Restoring theta‐like rhythmicity in rats restores initial learning in the Morris water maze

McNaughton, Neil; Ruan, Ming; Woodnorth, Mary-Anne

doi:10.1002/hipo.20235

Cited by 204 publications

(216 citation statements)

References 52 publications

(53 reference statements)

Supporting

Mentioning

200

Contrasting

Order By: Relevance

“…It was suggested that restoring theta-range rhythmicity restores hippocampal function (McNaughton, Ruan, & Woodnorth, 2006). The theta rhythm may also play a role in information processing using an attentional double-gating mechanism, "filtering-in" signals for effective registration and encoding of selected information and additionally "filteringout" interfering inputs (Vinogradova, 1995).…”

Section: Introductionmentioning

confidence: 99%

Ketamine Modulates Theta and Gamma Oscillations

Lazarewicz¹,

Ehrlichman²,

Maxwell³

et al. 2010

Journal of Cognitive Neuroscience

195

163

View full text Add to dashboard Cite

Ketamine, an N-methyl-D-aspartate (NMDA) receptor glutamatergic antagonist, has been studied as a model of schizophrenia when applied in subanesthetic doses. In EEG studies, ketamine affects sensory gating and alters the oscillatory characteristics of neuronal signals in a complexmanner. We investigated the effects of ketamine on in vivo recordings from the CA3 region of mouse hippocampus referenced to the ipsilateral frontal sinus using a paired-click auditory gating paradigm. One issue of particular interest was elucidating the effect of ketamine on background network activity, poststimulus evoked and induced activity. We find that ketamine attenuates the theta frequency band in both background activity and in poststimulus evoked activity. Ketamine also disrupts a late, poststimulus theta power reduction seen in control recordings. In the gamma frequency range, ketamine enhances both background and evoked power, but decreases relative induced power. These findings support a role for NMDA receptors in mediating the balance between theta and gamma responses to sensory stimuli, with possible implications for dysfunction in schizophrenia. In EEG studies, ketamine affects sensory gating and alters the oscillatory characteristics of neuronal signals in a complex manner. We investigated the effects of ketamine on in vivo recordings from the CA3 region of mouse hippocampus referenced to the ipsilateral frontal sinus using a paired-click auditory gating paradigm. One issue of particular interest was elucidating the effect of ketamine on background network activity, poststimulus evoked and induced activity. We find that ketamine attenuates the theta frequency band in both background activity and in poststimulus evoked activity. Ketamine also disrupts a late, poststimulus theta power reduction seen in control recordings. In the gamma frequency range, ketamine enhances both background and evoked power, but decreases relative induced power. These findings support a role for NMDA receptors in mediating the balance between theta and gamma responses to sensory stimuli, with possible implications for dysfunction in schizophrenia. ■ Disciplines Physical Sciences and Mathematics | Physics

show abstract

Section: Introductionmentioning

confidence: 99%

Ketamine Modulates Theta and Gamma Oscillations

Lazarewicz¹,

Ehrlichman²,

Maxwell³

et al. 2010

Journal of Cognitive Neuroscience

195

163

View full text Add to dashboard Cite

show abstract

“…Since decreased and increased theta activity correlate with cognitive deficit and improvement, respectively (Kinney et al, 1999;Nolan et al, 2004;McNaughton et al, 2006), compromised theta activity during epileptogenesis could be an important contributing factor for cognitive dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Early Deficits in Spatial Memory and Theta Rhythm in Experimental Temporal Lobe Epilepsy

Chauvière¹,

Rafrafi²,

et al. 2009

View full text Add to dashboard Cite

Patients with temporal lobe epilepsy (TLE), the most common form of epilepsy in adults, often display cognitive deficits. The time course and underlying mechanisms of cognitive decline remain unknown during epileptogenesis (the process leading to epilepsy). Using the rat pilocarpine model of TLE, we performed a longitudinal study to assess spatial and nonspatial cognitive performance during epileptogenesis. In parallel, we monitored interictal-like activity (ILA) in the hippocampal CA1 region, as well as theta oscillations, a brain rhythm central to numerous cognitive processes. Here, we report that spatial memory was altered soon after pilocarpine-induced status epilepticus, i.e., already during the seizure-free, latent period. Spatial deficits correlated with a decrease in the power of theta oscillations but not with the frequency of ILA. Spatial deficits persisted when animals had spontaneous seizures (chronic stage) without further modification. In contrast, nonspatial memory performances remained unaffected throughout. We conclude that the reorganization of hippocampal circuitry that immediately follows the initial insult can affect theta oscillation mechanisms, in turn, resulting in deficits in hippocampusdependent memory tasks. These deficits may be dissociated from the process that leads to epilepsy itself but could instead constitute, as ILA, early markers in at-risk patients and/or provide beneficial therapeutic targets.

show abstract

“…We also proved that arti cial replacement of blocked RSA repairs behavioural dysfunction [91] (the first proof that any EEG rhythmicity is functional in and of itself ); and that changes in RSA mediate the action of anxiolytics on behavioural inhibition in an approach-avoidance conflict [92]. Thus RSA appears to be not just a reliable model of anxiolytic action but to be a significant neural substrate of an anxietyrelated process.…”

Section: Rhythmical Slow Activity (Rsa Theta) As a Potential Anxietymentioning

confidence: 60%

Development of a theoretically-derived human anxiety syndrome biomarker

McNaughton

2014

Translational Neuroscience

Self Cite

View full text Add to dashboard Cite

"Anxiety disorders" are extremely common; and are a major source of health costs and lost work days. Their diagnosis is currently based on clinical symptom check lists and there are no biological markers to diagnose speci c syndromal causes. This paper describes: 1) a detailed theory of the brain systems controlling anxiolytic-insensitive threat-avoidance and anxiolytic-sensitive threat-approach -where, in specific brain structures, activity generates specific normal behaviours, hyperactivity generates abnormal behaviours, and hyper-reactivity (hypersensitivity to input) generates specific clinical syndromes; 2) a rodent model of systemic anxiolytic action (rhythmical slow activity), linked to the theory, that over a period of 40 years has shown predictive validity with no false positives or false negatives -and which is likely to assay the sensitivity of endogenous systems that control anxiety; and, 3) derivation from this rodent-based theory of a specific non-invasive biomarker (goal-conflict-specific rhythmicity) for the threat-approach system in humans. This new biomarker should allow division of untreated "anxiety" patients, with superficially similar clusters of symptoms, into distinct high scoring (syndromal) and low scoring groups with different treatment-responses. This would be the first theoretically-derived biomarker for any mental disorder and should: 1) predict treatment efficacy better than current symptom-based diagnoses; 2) provide a human single dose test of novel anxiolytics; 3) provide a starting point for developing biomarkers for other "anxiety" syndromes; and so, 4) greatly improve treatment outcomes and cost-effectiveness.

show abstract

Restoring theta‐like rhythmicity in rats restores initial learning in the Morris water maze

Cited by 204 publications

References 52 publications

Ketamine Modulates Theta and Gamma Oscillations

Ketamine Modulates Theta and Gamma Oscillations

Early Deficits in Spatial Memory and Theta Rhythm in Experimental Temporal Lobe Epilepsy

Development of a theoretically-derived human anxiety syndrome biomarker

Contact Info

Product

Resources

About