Little is known about the effects of inhalant anaesthetics on the avian electroencephalogram (EEG). The effects of halothane on the avian EEG are of interest, as this agent has been widely used to study nociception and analgesia in mammals. The objective of this study was to characterize the effects of halothane anaesthesia on the EEG of the chicken. Twelve female Hyline Brown chickens aged 8–10 weeks were anaesthetized with halothane in oxygen. For each bird, anaesthesia was progressively increased from 1–1.5 to 2 times the Minimum Anesthetic Concentration (MAC), then progressively decreased again. At each concentration, a sample of EEG was recorded after a 10‐min stabilization period. The mean Total Power (PTOT), Median Frequency (F50) and 95% Spectral Edge Frequency (F95) were calculated at each halothane MAC, along with the Burst Suppression Ratio (BSR). Burst suppression was rare and BSR did not differ between halothane concentrations. Increasing halothane concentration from 1 to 2 MAC resulted in a decrease in F50 and increase in PTOT, while F95 increased when MAC was reduced from 1.5 to 1. The results indicate dose‐dependent spectral EEG changes consistent with deepening anaesthesia in response to increasing halothane MAC. As burst suppression was rare, even at 1.5 or 2 times MAC, halothane may be a suitable anaesthetic agent for use in future studies exploring EEG activity in anaesthetized birds.
The reliable assessment and management of avian pain is important in the context of animal welfare. Overtly expressed signs of pain vary substantially between and within species, strains and individuals, limiting the use of behaviour in pain studies. Similarly, physiological indices of pain can also vary and may be confounded by influence from non-painful stimuli. In mammals, changes in the frequency spectrum of the electroencephalogram (EEG) recorded under light anaesthesia (the minimal anaesthesia model; MAM) have been shown to reliably indicate cerebral responses to noxious stimuli in a range of species. The aim of the current study was to determine whether the MAM can be applied to the study of nociception in birds. Ten chickens were lightly anaesthetised with halothane and their EEG recorded using surface electrodes during the application of supramaximal mechanical, thermal and electrical noxious stimuli. Spectral analysis revealed no EEG responses to any of these stimuli. Given that birds possess the neural apparatus to detect and process pain, and that the applied noxious stimuli elicit behavioural signs of pain in conscious chickens, this lack of response probably relates to methodological limitations. Anatomical differences between the avian and mammalian brains, along with a paucity of knowledge regarding specific sites of pain processing in the avian brain, could mean that EEG recorded from the head surface is insensitive to changes in neural activity in the pain processing regions of the avian brain. Future investigations should examine alternative electrode placement sites, based on avian homologues of the mammalian brain regions involved in pain processing.
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