The serotonergic inhibition of slowly bursting cells in the intergeniculate leaflet of the rat.
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| Title: | The serotonergic inhibition of slowly bursting cells in the intergeniculate leaflet of the rat. |
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| Authors: | Blasiak, T. (AUTHOR), Siejka, S. (AUTHOR), Raison, S. (AUTHOR), Pevet, P. (AUTHOR), Lewandowski, M. H. (AUTHOR) |
| Source: | European Journal of Neuroscience. Nov2006, Vol. 24 Issue 10, p2769-2780. 12p. 2 Diagrams, 6 Graphs. |
| Subjects: | Rats, Cells, Electric stimulation, Wounds & injuries, Vestibular nuclei, Serotoninergic mechanisms |
| Abstract: | Electrophysiological studies combined with local neurotoxic lesions were conducted on anaesthetized rats in order to determine whether the dorsal raphe nucleus (DRN) inhibits the intergeniculate leaflet (IGL) of the lateral geniculate nucleus by means of innervation by serotonin-containing fibres. In the control animals, electrical stimulation of the DRN induced the long-latency and long-lasting inhibition of the neuronal firing of the IGL cells that are characterized by rhythmic, slow-bursting activity in light conditions. The electrical destruction of the DRN resulted in an increase in the firing rate of the recorded IGL cells, whilst at the same time not affecting the rhythmic, bursting pattern of the activity. In the second group of animals, local neurotoxic lesion of serotonergic fibres was performed by injection of the toxin 5,7-dihydroxytryptamine into the IGL. After 10 days of postoperative recovery, electrophysiological experiments were performed on the toxin-treated rats. In these animals, electrical stimulation as well as electrical lesion of the DRN did not induce any change in the firing of the slowly bursting cells in the 5,7-dihydroxytryptamine-injected IGL. The results obtained provide evidence that inhibition of the IGL slowly bursting cells, by innervation from the dorsal raphe, is mediated by the release of serotonin. Furthermore, the observed serotonergic inhibition of the light-dependent activity of slowly bursting cells can contribute to the neuronal mechanism gating the information that flows through this nucleus to the vestibular, visuomotor, circadian and sleep/arousal systems, with which the IGL is strongly interconnected. [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | Electrophysiological studies combined with local neurotoxic lesions were conducted on anaesthetized rats in order to determine whether the dorsal raphe nucleus (DRN) inhibits the intergeniculate leaflet (IGL) of the lateral geniculate nucleus by means of innervation by serotonin-containing fibres. In the control animals, electrical stimulation of the DRN induced the long-latency and long-lasting inhibition of the neuronal firing of the IGL cells that are characterized by rhythmic, slow-bursting activity in light conditions. The electrical destruction of the DRN resulted in an increase in the firing rate of the recorded IGL cells, whilst at the same time not affecting the rhythmic, bursting pattern of the activity. In the second group of animals, local neurotoxic lesion of serotonergic fibres was performed by injection of the toxin 5,7-dihydroxytryptamine into the IGL. After 10 days of postoperative recovery, electrophysiological experiments were performed on the toxin-treated rats. In these animals, electrical stimulation as well as electrical lesion of the DRN did not induce any change in the firing of the slowly bursting cells in the 5,7-dihydroxytryptamine-injected IGL. The results obtained provide evidence that inhibition of the IGL slowly bursting cells, by innervation from the dorsal raphe, is mediated by the release of serotonin. Furthermore, the observed serotonergic inhibition of the light-dependent activity of slowly bursting cells can contribute to the neuronal mechanism gating the information that flows through this nucleus to the vestibular, visuomotor, circadian and sleep/arousal systems, with which the IGL is strongly interconnected. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 0953816X |
| DOI: | 10.1111/j.1460-9568.2006.05162.x |
