Prolongation in expiration evoked from ventrolateral pons of adult rats

Abstract

Activation of neurons in the ventrolateral (vl) pons was hypothesized to alter the breathing pattern because previous studies demonstrated apneusis after inhibiting neuronal activity with bilateral muscimol (10 mM) microinjections into the vl pons (17). The excitatory amino acid L-glutamate (10 mM) was microinjected (10-100 nl) into the vl pons in anesthetized, vagotomized, paralyzed, and ventilated adult rats (n = 8). In four of these animals, the target site was approached from the ventral surface of the pons to avoid penetrating the dorsolateral (dl) pons. The expiratory phase was prolonged transiently and concurrently with the microinjection. The location of the injection sites included the A5 area, was independent of the approach, and was distinct from the dl pons. These results complement our previous data and indicate that neurons located in the vl pons influence respiration specifically by prolonging expiration when activated and by delaying the inspiratory-to-expiratory phase transition when inhibited.

Cytoarchitecture of Pneumotaxic Integration of Respiratory and Nonrespiratory Information in the Rat

“…Although the labeling was unable to go beyond vl-pons, it is highly possible that these axonal projections were en route to the medulla, as suggested by previous neural tracing studies that demonstrated strong efferent projections from both dl-pons and vl-pons to the VRG and DRG (for review, see . These axons could also terminate or send out branches within vl-pons, as demonstrated by recent anterograde labeling (Dawid Milner et al, 2003) and orthodromic/antidromic electrostimulation (Jodkowski et al, 1994(Jodkowski et al, , 1997Dawid Milner et al, 2001) studies. Thus, pneumotaxic neurons may modulate medullary respiratory neurons either directly through axons of passage via vl-pons or indirectly through relay neurons in vl-pons.…”

“…Thus, pneumotaxic neurons may modulate medullary respiratory neurons either directly through axons of passage via vl-pons or indirectly through relay neurons in vl-pons. This cytoarchitecture explains why electrical or chemical stimulation delivered at the vl-pons prolonged the expiratory phase and its lesioning or inhibition caused apneusis, as with mPB-KF (Jodkowski et al, 1994(Jodkowski et al, , 1997. As such, the vl-pons may be considered as auxiliary to the traditional pneumotaxic center in dl-pons.…”

“…Many of these functions involve other dl-pons loci beyond the mPB-KF complex, such as the lateral parabrachial (lPB) nucleus, intertrigeminal nucleus (IT), and ventrolateral principal trigeminal sensory nucleus (Pr5). In addition, various subregions of the ventrolateral pons (vl-pons), such as the A5 noradrenergic neuron group and the lateral reticular formation, have been shown to modulate the respiratory rhythm (Jodkowski et al, 1994(Jodkowski et al, , 1997Jacquin et al, 1996;Borday et al, 1997). The variety of respiratory-related functions demonstrated in varying pontine loci suggests an extended organization of the pneumotaxic center in integrating multiplex physiological information.…”

A5 cells are silenced when REM sleep-like signs are elicited by pontine carbachol

“…They have extensive axonal projections that include cardiorespiratory and motor regions of the brain stem and spinal cord (1,8,9,23,36). Through these projections, they may control, among others, sympathetic and respiratory outputs and, via projection to the hypoglossal (XII) motor nucleus, may mediate noradrenergic excitation of XII motoneurons (5,22,27,40,49). XII motoneurons are of particular interest because they innervate the genioglossus muscle of the tongue, an important airway dilator.…”

Effect of hypothermia on respiratory rhythm generation in hamster brainstem–spinal cord preparations

“…Inputs from the pons (the medial parabrachial and Kölliker-Fuse nuclei, collectively referred to as the parabrachial complex (PbC) and the A5 noradrenergic nucleus) are well known to influence breathing in vivo (see Bianchi et al, 1995 for review;Jodkowski et al, 1997) and in vitro (see Ballanyi et al, 1999 for review). In rat brainstem-spinal cord preparations, inputs arising from the A5 noradrenergic nucleus act to reduce fictive breathing frequency (Hilaire et al, 1989).…”