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Study of Brain Plasticity Ramps up in the 1970s: New Phenomena and New Explanations
Author(s) -
Gerald Schneider
Publication year - 2011
Publication title -
brain behavior and evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.05
H-Index - 77
eISSN - 1421-9743
pISSN - 0006-8977
DOI - 10.1159/000330062
Subject(s) - neuroscience , plasticity , neuroplasticity , psychology , cognitive science , developmental plasticity , cognitive psychology , biology , physics , thermodynamics
ranged with Nauta to join his lab for postdoctoral work after receiving my graduate degree. He was interested in the plan to undertake neuroanatomical studies of animals with early brain damage. We discussed using paradigms that had not long before been used to find evidence of collateral sprouting in the spinal cord and brain of adult cats and rats after selective damage to axonal pathways. Nauta and I began the project by making lesions of visual cortex in neonatal cats. However, we found it difficult to keep the kittens alive, and I suggested that we try using hamsters for the project. I was already very familiar with Syrian hamsters from my thesis studies of behavioral effects of lesions of the visual system, and hamsters have a special advantage for studies of early brain damage – they are born in a very immature state, on the sixteenth day of gestation. Soon we were making visual cortex lesions in hamster nestlings. Walle Nauta was a very experienced and skillful surgeon, whereas I was still acquiring surgical skills. Nauta operated on the first hamsters in the experiments, removing the visual cortex. When I attempted the same surgery on my own, in some cases the lesion was too deep and there was damage to the underlying superior colliculus. When I traced the retinal projections in the first case in which the In the autumn of 1966, shortly after completion of PhD thesis work, I began experiments on brain damage inflicted early in life. In the thesis work I had done experimental studies of behavioral effects of brain damage – published in two papers [Schneider, 1967, 1969]. This work led to my experimental quest to find underlying mechanisms that could explain why behavioral effects of early lesions were so different from effects of adult lesions. I knew that there may be neuroanatomical changes after damage when the brain was still developing – changes that did not occur after damage suffered later in life. I felt that if no alterations in pathways occurred, then some basic assumptions we were making about brain-behavior relationships might have to be called into question. My hope was to do postdoctoral work with the well-known neuroanatomist Walle J.H. Nauta, the inventor of silver-staining methods for tracing axonal pathways (at that time, the most sensitive methods for tract tracing). When I discussed this plan with my department head at MIT, HansLucas Teuber, he told me that Nauta would soon be coming to MIT as the first neuroanatomist to join a psychology department faculty. After Professor Nauta had arrived and set up his laboratory, I made his acquaintance and began interacting with people working in his lab. Soon I had arPublished online: August 26, 2011

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