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L S Carman

Publications and source records attributed to L S Carman.

5 recordsLinked to original sources
PubMed1992

Orienting behavior in hamsters with lesions of superior colliculus, pretectum, and visual cortex.

We examined cortical and subcortical mediation of visual locomotor orienting function by comparing the behavior of hamsters with discrete bilateral lesions affecting the pretectum, superior colliculus (SC), or visual cortex (VC). Orienting and approach to stationary targets was evaluated by measuring the accuracy of hamsters' approaches to small black apertures, located at eye level along the wall of a circular white arena. Hamsters with bilateral ablation of the visual cortex were slightly impaired for approaches to central field targets, whereas those with ibotenic acid lesions of the pretectum (which spares fibers of passage and thus leaves tectal afferents intact) were totally unimpaired. Hamsters with transection of the brachium of SC (BSC) at the prectectal-SC (PT-SC) border were severely impaired in their ability to approach stationary targets in central and peripheral fields. Thus, we did not detect any of the central field sparing that has been reported by others for rodents with similar lesions. Several possible reasons for the disparity between our results and those of others are discussed. Overall, our results indicate that in hamsters the SC is essential for normal visually guided approach to dark, stationary targets throughout the visual field. Further, our results and qualitative observations indicate that the approach errors are most likely due to deficits of visuomotor integration rather than to a lack of visual scanning.

Animals↗
PubMed1992

Aberrant retinal projections to midbrain targets mediate spared visual orienting function in hamsters with neonatal lesions of superior colliculus.

Rodents, cats, and most nonmammalian vertebrates with bilateral tectal deafferentation or ablation in adulthood are extremely deficient at orienting to visual stimuli; yet animals with neonatal lesions of superficial layers of the superior colliculus (SC) show partial sparing of this response, particularly for targets in the central visual field. In this study, we sought to determine whether these spared orienting abilities are mediated by aberrant retinal projections to the remaining intermediate layers of the SC, or whether visual cortex (VC) mechanisms or alternative behavioral strategies are responsible. Neonatal golden hamsters received either bilateral heat lesions of the SC (rlSC), or a heat lesion of the right SC and enucleation of the right eye (rSCrE). This latter procedure causes axons from the left eye to recross the tectal midline and terminate in the "wrong" (left) SC (Schneider 1973). As adults, both groups of hamsters were extremely deficient in visually guided approach to stationary targets, although rlSC-lesioned hamsters showed some sparing for central field targets and rSCrE-lesioned hamsters often made wrong-direction turns for targets in the left peripheral field. We then subjected both groups of neonatally lesioned hamsters to bilateral aspiration lesions of the VC. Retesting showed no change in visual orienting behavior as a result of the cortical lesions. Labeling of the optic tract with horseradish peroxidase (HRP) revealed abundant aberrant retinal projections to remaining intermediate layers of the SC and thalamic nucleus lateralis posterior (LP), as well as supernormal innervation of pretectal nuclei, the dorsal terminal nucleus of the accessory optic tract, and the ventral nucleus of the lateral geniculate body (LGv). We conclude that the spared visual orienting capabilities of hamsters with rlSC and rSCrE lesions are mediated by the aberrant midbrain projections, and that cortical mechanisms are not involved in spared visual orienting functions following these neonatal lesions.

Animals↗
PubMed1991

Partial lesion of the substantia nigra: relation between extent of lesion and rotational behavior.

Recent work, largely carried out in primate models of Parkinson's disease (PD), indicates that residual dopaminergic neurons in the midbrain and their axons to the nucleus accumbens and striatum can be stimulated to sprout collateral axons, reinnervate the striatum, and cause a behavioral recovery. We sought to create a partial lesion model of PD in the rat that would (i) mimic the pattern of cell loss in human patients in early stages of PD, and (ii) permit examination of experimental manipulations that promote sprouting of axons of the surviving dopaminergic cells in the midbrain. Rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra pars compacta (SNpc) were tested weekly for rotational asymmetry following administration of apomorphine or amphetamine. After completion of behavioral testing, the animals were sacrificed and the brains immunolabeled for tyrosine hydroxylase (TH). Analysis of anatomical and behavioral data revealed a strong correlation between number of remaining TH-immunoreactive cells in the SNpc and the number of rotations induced by apomorphine. There was no significant correlation between number of remaining TH-immunoreactive nigral neurons and number of rotations induced by amphetamine. We also examined the relation between area in the denervated striatum with remaining TH-immunoreactive axons, number of TH-immunoreactive cells in the lesioned SNpc, and rotational behavior. As expected, there was a strong correlation between area innervated by TH-immunoreactive axons and number of remaining TH-immunoreactive neurons in the lesioned SNpc. Total extent of innervation was also correlated with number of apomorphine-induced rotations but not with number of amphetamine-induced rotations.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗