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Stimulation of the nasal passages with ammonia vapors can initiate a nasopharyngeal response that resembles the diving response. This response consists of a sympathetically mediated increase in peripheral vascular resistance, parasympathetically mediated bradycardia and an apnea. The current study investigated the role of the anterior ethmoidal nerve (AEN) in the nasopharyngeal response in the rat, as it is thought that the AEN provides the main sensory innervation of the nasal passages. When both AENs were intact, nasal stimulation caused significant bradycardia, hypertension, and apnea and produced Fos label ventrally within the ipsilateral medullary dorsal horn (MDH) and paratrigeminal nucleus just caudal to the obex. This labeling presumably represents activation of second-order trigeminal neurons. When only one AEN was intact, the nasopharyngeal response was slightly attenuated, and a similar pattern of Fos labeling was only seen in the trigeminal nucleus ipsilateral to the intact AEN. The trigeminal labeling contralateral to the intact AEN was significantly reduced. When both AENs were cut, the nasopharyngeal response to nasal stimulation consisted of only a slight apnea and an increase in arterial pressure; the resultant Fos labeling within the trigeminal nucleus was significantly reduced. Cutting both AENs but not stimulating the nasal passages also produced some Fos labeling within the trigeminal nucleus. These findings suggest that a single AEN can provide sufficient afferent input to initiate the cardiorespiratory changes consistent with the nasopharyngeal response. We conclude that the AEN provides a unique afferent contribution that is capable of producing the diving response.
The distribution of labeled neurons in the brain and spinal cord was studied after injecting the Bartha strain of pseudorabies virus (PRV) into the sciatic nerve to provide a baseline for studying neural circuitry after spinal cord injury (SCI) and regeneration. Following a single injection of viral particles into the left sciatic nerve, PRV labeling was found in the spinal cord at 2 days post-injection (p.i.). Increasing complexity in viral labeling from the spinal cord to supraspinal regions became apparent with increasing survival time. In brain regions, several neuronal groups that regulate sympathetic outflow, such as the rostroventrolateral medulla, the lateral paragigantocellular nuclei, and the A5 cells, were densely labeled. However, relatively sparse labeling was noticed in the lateral vestibular nuclei, the red nucleus and the motor cortex whose spinal projections regulate somatic motor function, although those areas were abundantly labeled with Fast blue (FB) in a double-labeling experiment in which FB was co-injected into the lumbar cord. The pattern of viral labeling became more complex beyond 5 days p.i. when increased numbers of cell groups were labeled with PRV but not FB. In addition, some infected neurons started to lyse, as evidenced by a decrease in viral labeling at 7 days p.i. Thus, the 5th day post-viral injection would appear to be an appropriate survival time to obtain maximal labeling with acceptable specificity. We suggest that transneuronal labeling using PRV should be appropriate for studying multi-neural circuitry after SCI and regeneration.
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