Chirp-evoked potentials in the awake and anesthetized rat. A procedure to assess changes in cortical oscillatory activity
M. Pérez-Alcázar, M.J. Nicolás, M. Valencia, M. Alegre, J. Iriarte and J. Artieda
Neurophysiology Laboratory, Neuroscience Area, CIMA and Clínica Universitaria, Universidad de Navarra, Pamplona, Spain
Data: 7/Nov/2007Neurofisiologia [ES]
Steady-state potentials are oscillatory responses generated by rhythmic stimulation of a sensory pathway.
The frequency of the response, which follows the frequency of stimulation and potentially indicates the preferential working frequency of the auditory neural network, is maximal at a stimulus rate of 40 Hz for auditory stimuli in humans, but may be different in other species.
Our aim was to explore the responses to different frequencies in the rat. The stimulus was a tone modulated in amplitude by a sinusoid with linearly-increasing frequency from 1 to 250 Hz ("chirp"). Time-frequency transforms were used for response analysis in 12 animals, awake and under ketamine/xylazine anesthesia. We studied whether the responses were due to increases in amplitude or to phase-locking phenomena, using single-sweep time-frequency transforms and inter-trial phase analysis.
A progressive decrease in the amplitude of the response was observed from the maximal values (around 15 Hz) up to the limit of the test (250 Hz). The high-frequency component was mainly due to phase-locking phenomena with a smaller amplitude contribution. Under anesthesia, the amplitude and phase-locking of lower frequencies (under 100 Hz) decreased, while the phase-locking over 200 Hz increased. In conclusion, amplitude-modulation following responses differ between humans and rats in response range and frequency of maximal amplitude. Anesthesia with ketamine/xylazine modifies differentially the amplitude and the phase-locking of the responses.
These findings should be taken into account when assessing the changes in cortical oscillatory activity related to different drugs, in healthy rodents and in animal models of neurodegenerative diseases.
CITAÇÃO DO ARTIGO Exp Neurol. 2008 Mar;210(1):144-57
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