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Recovery of frontal cortex-mediated visual behaviors following neurotrophic rescue of axotomized neurons in medial frontal cortex
Journal article   Open access   Peer reviewed

Recovery of frontal cortex-mediated visual behaviors following neurotrophic rescue of axotomized neurons in medial frontal cortex

F Haun and T J Cunningham
The Journal of neuroscience, v 13(2), pp 614-622
Feb 1993
DOI: https://doi.org/10.1523/JNEUROSCI.13-02-00614.1993
PMID: 8426229
Featured in Collection :   UN Sustainable Development Goals @ Drexel
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https://doi.org/10.1523/JNEUROSCI.13-02-00614.1993View
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Abstract

Cell Survival Culture Techniques Rats Neurons - cytology Occipital Lobe - physiology Axons - physiology Visual Cortex - surgery Pattern Recognition, Visual - physiology Frontal Lobe - physiology Visual Cortex - physiology Discrimination Learning - physiology Vision, Ocular - physiology Animals Culture Media Occipital Lobe - embryology Neurons - physiology Parietal Lobe - physiology Nerve Growth Factors - physiology Parietal Lobe - surgery Frontal Lobe - embryology
Unilateral lesions extending across the boundary region of visual and parietal cortex in adult rats result in the death of 20-35% of neurons in layers II-III of the caudal third of medial frontal cortex ipsilaterally, a neuron population labeled with 3H-thymidine on the 19th day of gestation (E19). Additionally, there is a consistent 15% loss of these labeled neurons in an area between 50% and 60% of the distance along the caudal-rostral extent of medial frontal cortex, an area that may function analogously to the frontal eye field of primates. All of these neurons are rescued from axotomy-induced death by delivering into the posterior cortex lesion cavity for 2 weeks a macromolecular fraction of culture medium conditioned by embryonic primordia of the frontal-occipital pathway (CM). Moreover, the rescue is apparently permanent, with normal numbers of these neurons present in CM animals 6-7 weeks after the neurotrophic factor is no longer being supplied exogenously. Behaviorally, control operates receiving a similarly prepared fraction of unconditioned medium are significantly impaired in the number of trials needed to learn two visual discrimination tasks. This deficit is attributable in part to a bias in erroneous responses to the side contralateral to the lesion. The error bias reflects a failure to inhibit repeated incorrect responding contralaterally. In contrast, the CM animals learn both visual tasks in a normal number of trials and have no contralateral error bias. Rather, all CM animals have an contralateral error bias. Rather, all CM animals have an ipsilateral error bias (interpreted as an unmasking of the contralateral neglect expected after a parietal cortex lesion).

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