The diving response is characterized by bradycardia, apnea, and increased peripheral resistance. This reflex response is initiated by immersing the nose in water. Because the anterior ethmoidal nerve (AEN) innervates the nose, our hypothesis was that intact AENs are essential for initiating the diving response in voluntarily diving rats. Heart rate (HR) and arterial blood pressure (BPa) were monitored using implanted biotransmitters. Sprague-Dawley rats were trained to voluntarily swim 5 m underwater. During diving, HR decreased from 480 ± 15 to 99 ± 5 bpm and BPa increased from 136 ± 2 to 187 ± 3 mmHg. Experimental rats (N = 9) then received bilateral AEN sectioning, while Sham rats (N = 8) did not. During diving in Experimental rats 7 days after AEN surgery, HR decreased from 478 ± 13 to 76 ± 4 bpm and BPa increased from 134 ± 3 to 186 ± 4 mmHg. Responses were similar in Sham rats. Then, during nasal stimulation with ammonia vapors in urethane-anesthetized Experimental rats, HR decreased from 368 ± 7 to 83 ± 4 bpm, and BPa increased from 126 ± 7 to 175 ± 4 mmHg. Responses were similar in Sham rats. Thus, 1 week after being sectioned the AENs are not essential for initiating a full cardiorespiratory response during both voluntary diving and nasal stimulation. We conclude that other nerve(s) innervating the nose are able to provide an afferent signal sufficient to initiate the diving response, although neuronal plasticity within the medullary dorsal horn may be necessary for this to occur.

In response to stimulation of the nasal passages with volatile ammonia vapors, the nasopharyngeal reflex produces parasympathetically mediated bradycardia, sympathetically mediated increased peripheral vascular tone, and apnea. The anterior ethmoidal nerve (AEN), which innervates the anterior nasal mucosa, is thought to be primarily responsible for providing the sensory afferent signals that initiate these protective reflexes, as bilateral sectioning causes an attenuation of this response. However, recent evidence has shown cardiovascular responses to nasal stimulation with ammonia vapors are fully intact 9 days after bilateral AEN sectioning, and are similar to control animals without bilaterally sectioned AENs. To investigate this restoration of the nasopharyngeal response, we recorded the cardiorespiratory responses to nasal stimulation with ammonia vapors immediately after, and 3 and 9 days after, bilateral AEN sectioning. We also processed brainstem tissue for Fos to determine how the restoration of the nasopharyngeal response would affect the activity of neurons in the medullary dorsal horn (MDH), the part of the ventral spinal trigeminal nucleus caudalis region that receives primary afferent signals from the nose and nasal passages. We found 3 days after bilateral AEN sectioning the cardiorespiratory responses to nasal stimulation are partially restored. The bradycardic response to nasal stimulation is significantly more intense 3 days after AEN sectioning compared to Acute AEN sectioning. Surprisingly, 3 days after AEN sectioning the number of Fos-positive neurons within MDH decreased, even though the cardiorespiratory responses to nasal stimulation intensified. Collectively these findings indicate that, besides the AEN, there are alternate sensory pathways that can activate neurons within the trigeminal nucleus in response to nasal stimulation. The findings further suggest trigeminal neuronal plasticity involving these alternate sensory pathways occurs in as few as 3 days after bilateral AEN sectioning. Finally, activation of even a significantly reduced number of MDH neurons is sufficient to initiate the nasopharyngeal response.