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

Maxwell, Christina R.; Liang, Yuling; Weightman, Bryanne D; Kanes, Stephen; Abel, Ted; Gur, Raquel E.; Turetsky, Bruce I.; Bilker, Warren B.; Lenox, Robert H.; Siegel, Steven J.

doi:10.1038/sj.npp.1300376

Cited by 64 publications

(63 citation statements)

References 44 publications

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“…The electrode pedestal was secured to the skull using dental cement and Super Glue. All surgical procedures were consistent with previously published descriptions , Connolly et al, 2004, Maxwell et al, 2004a, Maxwell et al, 2004b, Siegel et al, 2005, Metzger et al, 2006.…”

Section: Surgerysupporting

confidence: 57%

“…In fact, a recent study on the effects of nicotine on ERP components demonstrated opposite effects of nicotine on the P20 and N40 amplitudes in mice with nicotine increasing P20 amplitude and decreasing N40 amplitude (Metzger et al, 2006). We believe the mouse P20 and N40 to be analogous to the human P50 and N100 respectively based on previous research in our lab and others , Connolly et al, 2004, Maxwell et al, 2004a, Maxwell et al, 2004b, Umbricht et al, 2004, Siegel et al, 2005, Metzger et al, 2006. Thus, we have chosen to analyze the components independently in this study.…”

Section: Introductionmentioning

confidence: 99%

“…Models of the ERP changes associated with schizophrenia have been used to explore potential mechanisms for the observed ERP deficits and as a tool for the development of new therapeutic agents (Stevens and Wear, 1997, Stevens et al, 1998, Simosky et al, 2003, Connolly et al, 2004, Maxwell et al, 2004a, Maxwell et al, 2004b, Umbricht et al, 2004. Although many studies propose the P20/N40 waveform difference in mice to be analogous to the human P50 Wear, 1997, Simosky et al, 2003), recently several studies have indicated that the P20 and N40 waveforms respond independently to pharmacological and behavioral manipulations (Connolly et al, 2004, Maxwell et al, 2004a, Maxwell et al, 2004b, Umbricht et al, 2004, Metzger et al, 2006. In fact, a recent study on the effects of nicotine on ERP components demonstrated opposite effects of nicotine on the P20 and N40 amplitudes in mice with nicotine increasing P20 amplitude and decreasing N40 amplitude (Metzger et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Mecamylamine blocks nicotine-induced enhancement of the P20 auditory event–related potential and evoked gamma

Phillips¹,

Ehrlichman²,

Siegel³

2007

Neuroscience

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Cigarette smoking is significantly more prevalent in individuals with schizophrenia than in nonaffected populations. Certain neurocognitive deficits and disruptions common in schizophrenia may be altered by smoking, leading to the hypothesis that schizophrenics engage in smoking behavior to alleviate specific neurocognitive symptoms of the disorder. Additionally, research suggests that individuals with schizophrenia have altered auditory event related potentials (ERPs) and abnormalities in evoked gamma oscillations which are both indices of sensory information processing. This study was conducted to examine the effect of acute administration of nicotine and the non-specific nicotinic antagonist mecamylamine on the P20 and N40 components of the auditory event related potential (ERP) and evoked gamma oscillations in mice. Acute nicotine (1 mg/kg) significantly increased P20 amplitude, an effect that was blocked by pretreatment with mecamylamine (2 mg/kg). Additionally, acute nicotine increased the normal burst of evoked gamma following an auditory stimulus. The increase in evoked gamma was also blocked by mecamylamine pretreatment. Although acute nicotine decreased amplitude of the N40 component, this decrease was not attenuated by mecamylamine. These results replicate findings that nicotine may enhance early sensory information processing through the nicotinic acetylcholinergic receptor system in an established model (ERPs) and extend these findings in an emerging, novel model (evoked gamma oscillations) of sensory information processing. The results also support the hypothesis that nicotine may be beneficial to individuals with deficits in neurocognitive functions, such as those suffering from schizophrenia.

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Section: Surgerysupporting

confidence: 57%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mecamylamine blocks nicotine-induced enhancement of the P20 auditory event–related potential and evoked gamma

Phillips¹,

Ehrlichman²,

Siegel³

2007

Neuroscience

View full text Add to dashboard Cite

show abstract

“…Our initial hypothesis to find a similar profile in the NR1 mutant mice was based on studies in rats, non-human primates and healthy volunteers, in which such a profile was reproduced by acute application of NMDAR antagonists, pointing to a possible involvement of the NMDAR in this deficit (Javitt et al, 2000a;Ehlers et al, 1992;Umbricht et al, 2004a). Furthermore, previous studies have shown that the mouse AEP peaks P1, N1, and P2 display refractory curves comparable to their putative human correlates (P1, N1, P2) (Umbricht et al, 2004b;Maxwell et al, 2004). Also, in two mouse studies that investigated the effects of pharmacological NMDAR blockade P1 was increased and N1 changed dependent on mouse strain (Maxwell et al, 2006;Connolly et al, 2004).…”

Section: Aep Peak Refractorinessmentioning

confidence: 72%

“…Early auditory sensory processing deficits in NR1 mutants S Bickel et al schizophrenia, and (2) the P1 and N1 peaks in mice do not represent the associate human peaks although the available evidence speaks against that (Umbricht et al, 2004b;Maxwell et al, 2004).…”

Section: Aep Peak Refractorinessmentioning

confidence: 99%

Early Auditory Sensory Processing Deficits in Mouse Mutants with Reduced NMDA Receptor Function

Bickel

Lipp

Umbricht

2007

Neuropsychopharmacol

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Cognitive deficits in schizophrenia include impairments at automatic, preattentive stages of sensory information processing. These deficits are evident in the prepulse inhibition-(PPI) and habituation of the auditory startle response paradigm, the paired tone paradigm in the EEG, and the peak recovery function of auditory evoked potentials (AEP). Administration of NMDA receptor antagonists reliably disrupts PPI and habituation of the startle, but not gating of AEPs in rodents. In the peak recovery paradigm, patients with schizophrenia and primates treated with NMDA receptor antagonists show reduced maximal response at long interstimulus intervals (ISI), but normal responses at short ISIs. Thus reduced NMDA receptor signalling may underlie alterations in these paradigms observed in schizophrenia. We tested the paradigms mentioned in mouse mutants with reduced expression of the NR1 subunit of the NMDA receptor (N ¼ 15) and their wild-type littermates (N ¼ 16). The NR1 mutant mice showed impaired habituation and PPI of the auditory startle response, as well as impaired gating in the paired tone paradigm. Deficits between the two gating measures did not correlate, corroborating previous evidence that these paradigms measure distinct processes. In the peak recovery paradigm, the NR1 mutants showed increased responses of the AEPs P1 and N1 at short ISIs but no difference between groups were observed at long ISIs. In conclusion, the NR1 hypomorphic mice modelled sensory and sensorimotor gating and startle habituation deficits observed in schizophrenia, but failed to model alterations in the peak recovery function.

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

Cited by 64 publications

References 44 publications

Mecamylamine blocks nicotine-induced enhancement of the P20 auditory event–related potential and evoked gamma

Mecamylamine blocks nicotine-induced enhancement of the P20 auditory event–related potential and evoked gamma

Early Auditory Sensory Processing Deficits in Mouse Mutants with Reduced NMDA Receptor Function

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

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