NMDA receptors mediate neuronal burst firing in rat somatosensory cortex in vivo

Kobayashi, Toshinori; Nagao, Takeki; Fukuda, H; Tp, Hicks; Ji, Oka

doi:10.1097/00001756-199306000-00034

Cited by 17 publications

(10 citation statements)

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“…These findings suggest that NMDA-mediated currents along with R-type currents are the key players underlying somatic bursting, in accordance with the recent findings of [41]. Overall, our results add to a large body of previous work regarding the role of NMDA and voltage dependent calcium channels in promoting somatic bursting [41], [50], [51], [52], [53], [54], [55], [56].…”

Section: Resultssupporting

confidence: 92%

Encoding of Spatio-Temporal Input Characteristics by a CA1 Pyramidal Neuron Model

et al. 2010

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The in vivo activity of CA1 pyramidal neurons alternates between regular spiking and bursting, but how these changes affect information processing remains unclear. Using a detailed CA1 pyramidal neuron model, we investigate how timing and spatial arrangement variations in synaptic inputs to the distal and proximal dendritic layers influence the information content of model responses. We find that the temporal delay between activation of the two layers acts as a switch between excitability modes: short delays induce bursting while long delays decrease firing. For long delays, the average firing frequency of the model response discriminates spatially clustered from diffused inputs to the distal dendritic tree. For short delays, the onset latency and inter-spike-interval succession of model responses can accurately classify input signals as temporally close or distant and spatially clustered or diffused across different stimulation protocols. These findings suggest that a CA1 pyramidal neuron may be capable of encoding and transmitting presynaptic spatiotemporal information about the activity of the entorhinal cortex-hippocampal network to higher brain regions via the selective use of either a temporal or a rate code.

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Section: Resultssupporting

confidence: 92%

Encoding of Spatio-Temporal Input Characteristics by a CA1 Pyramidal Neuron Model

et al. 2010

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“…The mechanisms that govern burst firing are likely to be a combination of intrinsic neural properties and local network connectivity (24,38,45,46). The bursting that we describe here is a period in a spike train that has a higher discharge rate than other periods in the same spike train.…”

Section: Discussionmentioning

confidence: 99%

“…It is generally thought that bursting arises from stimulation of NMDA receptors and opening of L-type calcium channels, which leads to sustained depolarization and increased probability of action potential generation in response to subsequent synaptic events (24,38). Thus, the lack of sustained NMDA receptor-mediated membrane depolarization would decrease the probability of successive action potential generation, and reduce the number of closely spaced spikes and burst activity (39)(40)(41)(42).…”

Section: Discussionmentioning

confidence: 99%

NMDA receptor hypofunction produces concomitant firing rate potentiation and burst activity reduction in the prefrontal cortex

Jackson

Homayoun

Moghaddam

2004

Proc. Natl. Acad. Sci. U.S.A.

392

321

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Cognitive deficits associated with frontal lobe dysfunction are a determinant of long-term disability in schizophrenia and are not effectively treated with available medications. Clinical studies show that many aspects of these deficits are transiently induced in healthy individuals treated with N-methyl-D-aspartate (NMDA) antagonists. These findings and recent genetic linkage studies strongly implicate NMDA receptor deficiency in schizophrenia and suggest that reversing this deficiency is pertinent to treating the cognitive symptoms of schizophrenia. Despite the wealth of behavioral data on the effects of NMDA antagonist treatment in humans and laboratory animals, there is a fundamental lack of understanding about the mechanisms by which a general state of NMDA deficiency influences the function of cortical neurons. Using ensemble recording in freely moving rats, we found that NMDA antagonist treatment, at doses that impaired working memory, potentiated the firing rate of most prefrontal cortex neurons. This potentiation, which correlated with expression of behavioral stereotypy, resulted from an increased number of irregularly discharged single spikes. Concurrent with the increase in spike activity, there was a significant reduction in organized bursting activity. These results identify two distinct mechanisms by which NMDA receptor deficiency may disrupt frontal lobe function: an increase in disorganized spike activity, which may enhance cortical noise and transmission of disinformation; and a decrease in burst activity, which reduces transmission efficacy of cortical neurons. These findings provide a physiological basis for the NMDA receptor deficiency model of schizophrenia and may clarify the nature of cortical dysfunction in this disease.N -methyl-D-aspartate (NMDA) receptors are increasingly implicated in schizophrenia. The majority of genes that have so far been linked to increased susceptibility to develop schizophrenia can modulate NMDA receptor-mediated signal transduction (1, 2), suggesting that NMDA receptors are a critical component of genetic vulnerability to develop schizophrenia. Recreational or investigator-administered exposure to drugs that have antagonist activity at NMDA receptors produces a transient state of psychosis and schizophrenia-like cognitive deficits (3-5). In fact, double-blind clinical studies suggest that the cognitive deficits produced by NMDA antagonists in healthy volunteers are nearly identical to the deficits observed in patients with schizophrenia (6). Based on these pharmacological and genetic linkage studies, the NMDA antagonist treatment is considered a mechanistically relevant model for cognitive deficits of schizophrenia (7-10). Understanding the impact of this treatment on cellular mechanisms that support the expression of abnormal cognition is critical for understanding the impact of an underlying NMDA dysfunction on the disease process and for defining better treatments. However, despite a large body of literature that has characterized the behavioral aspects of...

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“…Specifically, bursts as a unit of neural information have been postulated to play important roles in brain function [36, 42–44]. Compared with single spikes, presynaptic bursting of action potentials can be more reliably transmitted to the postsynaptic neurons and increase the probability of information transmission between neurons [45, 46]. Moreover, several lines of evidence indicated that bursts have a special role in synaptic plasticity [36].…”

Section: Discussionmentioning

confidence: 99%

Decreased Neuronal Bursting and Phase Synchrony in the Hippocampus of Streptozotocin Diabetic Rats

Qiao

Xie

et al. 2014

Journal of Diabetes Research

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Diabetic encephalopathy is one of the complications of diabetes. Cognitive dysfunction is the main consequence. Previous findings from neuroanatomical and in vitro electrophysiological studies showed that the structure and function of the hippocampus is impaired in diabetes, which may underlie the cognitive dysfunction induced by diabetes. However the study of electrophysiological abnormality of hippocampal neurons in intact networks is sparse. In the current study, we recorded the spontaneous firing of neurons in hippocampal CA1 area in anesthetized streptozotozin (STZ)-diabetic and age-matched control rats. Profound reduction in burst activity was found in diabetic rats. Compared to control rats, the intra-burst inter-spike intervals were prolonged significantly in diabetic rats, while the burst ratio and the mean number of spikes within a burst decreased significantly. Treatment with APP 17-mer peptide retarded the effects of diabetes on these parameters. In addition, the average PLV of diabetic rats was lower than that of control rats. These findings provide in vivo electrophysiological evidence for the impairment of hippocampal function in STZ-diabetic rats, and may have some implications in the mechanisms associated with cognitive deficits in diabetes.

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NMDA receptors mediate neuronal burst firing in rat somatosensory cortex in vivo

Cited by 17 publications

References 0 publications

Encoding of Spatio-Temporal Input Characteristics by a CA1 Pyramidal Neuron Model

Encoding of Spatio-Temporal Input Characteristics by a CA1 Pyramidal Neuron Model

NMDA receptor hypofunction produces concomitant firing rate potentiation and burst activity reduction in the prefrontal cortex

Decreased Neuronal Bursting and Phase Synchrony in the Hippocampus of Streptozotocin Diabetic Rats

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