Introduction

After a penetrating injury, neurons of the adult mammalian central nervous system (CNS) show only a limited and transient ability to regenerate, so that any motor and sensory deficits incurred are permanent. This is in direct contrast to the situation in the fetal and perinatal CNS, where neurons show a remarkable growth capacity after injury, with negligible consequent functional deficits. Our laboratory has been studying the differences in cellular and trophic responses that underlie the developmental changes in the CNS wounding response.

The cellular response to injury

The mature CNS

The response to injury in the adult CNS is characterized by three sequential and overlapping events: acute haemorrhage and inflammation, followed by glial/collagen scar formation, which is accompanied by an abortive regeneration response by axotomized neurons (Maxwell et al., 1990a). Briefly, at first the lesion is haemorrhagic and extravasated platelets play a major role in initiating both clotting in the lesion lumen and vasoconstriction in the wound edges associated with oedema and necrosis. Polymorphs, monocytes and later macrophages appear in large numbers. Their concentration in the wound is probably controlled by a homing response organized both by platelet factors and also by the expression of addressins on the endothelium of the brain vasculature and counter-receptors on leukocytes, as elsewhere in the body, although little is known of the details of this process in the damaged CNS. By 3–5 days, most of the extravasated erythrocytes have disappeared. The wound and its margins are filled with macrophages, monocytes and a few polymorphs. Fibroblasts and collagen fibres first appear at this stage to form a mesenchymal core in which extracellular matrix molecules, such as laminin and fibronectin, are deposited.