Neurogenesis and Regeneration of Nervous Tissue

In adults, neurogenesis occurs mainly in the hippocampus due to inhibitory influences from neuroglia, particularly oligodendrocytes, and the absence of growth-stimulating cues in other brain regions. The myelin produced by oligodendrocytes actively inhibits neuronal regeneration, making neurogenesis almost non-existent outside the hippocampus.

After spinal cord injury, astrocytes proliferate rapidly and form scar tissue that physically blocks regeneration. Combined with myelin inhibition from oligodendrocytes, this makes brain and spinal cord injuries typically irreversible. In contrast, peripheral nerve injuries have much higher capacity for repair when the cell body remains intact.

Peripheral nerve regeneration begins with Wallerian degeneration, where the injured axon and myelin sheath degrade while the neurolemma remains intact. Macrophages clear debris, Schwann cells multiply and form a regeneration tube, and increased RNA and protein synthesis promotes axon regrowth to complete regeneration.

For peripheral nerve regeneration, the neuron cell body must remain intact and Schwann cells must stay functional. If the injury gap is too large or filled with collagen fibers, new axons cannot grow across the damaged region, preventing successful regeneration.

Wallerian degeneration is the degradation of the injured axon and myelin sheath distal to the damage site. During this process, the region swells and breaks into fragments while the neurolemma remains intact. This allows macrophages to clear debris and enables Schwann cells to prepare the regeneration pathway.

After injury, Schwann cells multiply and grow toward each other across the damaged area, forming a regeneration tube that guides new axon growth. This tube provides structural support and chemical cues necessary for axons to regrow and restore nerve function.

Chromatolysis is the disintegration of Nissl bodies in the neuron cell body following axonal damage. This process indicates the neuron is responding to injury and preparing for regeneration by increasing RNA and protein synthesis to rebuild the damaged axon and restore function.