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Search Results: 1 - 10 of 191860 matches for " Hampson Robert E "
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A Pilot Study into the Effects of the CB1 Cannabinoid Receptor Agonist WIN55,212-2 or the Antagonist/Inverse Agonist AM251 on Sleep in Rats
Anushka V. Goonawardena,Andrea Plano,Lianne Robinson,Bettina Platt,Robert E. Hampson,Gernot Riedel
Sleep Disorders , 2011, DOI: 10.1155/2011/178469
Abstract: The plant cannabinoid Δ9-tetrahydrocannabinol and the endocannabinoid anandamide increase the amount of sleep via a CB1 receptor mediated mechanism. Here, we explored the use of a novel electroencephalogram (EEG) recording device based on wireless EEG microchip technology (Neurologger) in freely-moving rats, and its utility in experiments of cannabinoids-induced alterations of EEG/vigilance stages. EEG was recorded through epidural electrodes placed above pre-frontal and parietal cortex (overlaying the dorsal hippocampus). As cannabinoids, we acutely administered the full synthetic CB1 receptor agonist, WIN55,212-2 (1?mg/kg), and the antagonist/inverse agonist, AM251 (2?mg/kg), either alone or together through the intraperitoneal route. WIN55,212-2 increased the total amount of NREM sleep and the length of each NREM bout, but this was unlikely due to CB1 receptor activation since it was not prevented by AM251. However, WIN55,212-2 also lowered overall EEG spectral power especially in theta and alpha frequency bands during wakefulness and NREM sleep, and this effect was reversed by AM251. The antagonist/inverse agonist caused no sleep alterations by itself and moderately increased spectral power in Theta, alpha and beta frequency bands during NREM sleep when administered on its own. Implications of endocannabinoid modulation of the sleep-wake cycle and its possible interactions with other transmitter systems are considered. 1. Introduction It is widely known that the active ingredient of marijuana, Δ9-Tetrahydrocannabinol (Δ9-THC), modulates the sleep-wake cycle. During the 1970s and 1980s, several experiments carried out in humans and rats demonstrated that Δ9-THC was able to increase sleep [1–5]. Similar effects can be evoked by the endocannabinoid arachidonylethanolamide (anandamide), including the modulation of food intake, body temperature, locomotor activity, pain perception, sexual behavior, learning and memory, and sleep [6, 7]. Santucci and coworkers [8] were the first to study the physiological role of endocannabinoids on sleep. They systemically administered the CB1 receptor antagonist/inverse agonist, SR141716A (SR), to rats and observed a dose-dependent increase in wakefulness (W) and a reduction in both slow-wave (SWS) and rapid eye movement (REM) sleep. This indicated that the wake-promoting properties of SR arise as a result of the inhibition of the endocannabinoid tone on CB1 receptors [9] and/or due to an inverse agonism [10, 11] on the same subset of G-protein coupled receptors. Indeed, endocannabinoids such as anandamide also
Facilitation of Task Performance and Removal of the Effects of Sleep Deprivation by an Ampakine (CX717) in Nonhuman Primates
Linda J. Porrino,James B. Daunais,Gary A. Rogers,Robert E. Hampson,Sam A. Deadwyler
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0030299
Abstract: The deleterious effects of prolonged sleep deprivation on behavior and cognition are a concern in modern society. Persons at risk for impaired performance and health-related issues resulting from prolonged sleep loss would benefit from agents capable of reducing these detrimental effects at the time they are sleep deprived. Agents capable of improving cognition by enhancing brain activity under normal circumstances may also have the potential to reduce the harmful or unwanted effects of sleep deprivation. The significant prevalence of excitatory α-amino-3-hydroxy-5-methyl-4-isoxazolepr?opionicacid (AMPA) glutamatergic receptors in the brain provides a basis for implementing a class of drugs that could act to alter or remove the effects of sleep deprivation. The ampakine CX717 (Cortex Pharmaceuticals), a positive allosteric modulator of AMPA receptors, was tested for its ability to enhance performance of a cognitive, delayed match-to-sample task under normal circumstances in well-trained monkeys, as well as alleviate the detrimental effects of 30–36 h of sleep deprivation. CX717 produced a dose-dependent enhancement of task performance under normal alert testing conditions. Concomitant measures of regional cerebral metabolic rates for glucose (CMRglc) during the task, utilizing positron emission tomography, revealed increased activity in prefrontal cortex, dorsal striatum, and medial temporal lobe (including hippocampus) that was significantly enhanced over normal alert conditions following administration of CX717. A single night of sleep deprivation produced severe impairments in performance in the same monkeys, accompanied by significant alterations in task-related CMRglc in these same brain regions. However, CX717 administered to sleep-deprived monkeys produced a striking removal of the behavioral impairment and returned performance to above-normal levels even though animals were sleep deprived. Consistent with this recovery, CMRglc in all but one brain region affected by sleep deprivation was also returned to the normal alert pattern by the drug. The ampakine CX717, in addition to enhancing cognitive performance under normal alert conditions, also proved effective in alleviating impairment of performance due to sleep deprivation. Therefore, the ability to activate specific brain regions under normal alert conditions and alter the deleterious effects of sleep deprivation on activity in those same regions indicate a potential role for ampakines in sustaining performance under these types of adverse conditions.
Facilitation of task performance and removal of the effects of sleep deprivation by an ampakine (CX717) in nonhuman primates.
Porrino Linda J,Daunais James B,Rogers Gary A,Hampson Robert E
PLOS Biology , 2005,
Abstract: The deleterious effects of prolonged sleep deprivation on behavior and cognition are a concern in modern society. Persons at risk for impaired performance and health-related issues resulting from prolonged sleep loss would benefit from agents capable of reducing these detrimental effects at the time they are sleep deprived. Agents capable of improving cognition by enhancing brain activity under normal circumstances may also have the potential to reduce the harmful or unwanted effects of sleep deprivation. The significant prevalence of excitatory alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamatergic receptors in the brain provides a basis for implementing a class of drugs that could act to alter or remove the effects of sleep deprivation. The ampakine CX717 (Cortex Pharmaceuticals), a positive allosteric modulator of AMPA receptors, was tested for its ability to enhance performance of a cognitive, delayed match-to-sample task under normal circumstances in well-trained monkeys, as well as alleviate the detrimental effects of 30-36 h of sleep deprivation. CX717 produced a dose-dependent enhancement of task performance under normal alert testing conditions. Concomitant measures of regional cerebral metabolic rates for glucose (CMRglc) during the task, utilizing positron emission tomography, revealed increased activity in prefrontal cortex, dorsal striatum, and medial temporal lobe (including hippocampus) that was significantly enhanced over normal alert conditions following administration of CX717. A single night of sleep deprivation produced severe impairments in performance in the same monkeys, accompanied by significant alterations in task-related CMRglc in these same brain regions. However, CX717 administered to sleep-deprived monkeys produced a striking removal of the behavioral impairment and returned performance to above-normal levels even though animals were sleep deprived. Consistent with this recovery, CMRglc in all but one brain region affected by sleep deprivation was also returned to the normal alert pattern by the drug. The ampakine CX717, in addition to enhancing cognitive performance under normal alert conditions, also proved effective in alleviating impairment of performance due to sleep deprivation. Therefore, the ability to activate specific brain regions under normal alert conditions and alter the deleterious effects of sleep deprivation on activity in those same regions indicate a potential role for ampakines in sustaining performance under these types of adverse conditions.
Facilitation of Task Performance and Removal of the Effects of Sleep Deprivation by an Ampakine (CX717) in Nonhuman Primates
Linda J Porrino,James B Daunais,Gary A Rogers,Robert E Hampson,Sam A Deadwyler
PLOS Biology , 2005, DOI: 10.1371/journal.pbio.0030299
Abstract: The deleterious effects of prolonged sleep deprivation on behavior and cognition are a concern in modern society. Persons at risk for impaired performance and health-related issues resulting from prolonged sleep loss would benefit from agents capable of reducing these detrimental effects at the time they are sleep deprived. Agents capable of improving cognition by enhancing brain activity under normal circumstances may also have the potential to reduce the harmful or unwanted effects of sleep deprivation. The significant prevalence of excitatory α-amino-3-hydroxy-5-methyl-4-isoxazolepr?opionicacid (AMPA) glutamatergic receptors in the brain provides a basis for implementing a class of drugs that could act to alter or remove the effects of sleep deprivation. The ampakine CX717 (Cortex Pharmaceuticals), a positive allosteric modulator of AMPA receptors, was tested for its ability to enhance performance of a cognitive, delayed match-to-sample task under normal circumstances in well-trained monkeys, as well as alleviate the detrimental effects of 30–36 h of sleep deprivation. CX717 produced a dose-dependent enhancement of task performance under normal alert testing conditions. Concomitant measures of regional cerebral metabolic rates for glucose (CMRglc) during the task, utilizing positron emission tomography, revealed increased activity in prefrontal cortex, dorsal striatum, and medial temporal lobe (including hippocampus) that was significantly enhanced over normal alert conditions following administration of CX717. A single night of sleep deprivation produced severe impairments in performance in the same monkeys, accompanied by significant alterations in task-related CMRglc in these same brain regions. However, CX717 administered to sleep-deprived monkeys produced a striking removal of the behavioral impairment and returned performance to above-normal levels even though animals were sleep deprived. Consistent with this recovery, CMRglc in all but one brain region affected by sleep deprivation was also returned to the normal alert pattern by the drug. The ampakine CX717, in addition to enhancing cognitive performance under normal alert conditions, also proved effective in alleviating impairment of performance due to sleep deprivation. Therefore, the ability to activate specific brain regions under normal alert conditions and alter the deleterious effects of sleep deprivation on activity in those same regions indicate a potential role for ampakines in sustaining performance under these types of adverse conditions.
Closing the loop in primate prefrontal cortex: inter-laminar processing
Ioan Opris,Peter F. Huettl,Theodore W. Berger,Robert E. Hampson,Sam A. Deadwyler
Frontiers in Neural Circuits , 2012, DOI: 10.3389/fncir.2012.00088
Abstract: Prefrontal cortical (PFC) activity in the primate brain emerging from minicolumnar microcircuits plays a critical role in cognitive processes dealing with executive control of behavior. However, the specific operations of columnar laminar processing in prefrontal cortex (PFC) are not completely understood. Here we show via implementation of unique microanatomical recording and stimulating arrays, that minicolumns in PFC are involved in the executive control of behavior in rhesus macaque nonhuman primates (NHPs) performing a delayed-match-to-sample (DMS) task. PFC neurons demonstrate functional interactions between pairs of putative pyramidal cells within specified cortical layers via anatomically oriented minicolumns. Results reveal target-specific, spatially tuned firing between inter-laminar (layer 2/3 and layer 5) pairs of neurons participating in the gating of information during the decision making phase of the task with differential correlations between activity in layer 2/3 and layer 5 in the integration of spatial vs. object-specific information for correct task performance. Such inter-laminar processing was exploited by the interfacing of an online model which delivered stimulation to layer 5 locations in a pattern associated with successful performance thereby closing the columnar loop externally in a manner that mimicked normal processing in the same task. These unique technologies demonstrate that PFC neurons encode and process information via minicolumns which provides a closed loop form of “executive function,” hence disruption of such inter-laminar processing could form the bases for cognitive dysfunction in primate brain.
Extraction and restoration of hippocampal spatial memories with non-linear dynamical modeling
Dong Song,Vasilis Z. Marmarelis,Robert E. Hampson,Sam A. Deadwyler,Theodore W. Berger
Frontiers in Systems Neuroscience , 2014, DOI: 10.3389/fnsys.2014.00097
Abstract: To build a cognitive prosthesis that can replace the memory function of the hippocampus, it is essential to model the input-output function of the damaged hippocampal region, so the prosthetic device can stimulate the downstream hippocampal region, e.g., CA1, with the output signal, e.g., CA1 spike trains, predicted from the ongoing input signal, e.g., CA3 spike trains, and the identified input-output function, e.g., CA3-CA1 model. In order for the downstream region to form appropriate long-term memories based on the restored output signal, furthermore, the output signal should contain sufficient information about the memories that the animal has formed. In this study, we verify this premise by applying regression and classification modelings of the spatio-temporal patterns of spike trains to the hippocampal CA3 and CA1 data recorded from rats performing a memory-dependent delayed non-match-to-sample (DNMS) task. The regression model is essentially the multiple-input, multiple-output (MIMO) non-linear dynamical model of spike train transformation. It predicts the output spike trains based on the input spike trains and thus restores the output signal. In addition, the classification model interprets the signal by relating the spatio-temporal patterns to the memory events. We have found that: (1) both hippocampal CA3 and CA1 spike trains contain sufficient information for predicting the locations of the sample responses (i.e., left and right memories) during the DNMS task; and more importantly (2) the CA1 spike trains predicted from the CA3 spike trains by the MIMO model also are sufficient for predicting the locations on a single-trial basis. These results show quantitatively that, with a moderate number of unitary recordings from the hippocampus, the MIMO non-linear dynamical model is able to extract and restore spatial memory information for the formation of long-term memories and thus can serve as the computational basis of the hippocampal memory prosthesis.
Donor/recipient enhancement of memory in rat hippocampus
Sam A. Deadwyler,Theodore W. Berger,Andrew J. Sweatt,Dong Song,Rosa H. M. Chan,Ioan Opris,Vasilis Z. Marmarelis,Robert E. Hampson
Frontiers in Systems Neuroscience , 2013, DOI: 10.3389/fnsys.2013.00120
Abstract: The critical role of the mammalian hippocampus in the formation, translation and retrieval of memory has been documented over many decades. There are many theories of how the hippocampus operates to encode events and a precise mechanism was recently identified in rats performing a short-term memory task which demonstrated that successful information encoding was promoted via specific patterns of activity generated within ensembles of hippocampal neurons. In the study presented here, these “representations” were extracted via a customized non-linear multi-input multi-output (MIMO) mathematical model which allowed prediction of successful performance on specific trials within the testing session. A unique feature of this characterization was demonstrated when successful information encoding patterns were derived online from well-trained “donor” animals during difficult long-delay trials and delivered via online electrical stimulation to synchronously tested na?ve “recipient” animals never before exposed to the delay feature of the task. By transferring such model-derived trained (donor) animal hippocampal firing patterns via stimulation to coupled na?ve recipient animals, their task performance was facilitated in a direct “donor-recipient” manner. This provides the basis for utilizing extracted appropriate neural information from one brain to induce, recover, or enhance memory related processing in the brain of another subject.
Functional connectivity studies of patients with auditory verbal hallucinations
Ralph E. Hoffman,Michelle Hampson
Frontiers in Human Neuroscience , 2012, DOI: 10.3389/fnhum.2012.00006
Abstract: Functional connectivity (FC) studies of brain mechanisms leading to auditory verbal hallucinations (AVHs) utilizing functional magnetic resonance imaging (fMRI) data are reviewed. Initial FC studies utilized fMRI data collected during performance of various tasks, which suggested frontotemporal disconnection and/or source-monitoring disturbances. Later FC studies have utilized resting (no-task) fMRI data. These studies have produced a mixed picture of disconnection and hyperconnectivity involving different pathways associated with AVHs. Results of our most recent FC study of AVHs are reviewed in detail. This study suggests that the core mechanism producing AVHs involves not a single pathway, but a more complex functional loop. Components of this loop include Wernicke's area and its right homologue, the left inferior frontal cortex, and the putamen. It is noteworthy that the putamen appears to play a critical role in the generation of spontaneous language, and in determining whether auditory stimuli are registered consciously as percepts. Excessive functional coordination linking this region with the Wernicke's seed region in patients with schizophrenia could, therefore, generate an overabundance of potentially conscious language representations. In our model, intact FC in the other two legs of corticostriatal loop (Wernicke's with left IFG, and left IFG with putamen) appeared to allow hyperconnectivity linking the putamen and Wernicke's area (common to schizophrenia overall) to be expressed as conscious hallucinations of speech. Recommendations for future studies are discussed, including inclusion of multiple methodologies applied to the same subjects in order to compare and contrast different mechanistic hypotheses, utilizing EEG to better parse time-course of neural synchronization leading to AVHs, and ascertaining experiential subtypes of AVHs that may reflect distinct mechanisms.
Transcranial Magnetic Stimulation and Connectivity Mapping: Tools for Studying the Neural Bases of Brain Disorders
M. Hampson,R. E. Hoffman
Frontiers in Systems Neuroscience , 2010, DOI: 10.3389/fnsys.2010.00040
Abstract: There has been an increasing emphasis on characterizing pathophysiology underlying psychiatric and neurological disorders in terms of altered neural connectivity and network dynamics. Transcranial magnetic stimulation (TMS) provides a unique opportunity for investigating connectivity in the human brain. TMS allows researchers and clinicians to directly stimulate cortical regions accessible to electromagnetic coils positioned on the scalp. The induced activation can then propagate through long-range connections to other brain areas. Thus, by identifying distal regions activated during TMS, researchers can infer connectivity patterns in the healthy human brain and can examine how those patterns may be disrupted in patients with different brain disorders. Conversely, connectivity maps derived using neuroimaging methods can identify components of a dysfunctional network. Nodes in this dysfunctional network accessible as targets for TMS by virtue of their proximity to the scalp may then permit TMS-induced alterations of components of the network not directly accessible to TMS via propagated effects. Thus TMS can provide a portal for accessing and altering neural dynamics in networks that are widely distributed anatomically. Finally, when long-term modulation of network dynamics is induced by trains of repetitive TMS, changes in functional connectivity patterns can be studied in parallel with changes in patient symptoms. These correlational data can elucidate neural mechanisms underlying illness and recovery. In this review, we focus on the application of these approaches to the study of psychiatric and neurological illnesses.
Potential Use and Challenges of Functional Connectivity Mapping in Intractable Epilepsy
Robert Todd Constable,Dustin Scheinost,Emily S. Finn,Michelle Hampson,F. Scott Winstanley
Frontiers in Neurology , 2013, DOI: 10.3389/fneur.2013.00039
Abstract: This review focuses on the use of resting-state functional magnetic resonance imaging data to assess functional connectivity in the human brain and its application in intractable epilepsy. This approach has the potential to predict outcomes for a given surgical procedure based on the pre-surgical functional organization of the brain. Functional connectivity can also identify cortical regions that are organized differently in epilepsy patients either as a direct function of the disease or through indirect compensatory responses. Functional connectivity mapping may help identify epileptogenic tissue, whether this is a single focal location or a network of seizure-generating tissues. This review covers the basics of connectivity analysis and discusses particular issues associated with analyzing such data. These issues include how to define nodes, as well as differences between connectivity analyses of individual nodes, groups of nodes, and whole-brain assessment at the voxel level. The need for arbitrary thresholds in some connectivity analyses is discussed and a solution to this problem is reviewed. Overall, functional connectivity analysis is becoming an important tool for assessing functional brain organization in epilepsy.
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