valproic acid (VPA) on certain behavioral measures are correlated with the postnatal age at which these behaviors are quantified (Markram et al, 2007; Markram and Markram, 2010, #68472)
In adults there were no significant differences in the startle responses for VPA-treated rats that received either a single injection of VPA (n = 8) or multiple injections of www.frontiersin.org
Summary
Several neurocognitive disorders in humans involve dysfunctional sensory processing. These include but are not limited to autism spectrum disorders, attention deficit/hyperactivity disorders, fetal valproate syndrome, and putative sensory processing disorders. Sensory deficiencies in these disorders may manifest as hypo or hypersensitivity to sensory stimuli. Many exposed children lag in motor function and coordination, speech and learning. They often have decreased social interactions, hyperactivity, and difficulties with attention. Humans exposed prenatally to VPA suffer from sensorimotor dysfunctions, most prominently hypersensitivity to innocuous sensory stimuli (Ardinger et al, 1988)
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