Affiliations: Davidson College, Davidson, NC 28035, USA
Note: [] Corresponding address: Stuart Dickson Professor, Laboratory of
Behavioral Neuroscience, Department of Psychology, Davidson College, Davidson,
North Carolina 28035, USA, Tel.: +1 704 894 2888; Fax:+1 704 894 2512; E-mail:
[email protected].
Abstract: Functional reorganization is often invoked to account for recovery
of function after central nervous system (CNS) injury. The mechanisms
underlying this possible reorganization, however, remain uncertain. In the last
30 years, studies of the hippocampal formation of rats have indicated that the
CNS is capable of undergoing significant changes in its pattern of connectivity
in response to injury. Here, we explore numerous examples of lesion-induced
alterations in hippocampal connectivity known as axonal sprouting. Both
homotypic and heterotypic sprouting occur in the denervated hippocampus after
unilateral entorhinal cortex lesions. We assess the behavioral relevance of
glutamatergic homotypic sprouting emerging from the surviving contralateral
entorhinal area (i.e., the crossed temporodentate projection) as well as the
heterotypic sprouting from the remaining surviving afferents (e. g., the
cholinergic septodentate pathway) to the hippocampus. Studies examining the
role of crossed temporodentate sprouting in recovery from memory deficits after
entorhinal cortex injury indicate that homotypic sprouting may indeed
contribute to a reorganization of cortical function resulting in recovered
mnemonic capacity. Heterotypic sprouting is not as clearly linked to recovery
of function after bilateral entorhinal injury. We propose a tripartite model
for functional reorganization based on homotypic sprouting, neurotrophic
factors, and altered inhibitory functioning to account for how relatively small
increases in surviving homotypic pathways might restore neurological
function.
