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Defining the selective pattern of synapse replacement that occurs in different areas of the damaged brain is essential for predicting the limits of functional compensation that can be achieved after various types of brain injury. Here we describe the time course of dendritic reorganization, spine loss and recovery, and synapse replacement in the striatum following a unilateral cortex ablation. We found that the time course for the transient loss and recovery of dendritic spines on medium spiny I (MSI) neurons, the primary postsynaptic target for corticostriatal axons, paralleled the time course for the removal of degenerating axon terminals from the neuropil and the formation of new synapses on MSI neurons. Reinnervation of the deafferented striatum occurred chiefly by axon terminals that formed asymmetric synapses with dendritic spines of MSI neurons, and the mean density of asymmetric synapses recovered to 86% of the sham-operated rat value by 30 days postlesion. In addition, the synaptic circuitry of the reconstructed striatum was characterized by an increase in the number of multiple synaptic boutons (MSBs), i.e., presynaptic axon terminals that make contact with more than one dendritic spine. Whether the postsynaptic contacts of MSBs are formed with the dendritic spines of the same or a different parent dendrite in the striatum is unknown. Nevertheless, these data suggest that the formation of MSBs is an essential part of the compensatory response to the loss of input from the ipsilateral cortex following the aspiration lesion and may serve to modulate activity-dependent adaptive changes in the reconstructed striatum that can lead to functional recovery.

We examined the relationship between age and urinary excretion of free cortisol in acutely stressed middle-aged and elderly persons. We observed that elderly persons under stress excreted larger amounts of urinary-free cortisol than did middle-aged persons; Pearson's r between age and cortisol = 0.38, p less than 0.05. When the sample was stratified by severity of depressive symptoms, the relationship between age and cortisol excretion was strongly accentuated among those with severe depressive symptoms (r = 0.62, p = 0.01) and diminished among those with milder symptoms (r = 0.25, N.S.). Potentially confounding factors such as diet, use of medications, and physical stature were controlled and did not explain the observations. The high depression scores in this acutely stressed sample were indicative of a higher severity of stress response and also a higher risk of occurrence of depressive syndromes. The depressive syndromes did not resemble depressive disorder of an endogenous nature.

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