Loudness dependency of the primary auditory cortex as an indicator of central serotonergic transmission: Combination of EEG and fMRI
Converging arguments from preclinical and clinical studies support the hypothesis that the loudness dependence of the auditory evoked N1/P2-response (LDAEP) is regulated by the level of central serotonergic neurotransmission. More specific, studies in behaving cats suggest that inhibition or activation of the serotonergic neurons in the dorsal raphe nucleus influences the loudness dependency only in the primary but not in the secondary auditory cortex (Juckel et al., 1999). With dipole source analysis or tomographic current source density analysis, activity of the primary and the secondary auditory cortex can be separated at least in parts (Mulert et al., 2002). The goal of the present investigation was to use the high spatial resolution of fMRI to get a more precise covering of the activity of the primary auditory cortex than it is possible with EEG based localisation approaches.
Juckel, G., Hegerl, U., Molnar, M., Csepe, V., and Karmos, G., 1999. Auditory evoked potentials reflect serotonergic neuronal activity–a study in behaving cats administered drugs acting on 5-HT1A autoreceptors in the dorsal raphe nucleus. Neuropsychopharmacology 21, 710–716.
Mulert, C., Juckel, G., Augustin, H., and Hegerl, U., 2002. Comparison between the analysis of the loudness dependency of the auditory N1/P2 component with LORETA and dipole source analysis in the prediction of treatment response to the selective serotonin reuptake inhibitor citalopram in major depression. Clin Neurophysiol 113, 1566–1572.