Role of ascending activating systems in the regulation of sensory processing in rats
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1
Department of Physiology and Neurobiology, Eötvös Loránd University, Hungary
The mechanisms of cortical processing of sensory inputs can be investigated by studying evoked potentials. Configuration and amplitude of midlatency components in auditory evoked potentials depend not only on the stimuli, but on the background EEG as well. Decreased activation of the cortex (high delta intensity) causes increased amplitudes of these peaks. The appearance of the large delta waves (0.5 - 4.0 Hz) in the cortical EEG – generated by the slow oscillation of membrane potentials of pyramidal cells – depends on the diminished activity of the ascending activating systems. To investigate the contribution of decreased activity in the different ascending activating systems to the increased amplitude of midlatency evoked potential components, we examined the effects of cholinergic, adrenergic, dopaminergic, and serotoninergic drugs – all causing EEG desynchronization. The alpha-2 adrenergic receptor antagonist yohimbine and the selective serotonin reuptake inhibitor fluoxetine increased the evoked potential amplitudes, though decreased delta power. The cholinesterase inhibitor eserine decreased both peak amplitudes and background delta intensity. The dopaminergic agonist apomorphine first decreased then increased delta power, but caused low peak amplitudes and shortened peak latencies in both phases. Our results indicate that while ascending activating systems influence delta power similarly, they have differential effects on sensory processing.
Conference:
12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009.
Presentation Type:
Poster Presentation
Topic:
Developmental neurobiology and subcortical functions
Citation:
Nagy
B,
Hajnik
T,
Toth
A and
Detari
L
(2009). Role of ascending activating systems in the regulation of sensory processing in rats.
Front. Syst. Neurosci.
Conference Abstract:
12th Meeting of the Hungarian Neuroscience Society.
doi: 10.3389/conf.neuro.01.2009.04.069
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Received:
02 Mar 2009;
Published Online:
02 Mar 2009.
*
Correspondence:
Bálint Nagy, Department of Physiology and Neurobiology, Eötvös Loránd University, Budapest, Hungary, nagyblint@yahoo.com