Relationship between cortical electrical and cardiac autonomic activities in the awake lizard, Gallotia galloti

Citation
L. De Vera et al., Relationship between cortical electrical and cardiac autonomic activities in the awake lizard, Gallotia galloti, J EXP ZOOL, 287(1), 2000, pp. 21-28
Citations number
44
Categorie Soggetti
Animal Sciences","Animal & Plant Sciences
Journal title
JOURNAL OF EXPERIMENTAL ZOOLOGY
ISSN journal
0022104X → ACNP
Volume
287
Issue
1
Year of publication
2000
Pages
21 - 28
Database
ISI
SICI code
0022-104X(20000615)287:1<21:RBCEAC>2.0.ZU;2-N
Abstract
ECG and EEG signals were simultaneously recorded in lizards, Gallotia gallo ti, both in control conditions and under autonomic nervous system (ANS) blo ckade, in order to evaluate possible relationships between the ANS control of heart rate and the integrated central nervous system activity in reptile s. The ANS blockers used were prazosin, propranolol, and atropine. Time-dom ain summary statistics were derived from the series of consecutive R-R inte rvals (RRI) of the ECG to measure beat-to-beat heart rate variability (HRV) , and spectral analysis techniques were applied to the EEG activity to asse ss its frequency content. Both prazosin and atropine did not alter the powe r spectral density (PSD) of the EEG low frequency (LF: 0.5-7.5 Hz) and high frequency (HF: 7.6-30 Hz) bands, whereas propranolol decreased the PSD in these bands. These findings suggest that central beta-adrenergic receptor m echanisms could mediate the reptilian waking EEG activity without taking pa rt any alpha(1)-adrenergic and/or cholinergic receptor systems. In 55% of t he lizards in control conditions, and in similar to 43% of the lizards unde r prazosin and atropine, a negative correlation between the coefficient of variation of the series of RRI value (CVRRI) and the mean power frequency ( MPF) of the EEG spectra was found, but not under propranolol. Consequently, the lizards' HRV-EEG-activity relationship appears to be independent of al pha(1)-adrenergic and cholinergic receptor systems and mediated by beta-adr energic receptor mechanisms. (C) 2000 Wiley-Liss, Inc.