Medullary respiratory-related neurons with axonal connections to rostral pons and their function in termination of inspiration

Abstract

In urethane-anaesthetized, paralyzed and artificially ventilated rabbits, medullary respiration-related neurons (RRU) were classified according to the phase relation of their burst discharge to phrenic nerve activity. Phase-bound inspiratory (I) or expiratory (E) neurons were discriminated from phase-spanning expiratory-inspiratory (EI) or inspiratory-expiratory (IE) units. Mechanisms of termination of inspiration by electrical stimulation of rostral pontine nuclei (Nc. parabrachialis medialis; Lc. coeruleus) were examined firstly to demonstrate whether RRU receive descending excitatory and inhibitory afferents as well as ascending efferents and secondly to analyse the time course of the neuronal pathways involved. Of 120 RRU, 38 neurons were demonstrated to receive pontine afferents. About 33% of all E neurons became orthodromically excited during rostral pons stimulation whereas 18.2% of all I cells became orthodromically inhibited. Some RRU were shown to project up to the rostral pons. 50% of these were of the phase-spanning IE type. The onset of inspiratory inhibition induced by rostral pons stimulation occurred 3.4 ms after the onset of single electrical pulse stimulation. Based on these results a neuronal model for a pontine mechanism terminating inspiration is proposed.

Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons

“…There are functional synaptic connections between KFN neurons and ventral respiratory group inspiratory and expiratory neurons (49), and computer modeling of the pontomedullary respiratory network suggests that the timing and patterns of discharge of all the neurons tested for opiate responsiveness in this study can be influenced by excitatory synaptic inputs from pontine neurons (46).…”

Red nucleus lesions abolish the biphasic respiratory response to isocapnic hypoxia in decerebrate young rabbits.

“…In 1936, Kabat reported that electrical stimulation within the medial part of the mesencephalic tegmentum elicited a decrease in ventilation. Later, others found that electrical stimulation in the caudal, ventromedial mesencephalon including the RN decreased RO (Baxter & OlszewN-ski, 1955;Evans & Pepler, 1974;Coles, 1987;Schmid et al 1988;Gallman et al 1991).…”

“…The parvicellular division receives input predominantly from the cerebral cortex and its sole efferent pathway is to the ipsilateral inferior olive; very little is known about its functional role. The magnocellular part of the RN receives input mainly from the interpositus is no evidence to indicate a pathway from the RN to the dorsal respiratory group (Edwards, 1972;Horst, Luiten, Kuipers, 1984) there is evidence for projections to the ventral respiratory group (Horst et al 1984), in particular to bulbospinal neurones in the region of the ambigual complex (Schmid et al 1988). Interestingly, Vibert, Caille, Bertrand, Gromysz & Hugelin (1979) observed that respiratorymodulated units could be recorded from the most ventral part of the RN in adult cats.…”

“…Putting the foregoing studies together, we felt that the role of mesencephalic structures in mediating the fall in RO in hypoxia merited further investigation. In adult cats and rabbits electrical stimulation in, or in the region of, the red nucleus (RN;Bassal & Bianchi, 1982; Gallman, Lawing & Millhorn, 1991) or in the rubrospinal tract (Schmid, Bohmer & Fallert, 1988) inhibits RO during normoxia. Our initial studies (Ackland, Waites, Noble & Hanson, 1995) showed clearly that electrical stimulation in the RN also inhibits RO in young rabbits.…”

Effects of Anesthetics, Sedatives, and Opioids on Ventilatory Control

“…Direct administration of morphine into the Kölliker-Fuse nucleus (KFN) and medial parabrachial nucleus regions slowed respiratory rhythm by prolonging the inspiratory and expiratory phases (286,287). There are functional synaptic connections between KFN neurons and ventral respiratory group (VRG) inspiratory and expiratory neurons (613), and computer modeling of the pontomedullary respiratory network suggests that the timing and patterns of discharge of all the neurons tested for opioid responsiveness in this study can be influenced by excitatory synaptic inputs from pontine neurons (591).…”