Serotonergic modulation of the P13 midlatency auditory evoked potential in the rat

Miyazato, Hiroshi; Skinner, R.D.; Crews, Tracy; Williams, Keith D.; García‐Rill, Edgar

doi:10.1016/s0361-9230(99)00257-9

Cited by 24 publications

(11 citation statements)

References 20 publications

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“…Considerable evidence exists on the involvement of the pedunculopontine nucleus (PPN) and/or its medial thalamic output projections in the activating reticular system (RAS), in the generation of the Vx-AEP component occuring at 11-15 ms (P14-N19 in the present study) [22,23,28,29,39]. The AI-AEP occuring at 6-9 ms (P7-N10 in the present study), is well established as primary cortical excitation of the AI in the primary auditory pathway [3].…”

Section: Neurophysiologic Parameters In Relation To Fear-conditioned mentioning

confidence: 76%

Vertex-recorded, rather than primary somatosensory cortex-recorded, somatosensory-evoked potentials signal unpleasantness of noxious stimuli in the rat

Stienen

Oostrom

Bos

et al. 2006

Brain Research Bulletin

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In the present study, we investigated in the rat whether vertex-or primary somatosensory cortex-recorded somatosensory-evoked potentials (Vx-SEP/SI-SEP, respectively) signal unpleasantness of noxious stimuli. Therefore, initially we characterised fentanyl effects (0, 20, 40 or 50 g/kg/h) on somatosensory and auditory processing by recording Vx-/SI-SEPs and vertex-and primary auditory cortex-recorded auditory-evoked potentials (Vx-/AI-AEPs, respectively). Subsequently, in a separate experiment, the animals were subjected to a Pavlovian fear-conditioning paradigm. The noxious stimuli applied to evoke Vx-/SI-SEPs (unconditioned stimulus (US)) were paired to a tone (conditioned stimulus (CS)) under 'steady state' conditions of 0, 20, 40 or 50 g/kg/h fentanyl. Vx-/SI-SEPs were recorded simultaneously during these trials. After CS-US presentation, CS-induced fear-conditioned behaviour was analysed in relation to the SEPs recorded during CS-US presentation and the AEPs recorded in the first experiment. While the SI-SEP and AI-AEP were minimally but significantly affected, fentanyl dose-dependently decreased the Vx-SEP and Vx-AEP. The decrease of the Vx-SEP and Vx-AEP was parallelled by the dose-dependent decrease of the amount of CS-induced fear-conditioned behaviour. These results suggest that the dose-dependent decrease of the Vx-SEP amplitude, rather than of the SI-SEP, indicates that the US was experienced as less unpleasant. Next to an altered US processing, altered CS processing contributed to the decrease of the amount of CS-induced fear-conditioned behaviour as indicated by the dose-dependent decrease of the Vx-AEP.

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Section: Neurophysiologic Parameters In Relation To Fear-conditioned mentioning

confidence: 76%

Vertex-recorded, rather than primary somatosensory cortex-recorded, somatosensory-evoked potentials signal unpleasantness of noxious stimuli in the rat

Stienen

Oostrom

Bos

et al. 2006

Brain Research Bulletin

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“…The hippocampal P20-N40 auditory evoked potential in rodents is thought to be analogous to the human P50 potential (Adler et al 1986(Adler et al , 1988Stevens et al 1996), though this opinion is not universally held (Connolly et al 2003;Maxwell et al 2004;Miyazato et al 1999Miyazato et al , 2000Teneud et al 2000). The rodent P20-N40 has been used to model the neurobiology and pharmacology of the human P50 processing deficit (Willot et al 1982;Stevens and Wear 1997;O'Neill et al 2003;Simosky et al 2001Simosky et al , 2003Stevens et al 1996Stevens et al , 1998.…”

Section: Introductionmentioning

confidence: 99%

Tropisetron improves deficient inhibitory auditory processing in DBA/2 mice: role of α7 nicotinic acetylcholine receptors

et al. 2005

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“…In addition to its selective α2 NE antagonist properties, yohimbine was proposed as a GABA antagonist (Dunn and Corbett 1992), a serotonin agonist (Papeschi et al 1971), and a dopamine antagonist (Scatton et al 1980). Each of these neurotransmitter classes have been shown to modulate P13 and/or N40 (Hershman et al 1995;Johnson et al 1998;Miyazato et al 1999aMiyazato et al , 2000bSiegel et al 2005). Future studies can build on the present data by utilizing more selective noradrenergic agents, as well as agents more selective for the other receptors that yohimbine has shown affinity for.…”

Section: General Commentsmentioning

confidence: 77%

Noradrenergic antagonism of the P13 and N40 components of the rat auditory evoked potential

et al. 2006

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This study demonstrated that noradrenergic activity differentially affects P13 and N40 components. As P13 and N40 are each models of human P50, these findings highlight the complex circuitry that likely underlies P50. An appreciation for these complexities is critical for understanding the mechanisms of the P50 suppression deficit in schizophrenia, which may be influenced by both trait and state factors.

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Serotonergic modulation of the P13 midlatency auditory evoked potential in the rat

Cited by 24 publications

References 20 publications

Vertex-recorded, rather than primary somatosensory cortex-recorded, somatosensory-evoked potentials signal unpleasantness of noxious stimuli in the rat

Vertex-recorded, rather than primary somatosensory cortex-recorded, somatosensory-evoked potentials signal unpleasantness of noxious stimuli in the rat

Tropisetron improves deficient inhibitory auditory processing in DBA/2 mice: role of α7 nicotinic acetylcholine receptors

Noradrenergic antagonism of the P13 and N40 components of the rat auditory evoked potential

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