Published online by Cambridge University Press: 05 March 2012
Today, we tend to think of the nervous system as a highly plastic structure in which the structure and function of synapses is continually being modified. With this view, we are not surprised by reports of neuronal growth following injury, and indeed, are perhaps surprised that it does not occur more extensively. This is in stark contrast to the view during the first half of the 20th century, based on the extensive work of Ramon y Cajal (1959), that the nervous system was “fixed and immutable”, and that neurons of the adult mammalian central nervous system (CNS) were incapable of any more than very limited and abortive growth. The origins of the shift in viewpoint can be traced to reports in the late 1960s and early 1970s that documented the formation of novel synaptic connections following CNS injury, especially the landmark study (Raisman, 1969) that provided the first electron microscopic evidence that neurons in the septal nucleus were reinnervated after their normal connections had been disrupted by lesions. Similar evidence was then obtained in studies of the superior colliculus (Lund and Lund, 1971) and olfactory bulb (Westrum and Black, 1971). What made these reports noteworthy was the demonstration of novel synaptic connections that had the potential of modifying circuit function.
Initially, these reports of neuronal growth in the mature nervous system were viewed with skepticism, and many felt that the growth occurred only in special circumstances, or was very limited in extent.