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

Citation
D. Mutolo et al., Respiratory responses to thyrotropin-releasing hormone microinjected into the rabbit medulla oblongata, AM J P-REG, 277(5), 1999, pp. R1331-R1338
Citations number
39
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
277
Issue
5
Year of publication
1999
Pages
R1331 - R1338
Database
ISI
SICI code
0363-6119(199911)277:5<R1331:RRTTHM>2.0.ZU;2-D
Abstract
The investigated the respiratory role of thyrotropin-releasing hormone (TRH ) input to medullary structures involved in the control of breathing in ane sthetized, vagotomized, paralyzed, and artificially ventilated rabbits. Mic roinjections (10-20 nl) of 1 or 10 mM TRH were performed in different regio ns of the ventral respiratory group (VRG), namely the rostral expiratory po rtion or Botzinger complex (Bot. c.), the inspiratory portion, the transiti on zone between these two neuronal pools, and the caudal expiratory compone nt. 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 micr oinjections in the Bot. c. and the 'directly caudally located region where a mix of inspiratory and expiratory neurons were encountered elicited depre ssant respiratory responses. TRH microinjections were completely ineffectiv e at sites within the inspiratory and the caudal expiratory components of t he VRG. TRH microinjections in either the DRG or the AP induced excitatory effects on inspiratory activity. The results show for the first time that T RH may exert inhibitory influences on respiration at medullary levels by ac ting on rostral expiratory neurons and that not only the DRG, as previously suggested, but also the AP may mediate TRH-induced excitatory effects on r espiration.