Source location of a 50 msec latency auditory evoked field component

Reite, Martin; Teale, Peter; Zimmerman, J. E.; Davis, Kathleen C.; Whalen, J.

doi:10.1016/0013-4694(88)90147-2

Cited by 141 publications

(68 citation statements)

References 11 publications

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“…The degree of memory impairment in the two subtypes did not differ. These and other results (Bell-McGinty et al, 2005) suggest that primary and secondary auditory cortices in the temporal lobe that generate the P50 component (LiegeoisChauvel et al, 1994;Reite et al, 1988) become involved as MCI progresses from isolated memory deficits (singledomain MCI) to additional cognitive dysfunctions involving language functions (multiple-domain MCI).…”

Section: Introductionmentioning

confidence: 82%

Cholinesterase inhibitors affect brain potentials in amnestic mild cognitive impairment

et al. 2007

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Amnestic mild cognitive impairment (MCI) is an isolated episodic memory disorder that hasa high likelihood of progressing to Alzheimer's disease. Auditory sensory cortical responses (P50, N100) have been shown to be increased in amplitude in MCI compared to older controls. We tested whether (1) cortical potentials to other sensory modalities (somatosensory and visual) were also affected in MCI and (2) cholinesterase inhibitors (ChEIs), one of the therapies used in this disorder, modulated sensory cortical potentials in MCI. Somatosensory cortical potentials to median nerve stimulation and visual cortical potentials to reversing checkerboard stimulation were recorded from 15 older controls and 15 amnestic MCI subjects (single domain). Results were analyzed as a function of diagnosis (Control, MCI) and ChEIs treatment (Treated MCI, Untreated MCI). Somatosensory and visual potentials did not differ significantly in amplitude in MCI subjects compared to controls.When ChEIs use was considered, somatosensory potentials (N20, P50) but not visual potentials (N70, P100, N150) were of larger amplitude in untreated MCI subjects compared to treated MCI subjects. Three individual MCI subjects showed increased N20 amplitude while off ChEIs compared to while on ChEIs. An enhancement of N20 somatosensory cortical activity occurs in amnestic single-domain MCI and is sensitive to modulation by ChEIs. IntroductionMild cognitive impairment (MCI) describes older individuals having cognitive impairments without accompanying functional impairments that characterize dementia (Petersen et al., 1999). Recent studies have suggested criteria for distinguishing among four subtypes of MCI based on the presence of both episodic memory impairment (amnestic or non-amnestic MCI) and other cognitive impairments (single-or multipledomain MCI) (Petersen, 2004). For example, amnestic singledomain MCI refers to patients with involvement of only memory deficit whereas amnestic multiple-domain MCI refers to patients with impairment of both memory and other cognitive domains such as language or executive function. MCI subjects have a high risk of converting to Alzheimer's disease Petersen et al., 1999) and show neuropathological features of β-amyloid plaques and neurofibrillary tangles similar to early Alzheimer's disease (Kordower et al., 2001;Mufson et al., 1999). These findings suggest that MCI can be a precursor of Alzheimer's disease. Cholinergic processes in neocortical areas are affected in Alzheimer's disease (Geula and Mesulam, 1989;Heckers et al., 1992) and are particularly apparent late in the course of

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Section: Introductionmentioning

confidence: 82%

Cholinesterase inhibitors affect brain potentials in amnestic mild cognitive impairment

et al. 2007

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“…That better gating can be evidenced both in individuals with relatively low (A1 + ) and high (9R) synaptic dopamine tone in the striatum suggests that the two genetic components (DRD2, DAT1) of dopamine neurotransmission may affect P50 inhibitory proneness through separate neural mechanisms. The observation that S 1 -P50, which is thought to initiate P50 inhibitory processes and is generated primarily in the superior temporal gyri of the primary auditory cortex (Makela et al, 1994;Pelizzone et al, 1987;Reite et al, 1988), is (along with P5-gating) also elevated in A1 + (but not 9R) allele carriers may argue that DRD2-related alterations in auditory habituation are primarily innervated via dopaminergic pathways in intrinsic (temporal lobe) brain regions.…”

Section: Discussionmentioning

confidence: 99%

The moderating role of the dopamine transporter 1 gene on P50 sensory gating and its modulation by nicotine

et al. 2011

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Although schizophrenia has been considered primarily a disease of dopaminergic neurotransmission, the role of dopamine in auditory sensory gating deficits in this disorder and their amelioration by smoking/nicotine is unclear. Hypothesizing that individual differences in striatal dopamine levels may moderate auditory gating and its modulation by nicotine, this preliminary study used the mid-latency (P50) auditory event-related potential (ERP) to examine the single dose (6 mg) effects of nicotine (vs. placebo) gum on sensory gating in 24 healthy nonsmokers varying in the genetic expression of the dopamine transporter (DAT). Consistent with an inverted-U relationship between dopamine level and the drug effects, individuals carrying the 9R (lower gene expression) allele, which is related to greater striatal dopamine levels, tended to evidence increased baseline gating compared to 10R (higher gene expression) allele carriers and showed a reduction in gating with acute nicotine. The present results may help to understand the link between excessive smoking and sensory gating deficits in schizophrenia and to explain the potential functional implications of genetic disposition on nicotinic treatment in schizophrenia. Keywords schizophrenia; P50; gating; dopamine transporter gene; nicotine; smoking Early theoretical models of information processing in schizophrenia postulated impairment in the preattentive, automatic processing of sensory input to be a contributing factor in the appearance of psychotic symptoms, perceptual disturbances, and various cognitive deficits that characterize this disorder (Venables, 1964). Meta-analyses and reviews of event-related potential (ERP) studies probing auditory sensory gating in a paired stimulus paradigm (involving the presentation two [ CIHR Author Manuscript CIHR Author Manuscript CIHR Author Manuscriptfound that ~90% of patients with schizophrenia as well as ~50% of their first-degree relatives exhibit insufficient inhibitory processing of repetitive, irrelevant acoustic stimuli (Bramon et al., 2004;De Wilde et al., 2007;Patterson et al., 2008). Typically assessed with the amplitude of the early (50 ms) positive ERP component, P50, abnormal auditory sensory gating has been evidenced by a relative inability to suppress P50 to S 2 , and is expressed by larger S 2 /S 1 ratio (rP50) and/or smaller S 1 minus S 2 difference (dP50) scores.Smoking and acute nicotine have transiently corrected deficient P50 processing in schizophrenia patients and their relatives, respectively (Adler et al., 1992(Adler et al., , 1993. In addition, in a rodent model of schizophrenia-like gating deficiency, studies assessing the P20-N40 ERP, which is an analogue of the human P50, have shown agonists and antagonists of the α7 nicotinic receptor to improve deficient S 2 inhibition and to block normal S 2 inhibition, respectively (Stevens et al., 1998(Stevens et al., , 1999Simosky et al., 2001). Other studies reporting gating improvements with nicotine in rodents and humans, however, have found increa...

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“…Generators of the P50, N100, and P200 components of the auditory evoked potential in humans have been localized within primary and secondary auditory cortex [1,20,30,32,34]. Accordingly, the amplitude changes seen in auditory evoked potentials in the intramodal and crossmodal tasks are likely due to changes in auditory cortical activity.…”

Section: Discussionmentioning

confidence: 99%

“…Diagnosis of MCI was similar to the criteria of Petersen et al [26]. MCI patients reported subjective memory complaints, and had scores Ͼ1.5 SD below the mean age-adjusted normative score on the WMS-R Logical 30). Four MCI and 9 AD subjects were taking the cholinesterase inhibitor donepezil for their memory complaints.…”

Section: Subjectsmentioning

confidence: 98%

Sensory cortical interactions in aging, mild cognitive impairment, and Alzheimer’s disease

Golob

Miranda

Johnson

et al. 2001

Neurobiology of Aging

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Progressive declines in memory function accompany normal aging, mild cognitive impairment (MCI), and Alzheimer's disease (AD). Neuropathological studies suggest that damage to neurons providing connections between cortical areas may contribute to memory impairments in AD. Because AD develops slowly, similar neuropathological changes, to a lesser degree, may be present in MCI and some asymptomatic elderly subjects. In this study we tested the hypothesis that corticocortical interactions between sensory regions are impaired in aging, MCI, and AD, as compared with young subjects. When sensory cortical evoked potentials are elicited by pairs of stimuli the amplitudes of potentials to the second stimulus are attenuated. Corticocortical interactions were assessed by presenting stimulus pairs in different modalities (auditory/visual). There were significant group differences in the degree that a visual stimulus attenuated subsequent auditory potentials (young Ͼ healthy elderly Ͼ MCI Ͼ AD). Control experiments indicated equivalent amplitude reductions for all groups to the second stimulus for stimulus pairs having the same modality. These findings are compatible with progressive declines in corticocortical processing in aging, MCI, and AD.

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Source location of a 50 msec latency auditory evoked field component

Cited by 141 publications

References 11 publications

Cholinesterase inhibitors affect brain potentials in amnestic mild cognitive impairment

Cholinesterase inhibitors affect brain potentials in amnestic mild cognitive impairment

The moderating role of the dopamine transporter 1 gene on P50 sensory gating and its modulation by nicotine

Sensory cortical interactions in aging, mild cognitive impairment, and Alzheimer’s disease

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