Electron microscopic analysis of lesion-induced changes in synaptic structure and immunogold labeling of neurotransmitters within the feline trigeminal nucleus.

This report uses lesion and postembedding immunogold protocols to examine the ultrastructural details of lesion-induced synaptic and neurotransmitter changes in the feline trigeminal nucleus. Electron microscopic (EM) analysis concentrated on lamina II (substantia gelatinosa) of the subnucleus pars caudalis (PC) which is one relay site or trigeminal fibers involved in nociception. Special attention was directed to analysis of reoccupation of synaptic sites vacated by primary afferent degeneration. Primary afferents are caused to degenerate by performing unilateral retrogasserian rhizotomy. After survival times of 1, 2, 6, and 7 days, sections of PC were processed for postembedding immunogold labeling with antibodies to the neurotransmitters gamma aminobutyric acid (GABA) and glutamate (Glu). The results show: (1) degenerating primary afferent terminals were easily identified in various stages of degeneration; (2) Glu immunoreactivity was observed in early forms of degenerated primary afferent terminals with clumped vesicles as well as in the highly distorted, electron dense terminals of later degeneration; and (3) some GABA immunoreactive terminals formed atypical synapses which exhibited both asymmetric (excitatory) and symmetric (inhibitory) synaptic densities. A possible model is presented of the progression of events following trigeminal nerve lesion which results in atypical synapse formation. Such altered synaptic relationships seen in PC following trigeminal rhizotomy may be related to hyperactivity that is seen in animals and to the atypical facial pain following nerve lesions in humans.