In a prior study (Jacquin et al., '86c), the response properties and projections of neonatally axotomized trigeminal (V) primary afferents were studied in the adult rat. Here, single‐unit recording, electrical stimulation, and receptive field (RF) mapping techniques were also used to assess the functional consequences of neonatal infraorbital nerve section upon postsynaptic cells in V brainstem subnucleus interpolaris (SpVi). Of 904 cells studied, 385 were from normal adults and 519 were from neonatally deafferented adults. Infraorbital nerve section at birth resulted in: (1) a substantial reduction in those areas of SpVi containing cells with infraorbital RFs, and only a slight increase in areas solely responsive to noninfraorbital surfaces, (2) an absence of orderly topography within cells expressing regenerate primary afferent inputs, (3) a slight increase in mean discharge latency to V ganglion or thalamic shocks, (4) an increased relative percentage of cells orthodromically activated by diencephalic or cerebellar shocks, (5) a decreased relative percentage of mystacial vibrissa‐sensitive local circuit neurons, with a corresponding increase in local circuit nociceptors and unresponsive cells, (6) an increased relative percentage of mystacial nociceptors, vibrissae, guard hair, and/or skin sensitive cells projecting to thalamus and/or cerebellum, (7) an increased percentage of local circuit neurons with RFs including more than one vibrissa, whereas projection neurons did not differ from normal in the number of vibrissae composing their RFs, and (8) an increased relative percentage of cells expressing interdivisional and intermodality convergence, split RFs, spontaneous activity, directional, high velocity, and neuroma sensitivity. Thus neonatal nerve section produces changes in topography, inputs, projection status, and responses of surviving postsynaptic neurons. Although many of these centrally observed alterations can be attributed to altered peripheral projections in axotomized V primary afferents, others must reflect central reorganization. The central mechanisms responsible for the synthesis of deafferentation‐induced RFs remain to be elucidated.
- nerve damage