Adenosine is considered to be a key regulator of sleep homeostasis by promoting slow-wave sleep through inhibition of the brain's arousal centers. However, little is known about the effect of adenosine on neuronal network activity at the cellular level in the neocortex. Here, we show that adenosine differentially modulates synaptic transmission between different types of neurons in cortical layer 4 (L4) through activation of pre- and/or postsynaptically located adenosine A1 receptors.
View Article and Find Full Text PDFOscillations in electrical activity are a characteristic feature of many brain networks and display a wide variety of temporal patterns. A network may express a single oscillation frequency, alternate between two or more distinct frequencies, or continually express multiple frequencies. In addition, oscillation amplitude may fluctuate over time.
View Article and Find Full Text PDFThe medial prefrontal cortex (mPFC) has been implicated in cognitive and executive processes including decision making, working memory and behavioral flexibility. Cortical processing depends on the interaction between distinct neuronal cell types in different cortical layers. To better understand cortical processing in the rat mPFC, we studied the diversity of pyramidal neurons using in vitro whole-cell patch clamp recordings and biocytin staining of neurons, followed by morphological analysis.
View Article and Find Full Text PDFThe neuromodulator adenosine is widely considered to be a key regulator of sleep homeostasis and an indicator of sleep need. Although the effect of adenosine on subcortical areas has been previously described, the effects on cortical neurons have not been addressed systematically to date. To that purpose, we performed in vitro whole-cell patch-clamp recordings and biocytin staining of pyramidal neurons and interneurons throughout all layers of rat prefrontal and somatosensory cortex, followed by morphological analysis.
View Article and Find Full Text PDFElectrical oscillations in neuronal network activity are ubiquitous in the brain and have been associated with cognition and behavior. Intriguingly, the amplitude of ongoing oscillations, such as measured in EEG recordings, fluctuates irregularly, with episodes of high amplitude alternating with episodes of low amplitude. Despite the widespread occurrence of amplitude fluctuations in many frequency bands and brain regions, the mechanisms by which they are generated are poorly understood.
View Article and Find Full Text PDFOngoing neuronal oscillations in vivo exhibit non-random amplitude fluctuations as reflected in a slow decay of temporal auto-correlations that persist for tens of seconds. Interestingly, the decay of auto-correlations is altered in several brain-related disorders, including epilepsy, depression and Alzheimer's disease, suggesting that the temporal structure of oscillations depends on intact neuronal networks in the brain. Whether structured amplitude modulation occurs only in the intact brain or whether isolated neuronal networks can also give rise to amplitude modulation with a slow decay is not known.
View Article and Find Full Text PDFBackground: The medial prefrontal cortex has been implicated in a variety of cognitive and executive processes such as decision making and working memory. The medial prefrontal cortex of rodents consists of several areas including the prelimbic and infralimbic cortex that are thought to be involved in different aspects of cognitive performance. Despite the distinct roles in cognitive behavior that have been attributed to prelimbic and infralimbic cortex, little is known about neuronal network functioning of these areas, and whether these networks show any interaction during fast network oscillations.
View Article and Find Full Text PDFThe single-copy mouse gene Ptprr gives rise to different protein tyrosine phosphatase (PTP) isoforms in neuronal cells through the use of distinct promoters, alternative splicing, and multiple translation initiation sites. Here, we examined the array of post-translational modifications imposed on the PTPRR protein isoforms PTPBR7, PTP-SL, PTPPBSgamma42 and PTPPBSgamma37, which have distinct N-terminal segments and localize to different parts of the cell. All isoforms were found to be short-lived, constitutively phosphorylated proteins.
View Article and Find Full Text PDFPsychopharmacology (Berl)
March 2006
Rationale: Nicotine affects many aspects of human cognition, including attention and memory. Activation of nicotinic acetylcholine receptors (nAChRs) in neuronal networks modulates activity and information processing during cognitive tasks, which can be observed in electroencephalograms (EEGs) and functional magnetic resonance imaging studies.
Objectives: In this review, we will address aspects of nAChR functioning as well as synaptic and cellular modulation important for nicotinic impact on neuronal networks that ultimately underlie its effects on cognition.
The stability of neuronal networks is thought to depend on synaptic transmission which provides activity-dependent maintenance signals for both synapses and neurons. Here, we tested the relationship between presynaptic secretion and neuronal maintenance using munc18-1-null mutant mice as a model. These mutants have a specific defect in secretion from synaptic and large dense-cored vesicles [Verhage et al.
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