Midlatency auditory evoked responses: differential effects of a cholinergic agonist and antagonist

Buchwald, Jennifer S.; Rubinstein, Eduardo H.; Schwafel, J.; Strandburg, Robert J.

doi:10.1016/0168-5597(91)90114-d

Cited by 102 publications

(69 citation statements)

References 30 publications

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“…Our findings (Jääskel-äinen et al 1999) and those of Buchwald et al (1991) have suggested that brain acetylcholine plays an important role in the generation of the Pa response. In these studies, the Pa/Pam amplitude was enhanced by muscarine receptor antagonist scopolamine, and was reduced by the agonist physostigmine.…”

Section: Resultssupporting

confidence: 62%

Serotonin Modulates Early Cortical Auditory Processing in Healthy Subjects. Evidence from MEG with Acute Tryptophan Depletion

Kähkönen

Ahveninen

Pennanen

et al. 2002

Neuropsychopharmacology

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We studied the effects of acute tryptophan depletion (ATD) on early cortical auditory processing. Middle-latency auditory evoked fields (MAEF) were investigated in 14 healthy subjects after 5 h of ATD or control mixture ingestion in a randomized, double-blinded, controlled crossover design study. MAEFs to monaural click stimuli (0.1-ms duration) were recorded with a 122-channel neuromagnetometer. Total plasma tryptophan (Trp),Low brain serotonin (5-HT) levels and function have been implicated in various psychopathologies including depression and anxiety. Acute tryptophan depletion (ATD) is a dietary intervention that rapidly lowers plasma tryptophan (Trp) and alters 5-HT synthesis, metabolism, and release in animals and humans (Young et al. 1985;Nishizawa et al. 1997;Stancampiano et al. 1997;Carpenter et al. 1998). It involves the administration of an amino acid mixture that lacks Trp, the amino acid precursor of serotonin. The effect of ATD on 5-HT synthesis and metabolism is twofold (Young et al. 1985). First, decline in plasma Trp occurs because the Trpdeficient amino acid mixture promotes synthesis of new proteins. Trp incorporated into protein comes from blood and tissue pools, and therefore its concentration in plasma and brain falls (Biggio et al. 1974;Gessa et al. Stancampiano et al. 1997). Magnetoencephalography (MEG) is a method for the measurement of extracranial magnetic fields produced by ionic current flow generated mainly by cortical pyramidal cells. MEG is a non-invasive method for functional brain studies with temporal resolution as high as electroencephalography (EEG), but with more accurate source localization . Because of cortical folding in the Sylvian fissure, MEG is ideally suited for the localization and measurement of supratemporal auditory cortical activity .Auditory evoked magnetic potentials (AEP) and fields (AEF), which allow the investigation underlying auditory processing, can be obtained by averaging EEG or MEG epochs time-locked to the presentation of auditory stimuli. The earliest cortical AEFs, the middlelatency AEFs (MAEFs), occur at about 20-70 ms from stimulus onset. The MAEFs are composed of several distinct deflections, with Pam peaking at approximately 30 ms and Nbm at about 45 ms.There is evidence to suggest that serotonergic activity may modulate auditory evoked potentials (Hegerl and Juckel 1993;Juckel et al. 1997;Dierks et al. 1999) and background EEG frequencies (Knott et al. 1999). The sound intensity dependence of auditory N1/P2 amplitude has been suggested to be a specific indicator of serotonin function (Hegerl and Juckel 1993;Juckel et al. 1997). Reduced serotonin function leads to higher intensity dependence of N1/P2 amplitude and vice versa. However, Dierks et al. (1999) were not able to confirm these findings using ATD in healthy subjects. In contract, this study showed that ATD decreases the intensity dependence of N1/P2 amplitudes. In the recent ATD study using a 52-g amino acid challenge, Hughes et al. (2000) found no changes in auditory N1, P2, or P3 ampl...

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Section: Resultssupporting

confidence: 62%

Serotonin Modulates Early Cortical Auditory Processing in Healthy Subjects. Evidence from MEG with Acute Tryptophan Depletion

Kähkönen

Ahveninen

Pennanen

et al. 2002

Neuropsychopharmacology

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“…We conclude that there are some indications that P50 amplitudes may be attenuated following donepezil treatment, but the effects of donepezil on P50 amplitudes in MCI need to be further investigated given the mixed results, which are likely due to the small number of subjects in the MCI subgroups. Previous studies have shown that acetylcholine can modulate the activity of auditory cortex (Buchwald et al, 1991;Metherate, 2004). There is also an increase in cholinergic enzyme activity in certain cortical regions in MCI (Dekosky et al, 2002).…”

Section: Cholinergic Transmission and The Long-latency P50 Component mentioning

confidence: 90%

Auditory brain-stem, middle- and long-latency evoked potentials in mild cognitive impairment

Irimajiri

Golob

Starr

2005

Clinical Neurophysiology

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Objective: Mild cognitive impairment (MCI) is a selective episodic memory deficit in the elderly with a high risk of Alzheimer's disease. The amplitudes of a long-latency auditory evoked potential (P50) are larger in MCI compared to age-matched controls. We tested whether increased P50 amplitudes in MCI were accompanied by changes of middle-latency potentials occurring around 50 ms and/or auditory brainstem potentials. Methods: Auditory evoked potentials were recorded from age-matched controls (nZ16) and MCI (nZ17) in a passive listening paradigm at two stimulus presentation rates (2/s, 1/1.5 s). A subset of subjects also received stimuli at a rate of 1/3 s. Results: Relative to controls, MCI subjects had larger long-latency P50 amplitudes at all stimulus rates. Significant group differences in N100 amplitude were dependent on stimulus rate. Amplitudes of the middle-latency components (Pa, Nb, P1 peaking at approximately 30, 40, and 50 ms, respectively) did not differ between groups, but a slow wave between 30 and 49 ms on which the middle-latency components arose was significantly increased in MCI. ABR Wave V latency and amplitude did not differ significantly between groups. Conclusions: The increase of long-latency P50 amplitudes in MCI reflects changes of a middle-latency slow wave, but not of transient middle-latency components. There was no evidence of group difference at the brain-stem level. Significance: Increased slow wave occurring as early as 50 ms may reflect neurophysiological consequences of neuropathology in MCI.

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“…At the same time, the values of the three parameters -RA, PA and Do in the anxiety group were higher than in the asthenia group. Thus, the RA index in the anxiety group (59.3 ± 2.13) was greater (U [15], [16] = 0; p <0.001) than in the asthenia group (49.7 ± 2.12). PA in the anxiety group (46.7 ± 3.81) also exceeded (U = 25, p <0.001) the values of the The indices of psychological testing of asthenia and anxiety groups showed signi icant exceeding values (U values from 0 to 25, p<0.001) of RA, PA, Ds, Do and Ao of both groups relative towards the comparison group (Fig.…”

Section: The Results Of Psychological Testing In Asthenia and Anxietymentioning

confidence: 93%

“…The latent periods of the P3 component and in the asthenia group are 312.0 ± 33.16 ms (U = 50; p <0.001), and in the anxiety group 320.0 ± 34.61 ms (U [15]; [16] = 87.5, p <0.05) were lower than in the CG (368.3 ± 37.15 ms) (Fig. 6).…”

Section: Erp In Asthenia and Anxiety Groups Compared To The Control Gmentioning

confidence: 99%

Evaluation of the evoked brain potentials of patients with asthenia and anxiety symptoms and the partial loss of sight

Tsira¹,

Abdryakhimov

Snegir

et al. 2017

PMGP

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Midlatency auditory evoked responses: differential effects of a cholinergic agonist and antagonist

Cited by 102 publications

References 30 publications

Serotonin Modulates Early Cortical Auditory Processing in Healthy Subjects. Evidence from MEG with Acute Tryptophan Depletion

Serotonin Modulates Early Cortical Auditory Processing in Healthy Subjects. Evidence from MEG with Acute Tryptophan Depletion

Auditory brain-stem, middle- and long-latency evoked potentials in mild cognitive impairment

Evaluation of the evoked brain potentials of patients with asthenia and anxiety symptoms and the partial loss of sight

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