Morphine microinjected into the nucleus tractus solitarius and rostral ventrolateral medullary nucleus enhances somatosympathetic A- and C-reflexes in anesthetized rats

Abstract

The modulatory effects of morphine microinjected into localized areas of the brainstem on somatosympathetic A- and C-reflexes were examined in urethane-anesthetized rats. Somatosympathetic A- and C-reflexes were elicited in a branch of the inferior cardiac nerve by electrical stimulation of myelinated (A) and unmyelinated (C) afferent fibers in the tibial nerve. Morphine (0.002–0.2 μg/50 nl) was microinjected into the rostral, intermediate and caudal parts of the nucleus tractus solitarius (NTS), the rostral ventrolateral medullary nucleus (RVLM), the caudal ventrolateral medullary nucleus (CVLM), the locus coeruleus (LC), the raphe magnus (RM), the periaqueductal gray (PAG), and the accumbens nucleus (Acb). Microinjections of morphine (0.2 μg) into the intermediate and caudal NTS produced significant augmentations of the A- and C-reflexes, C-reflexes being more markedly enhanced than A-reflexes. Microinjection of morphine (0.2 μg) into the RVLM produced a prominent increase in the C-reflex, the threshold dose for a significant increase being 0.02 μg morphine. Microinjection of morphine up to 0.2 μg/50 nl into the other areas mentioned above had no significant effect on either reflex component. All opiate-induced increases of the reflex discharges could be reversed by intravenous application of naloxone (2 mg/kg). The reflex augmentation induced by microinjection of morphine into the NTS may be caused by suppressing inhibitory baroreceptor information or by enhancing excitatory chemoreceptor information in the NTS. Augmentation of the C-reflex induced by microinjection of morphine into the RVLM may be caused by facilitating C-reflex pathways or by suppressing inhibitory neural circuits involved in the C-reflex within the RVLM.