A Parametric Study of the N40 Auditory Evoked Response in Rats

Boutros, Nashaat N.; Bonnet, Kenneth A.; Millana, Ronel B.; Liu, Jennifer

doi:10.1016/s0006-3223(97)00161-3

Cited by 47 publications

(21 citation statements)

References 20 publications

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“…The mechanisms by which exogenous cannabinoids such as THC might affect P50 gating are largely unknown, however consistent with rat models of sensory gating (Boutros et al, 1997;Boutros and Kwan, 1998;Dissanayake et al, 2013), as well as intracranial recordings in humans which have implicated hippocampal involvement (e.g., Grunwald et al, 2003), disrupted sensory gating in cannabis users might be due to the partial agonist effects of THC at CB1 receptors in the hippocampus in terms of reducing GABAergic inhibition of excitatory glutamatergic neurons (Dissanayake et al, 2013). This could lead to deficits in inhibitory processing, including reduced inhibitory inputs to P50 generators in auditory and frontal cortices.…”

Section: Discussionmentioning

confidence: 64%

Chronic effects of cannabis on sensory gating

Broyd

Greenwood

Croft

et al. 2013

International Journal of Psychophysiology

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Chronic cannabis use has been associated with neurocognitive deficits, alterations in brain structure and function, and with psychosis. This study investigated the effects of chronic cannabis use on P50 sensory-gating in regular users, and explored the association between sensory gating, cannabis use history and the development of psychotic-like symptoms. Twenty controls and 21 regular cannabis users completed a P50 paired-click (S1 and S2) paradigm with an inter-pair interval of 9. s. The groups were compared on P50 amplitude to S1 and S2, P50 ratio (S2/S1) and P50 difference score (S1-S2). While cannabis users overall did not differ from controls on P50 measures, prolonged duration of regular use was associated with greater impairment in sensory gating as indexed by both P50 ratio and difference scores (including after controlling for tobacco use). Long-term cannabis users were found to have worse sensory gating ratios and difference scores compared to short-term users and controls. P50 metrics did not correlate significantly with any measure of psychotic-like symptoms in cannabis users. These results suggest that prolonged exposure to cannabis results in impaired P50 sensory-gating in long-term cannabis users. While it is possible that these deficits may have pre-dated cannabis use and reflect a vulnerability to cannabis use, their association with increasing years of cannabis use suggests that this is not the case. Impaired P50 sensory-gating ratios have also been reported in patients with schizophrenia and may indicate a similar underlying pathology.

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Section: Discussionmentioning

confidence: 64%

Chronic effects of cannabis on sensory gating

Broyd

Greenwood

Croft

et al. 2013

International Journal of Psychophysiology

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“…In rats the N40, which was thought to be equivalent to the human P50, (Boutros et al, 1997), occurs simultaneously in scalp and intrahippocampal recordings (Bickford-Wimer et al, 1990). Via extrapolation, from animal to human data, the hippocampus was also considered central to the gating of the human P50.…”

Section: Discussionmentioning

confidence: 99%

Sensory gating in the human hippocampal and rhinal regions: Regional differences

et al. 2007

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To further explore the roles of medial temporal structures in mediating sensory gating of incoming irrelevant or redundant auditory input, twenty-seven patients with intractable epilepsy with depth electrodes implanted in the medial temporal lobe for presurgery evaluation underwent evoked response recording to auditory paired-stimuli (S1-S2). Seventeen subjects were diagnosed with left medial temporal lobe epilepsy (MTLE) and 10 with right MTLE. Only data from the nonlesion side were included. Twenty-three records from rhinal and anterior hippocampal regions, and 21 from posterior hippocampal regions were included in the analysis. The rhinal region had two prominent components (a negativity peaking around 200 ms followed by a positivity peaking around 400 ms). Both the anterior and posterior hippocampal regions exhibited a dominant negative potential peaking around 400 ms. These components were all composed predominantly of slower frequencies. In contrast, a negativity in the posterior hippocampus at around 100 ms was composed of slow and fast frequencies. All components but the early rhinal negativity were attenuated by stimulus repetition. This is the first report documenting that different regions of the medial temporal area are differentially involved in the processing of auditory input, most likely reflecting separate steps of processing. The data support the need for further exploration of the contribution of these regions to sensory gating. This information helps to increase our understanding of this basic but important and complex function.

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“…The neurobiology of sensory processing deficits in schizophrenia has been investigated with auditory ERPs in monkeys, cats, rats, and mice, using tasks similar to those used in humans (Boutros et al, 1997;de Bruin et al, 1999;Javitt et al, 2000;Pincze et al, 2001;Siegel et al, 2003;Simosky et al, 2003;Stevens et al, 2001Stevens et al, , 1997. To interpret the findings in these studies, it is important to understand the relationship between auditory evoked components in the species being studied and the analogous components in human.…”

Section: Introductionmentioning

confidence: 99%

Effects of Chronic Olanzapine and Haloperidol Differ on the Mouse N1 Auditory Evoked Potential

Maxwell

Liang

Weightman

et al. 2004

Neuropsychopharmacol

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Auditory evoked potentials have been used in a variety of animal models to assess information-processing impairments in schizophrenia. Previous mouse models have primarily employed a paired click paradigm to assess the transient measures of auditory gating. The current study uses stimulus trains at varied interstimulus intervals (ISI) between 0.25 and 8 s in mice to assess the effects of chronic olanzapine and haloperidol on auditory processing. Data indicate that olanzapine increases the amplitude of the N40, P80, and P20/N40 components of the auditory evoked potential, whereas haloperidol had no such effect. The ISI paradigm also allowed for an evaluation of several components of the mouse evoked potential to assess those that display response properties similar to the human P50 and N100. Data suggest that the mouse N40 displays an ISI response relationship that shares characteristics with the human N100, whereas the P20 appears more consistent with the human P50 across the ISI range evaluated in this task. This study suggests that olanzapine may help improve N100 impairments seen in schizophrenia, while haloperidol does not.

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A Parametric Study of the N40 Auditory Evoked Response in Rats

Cited by 47 publications

References 20 publications

Chronic effects of cannabis on sensory gating

Chronic effects of cannabis on sensory gating

Sensory gating in the human hippocampal and rhinal regions: Regional differences

Effects of Chronic Olanzapine and Haloperidol Differ on the Mouse N1 Auditory Evoked Potential

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