Age-dependent sparing of visual function after bilateral lesions of primary visual cortex.

Abstract

Bilateral lesions of primary visual cortex (PVC) sustained early in life induce the visual system to undergo structural and functional reorganization and produce modified neuronal networks capable of mediating visual abilities that would be impaired if the lesions occurred in adulthood. Reorganization after early lesion is also accompanied by degeneration of the lateral geniculate nucleus of the thalamus, and 90% of beta retinal ganglion cells die via retrograde degeneration. It is unclear whether the high potential of the system to reorganize after early lesion could overcome the effects of beta retinal ganglion cell death. Visual acuity, which depends on an intact beta-cell array, was impaired in cats that underwent PVC lesions on postnatal day 1 and indicated that neuroplastic potential was insufficient to overcome early lesion-induced maladaptive plasticity. Animals with lesions made at 1 month of age, a stage accompanied by high levels of neuroplastic potential but no death of beta cells, achieved acuity measures equivalent to intact animals. The authors conclude that visual signals are rerouted to subserve functionality when the lesion is made at 1 month of age, but not at 1 day of age.

Long-term effects of neonatal medial temporal ablations on socioemotional behavior in monkeys (Macaca mulatta).

“…The finding of more profound socioemotional disturbances after neonatal lesions suggests that the monkeys given lesions in adulthood retained at least some aspects of the socioemotional repertoire they had acquired during maturation, whereas the neonatally operated animals never succeeded in acquiring them. This finding also represents a reverse pattern from that commonly reported for other types of behavioral effects after early versus late cerebral damage (Goldman et al, 1970; Kennard, 1936, 1938; Kolb, 1987; Málková et al, 2000; Málková et al, 1995; Rushmore et al, 2008; Shupert et al, 1993; Webster, Ungerleider, & Bachevalier, 1995) indicating greater deficits after the adult than the infant lesions. Thus, the present findings have important implications for socioemotional as distinct from other types of behavioral and cognitive development after medial temporal damage in children.…”

“…In contrast, neonatal lesions of the medial temporal lobe in Group AH produced a severe and chronic loss of social interactions. This level of longlasting socioemotional impairment from neonatal lesions was not predicted, given the special degree of plasticity of the immature brain and the recovery of function that often follows early damage (Goldman, Rosvold, & Mishkin, 1970;Kennard, 1936Kennard, , 1938Kolb, 1987;Malkova, Bachevalier, Webster, & Mishkin, 2000;Ma ´lkova ´et al, 1995;Rushmore, Rigolo, Peer, Afifi, Valero-Cabre, & Payne, 2008;Shupert, Cornwell, & Payne, 1993;, raising the question of whether the impairment was nevertheless lower than would be expected from the same damage incurred in adulthood. To address this question, we prepared a new group of monkeys with the same medial temporal ablation as before, but one made when the animals were already fully mature adults.…”

Adult cortical plasticity following injury: Recapitulation of critical period mechanisms?

“…Interestingly, after an acute injury or stroke in the adult brain, maximal neuronal plasticity and recovery occur during a sensitive period that follows the cortical insult (Nudo R.J. et al, 1996, Kolb et al, 2000, Villablanca and Hovda, 2000, Coq and Xerri, 2001, Biernaskie et al, 2004, Barbay et al, 2006, Salter et al, 2006, Rushmore et al, 2008, Nielsen et al, 2013), and as we will explore below, the cascade of events that reconfigure cortical circuitry following deprivation-induced plasticity and plasticity following cortical injury are strikingly similar (see these excellent reviews on plasticity following cortical injury/stroke (Wieloch and Nikolich, 2006, Cramer, 2008, Murphy and Corbett, 2009, Overman and Carmichael, 2013). …”

Acute lesions of primary visual cortical areas in adult cats inactivate responses of neurons in higher visual cortices

“…However, cats with neonatal lesions of primary visual cortices (including chiefly areas 17 and 18) showed more sparing of vision in performance of visual cliff detection, orienting to suddenly appearing targets, and other visual tasks (Rushmore & Payne, 2004;Shupert et al, 1993;). These residual visual functions are likely mediated through plastic reorganization of visual pathways after lesions (Payne, 2004;Rushmore and Payne, 2004;Rushmore et al, 2008;, as demonstrated by previous morphological studies on post-lesion rewiring of visual circuits capable of mediating visual abilities (Kalil et al, 1991;Lomber et al, 1993Lomber et al, , 1995Payne& Lomber, 1998). Previous research found that a significant portion of neurons in posteromedial lateral suprasylvian (PMLS) cortex were responsive to moving gratings as well as simple and complex random dot kinematograms (RDKs) following early lesions of primary visual cortex in cats (Ouellette et al, 2007).…”