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1. Extracellular recordings of 125 neurons in the rostroventral medulla (RVM) were performed in 35 rats that were maintained in a light plane of anesthesia with methohexital. The neurons were classified as ON, OFF, or NEUTRAL cells, depending on their response to noxious heat applied to the tail. ON cells showed an increase in firing rate just before the tail flick (TF), OFF cells showed a decrease in firing rate just before the TF, and NEUTRAL cells showed no correlation between neural activity and the TF. 2. The effects of electrical stimulation of cervical vagal afferents (VAS) on 1) the activity of ON, OFF, and NEUTRAL cells, 2) TF latency, and 3) arterial blood pressure (ABP) were determined at intensities less than or equal to the intensity of VAS necessary to inhibit the TF reflex to a cutoff latency of 10 s. VAS excited 70.8% of the ON cells and inhibited 77.8% of the OFF cells at greater intensities, including intensities that inhibited the TF. However, 55.6% of the OFF cells inhibited by the threshold intensity of VAS to inhibit the TF reflex were excited by lesser intensities of VAS (less than 50% of the intensity that inhibited the TF) that facilitated the TF reflex, and 14.3% of the ON cells excited by the threshold intensity of VAS to inhibit the TF reflex were inhibited by lesser intensities of VAS. VAS had mixed effects on NEUTRAL cells. VAS excited 23.7% and inhibited 10.5% of the NEUTRAL cells that had somatic receptive fields. VAS excited 12.9% and inhibited 9.7% of the NEUTRAL cells that had no identified somatic receptive field. The excitation of ON cells and inhibition of OFF cells produced by VAS at the intensity to inhibit the TF are opposite to predicted outcomes on the basis of current theories on the function of ON and OFF cells in nociception. 3. VAS produced a depressor response at intensities ranging from approximately 50% to 100% of the VAS intensity necessary to inhibit the TF reflex to the cutoff latency. At lesser intensities, VAS occasionally produced a small pressor response. 4. ON and OFF cells generally showed marked fluctuations in background activity, shifting between active and inactive states. The levels of background neural activity were correlated with mean ABP. ABP levels were lower when ON cells were active and OFF cells were inactive than when ON cells were inactive and OFF cells active.(ABSTRACT TRUNCATED AT 250 WORDS)

1. Intravenous administration of 1.0 mg/kg of morphine produces inhibition of the nociceptive tail-flick (TF) reflex, hypotension, and bradycardia in the pentobarbital-anesthetized rat. The present experiments examined peripheral, spinal, and supraspinal relays for inhibition of the TF reflex and cardiovascular responses produced by morphine (1.0 mg/kg iv) in the pentobarbital-anesthetized rat using 1) bilateral cervical vagotomy, 2) spinal cold block or mechanical lesions of the dorsolateral funiculi (DLFs), or 3) nonselective local anesthesia or soma-selective lesions of specific CNS regions. Intravenous morphine-induced inhibition of responses of unidentified, ascending, and spinothalamic tract (STT) lumbosacral spinal dorsal horn neurons to noxious heating of the hindpaw were also examined in intact and bilateral cervical vagotomized rats. 2. Bilateral cervical vagotomy significantly attenuated inhibition of the TF reflex and bradycardia produced by intravenous administration of morphine. Bilateral cervical vagogtomy changed the normal depressor response produced by morphine into a sustained pressor response. Inhibition of the TF reflex in intact rats was not due to changes in tail temperature. 3. Spinal cold block significantly attenuated inhibition of the TF reflex, the depressor response, and the bradycardia produced by intravenous administration of morphine. However, bilateral mechanical transections of the DLFs failed to significantly affect either inhibition of the TF reflex or cardiovascular responses produced by this dose of intravenous morphine. 4. Microinjection of either lidocaine or ibotenic acid into the nuclei tracti solitarii (NTS), rostromedial medulla (RMM), or ventrolateral pontine tegmentum (VLPT) attenuated morphine-induced inhibition of the TF reflex. Similar microinjections into either the periaqueductal gray (PAG) or the dorsolateral pons (DLP) failed to affect morphine-induced inhibition of the TF reflex. 5. Microinjection of either lidocaine or ibotenic acid into the NTS, RMM, VLPT, DLP, or rostral ventrolateral medulla (RVLM) attenuated the depressor response produced by morphine, although baseline arterial blood pressure (ABP) was affected by ibotenic acid microinjections in the DLP. In all these cases, the microinjections failed to reveal a sustained pressor response as was observed with bilateral cervical vagotomy. Similar microinjections into the PAG failed to affect the depressor response produced by morphine. 6. The lidocaine and ibotenic acid microinjection treatments also showed that the bradycardic response produced by morphine depends on the integrity of the NTS, RMM, RVLM, and possibly the DLP, but not the PAG or VLPT.(ABSTRACT TRUNCATED AT 400 WORDS)

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