THE EFFECTS OF SOMATOSTATIN MICROINJECTIONS INTO THE SOLITARY TRACT NUCLEUS ON HERING — BREUER REFLEX

In the paper, the data concerning the effects of somatostatin microinjections into the solitary tract nucleus on Hering — Breuer reflex are presented. We found a stimulatory effect of somatostatin on the reflex by an increase of normalized expiratory duration. Thus, modulation of Hering-Breuer reflex is appeared to be a possible mechanism of somatostatin action at the level of dorsal respiratory group.

Respiratory responses to thyrotropin-releasing hormone microinjected into the rabbit medulla oblongata

We investigated the respiratory role of thyrotropin-releasing hormone (TRH) input to medullary structures involved in the control of breathing in anesthetized, vagotomized, paralyzed, and artificially ventilated rabbits. Microinjections (10–20 nl) of 1 or 10 mM TRH were performed in different regions of the ventral respiratory group (VRG), namely the rostral expiratory portion or Bötzinger complex (Böt. c.), the inspiratory portion, the transition zone between these two neuronal pools, and the caudal expiratory component. TRH microinjections were also performed in the dorsal respiratory group (DRG) and the area postrema (AP). Injection sites were localized by using stereotaxic coordinates and extracellular recordings of neuronal activity; their locations were confirmed by subsequent histological control. TRH microinjections in the Böt. c. and the directly caudally located region where a mix of inspiratory and expiratory neurons were encountered elicited depressant respiratory responses. TRH microinjections were completely ineffective at sites within the inspiratory and the caudal expiratory components of the VRG. TRH microinjections in either the DRG or the AP induced excitatory effects on inspiratory activity. The results show for the first time that TRH may exert inhibitory influences on respiration at medullary levels by acting on rostral expiratory neurons and that not only the DRG, as previously suggested, but also the AP may mediate TRH-induced excitatory effects on respiration.

Respiratory motor responses to cranial nerve afferent stimulation in rats

It was hypothesized that, because rats appear to lack a prominent disynaptic projection from the dorsal respiratory group to phrenic motoneurons (Phr), they would lack the short-latency excitation of Phr output seen in cats in response to stimulation of some cranial nerve afferents. Single-pulse superior laryngeal nerve (SLN) stimulation elicited a short-latency bilateral excitation of glossopharyngeal (IX) and hypoglossal (XII) nerves and an ipsilateral excitation of pharyngeal branch of vagus (PhX) in 67% of rats, but no excitation of Phr. Vagus (X) stimulation elicited a bilateral excitation of Phr and a predominantly ipsilateral excitation of IX and PhX. Single-pulse stimulation of SLN or X also elicited longer-latency, bilateral decreases in activity of all recorded nerves. Repetitive stimulation (50 Hz) of SLN or X suppressed inspiratory activity and prolonged expiration. Lung inflation (7.5 cmH2O) inhibited Phr and PhX activity; X stimulation inhibited Phr but prolonged PhX activity. In conclusion, rats predictably lack the SLN-induced short latency Phr excitation but exhibit other short latency reflexes for which the underlying circuitry is not clear.

Activity of respiratory neurons during hypoxia in the chemodenervated cat

Exposure of anesthetized paralyzed vagotomized peripherally chemodenervated cats to hypoxia results in initial depression and subsequent loss of the phrenic neurogram. To determine whether hypoxic respiratory depression results from the inhibition of respiratory premotor neurons by bulbospinal neurons of the Botzinger complex (Bot-E neurons), extracellular recordings were made of dorsal and ventral respiratory group bulbospinal inspiratory neurons and Bot-E neurons during acute hypoxic hypoxia. All neurons recorded decreased firing rate during hypoxia. Bot-E neurons became silent before the loss of phasic phrenic activity during hypoxia and commenced firing before or coincident with the return of the phrenic neurogram during reoxygenation. Inspiratory neurons ceased firing coincident with phrenic silence. Dorsal respiratory group and ventral respiratory group neurons that had a late onset of firing with respect to the phrenic neurogram during normoxia fired progressively earlier in inspiration during hypoxia, an effect that was reversed during reoxygenation. These data are consistent with inhibition and/or disfacilitation as the mechanism of hypoxic respiratory depression but suggest that Bot-E neurons are not the source of this inhibition.

Respiratory nuclei share synaptic connectivity with pontine reticular regions regulating REM sleep

Injection of cholinomimetics into the medial pontine reticular formation (mPRF) of intact, unanesthetized cat causes a rapid eye movement (REM) sleep-like state and respiratory depression. The mPRF contains no concentrations of respiratory neurons, and this study examined the hypothesis that respiratory depression evoked from the mPRF is synaptically mediated. The mPRF of conscious cats was injected with bethanechol to define an mPRF zone causing state-dependent respiratory depression. Bethanechol caused a 361% increase in the REM sleep-like state and a 37% decrease in minute ventilation. Additional cats were injected with the retrograde fluorescent tracers True Blue and either Fluoro-Gold or Diamidino Yellow aimed for the cholinoceptive mPRF or for the pontine respiratory group (PRG). After mPRF dye injection, 1) labeling was observed in the PRG, dorsal respiratory group (DRG), and ventral respiratory group (VRG); and 2) double-labeled cells were observed in the VRG and PRG. Dye injections into the PRG produced contralateral and ipsilateral fluorescent labeling of the mPRF, DRG, and VRG. Thus cholinoceptive regions of the mPRF involved in REM sleep generation have reciprocal monosynaptic connections with the PRG and receive monosynaptic projections from the DRG and VRG.

Organization of vestibular inputs to nucleus tractus solitarius and adjacent structures in cat brain stem

The vestibular system is involved in maintaining stable blood pressure and respiration during changes in posture and is essential for eliciting motion sickness-related vomiting. Because the nucleus tractus solitarius (NTS) participates in the regulation of sympathetic and inspiratory outflow and the triggering of emesis, we tested the hypothesis that this region receives vestibular inputs in cats. In one set of experiments, microinjections of the tracer Phaseolus vulgaris leucoagglutinin into the medial and inferior vestibular nuclei labeled projections to the middle and lateral regions of the NTS. In electrophysiological experiments, electrical stimulation of the vestibular nerve modified the firing rates of neurons located in the same regions. Some neurons with vestibular inputs received convergent signals from the abdominal vagus nerve and could potentially mediate motion sickness-related vomiting. Others received convergent baroreceptor inputs and could act as a substrate for some components of vestibulosympathetic reflexes. In contrast, inspiratory neurons in the dorsal respiratory group received little vestibular input, suggesting that vestibulorespiratory reflexes are mediated by cells located elsewhere.