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Frequency Adaptation (frequency + adaptation)
Selected AbstractsComputational constraints between retrieving the past and predicting the future, and the CA3-CA1 differentiationHIPPOCAMPUS, Issue 5 2004Alessandro Treves Abstract The differentiation between the CA3 and CA1 fields of the mammalian hippocampus is one of the salient traits that set it apart from the organization of the homologue medial wall in reptiles and birds. CA3 is widely thought to function as an autoassociator, but what do we need CA1 for? Based on evidence for a specific role of CA1 in temporal processing, I have explored the hypothesis that the differentiation between CA3 and CA1 may help solve a computational conflict. The conflict is between pattern completion, or integrating current sensory information on the basis of memory, and prediction, or moving from one pattern to the next in a stored sequence. CA3 would take care of the former, while CA1 would concentrate on the latter. I have found the hypothesis to be only weakly supported by neural network simulations. The conflict indeed exists, but two mechanisms that would relate more directly to a functional CA3-CA1 differentiation were found unable to produce genuine prediction. Instead, a simple mechanism based on firing frequency adaptation in pyramidal cells was found to be sufficient for prediction, with the degree of adaptation as the crucial parameter balancing retrieval with prediction. The differentiation between the architectures of CA3 and CA1 has a minor but significant, and positive, effect on this balance. In particular, for a fixed anticipatory interval in the model, it increases significantly the information content of hippocampal outputs. There may therefore be just a simple quantitative advantage in differentiating the connectivity of the two fields. Moreover, different degrees of adaptation in CA3 and CA1 cells were not found to lead to better performance, further undermining the notion of a functional dissociation. © 2004 Wiley-Liss, Inc. [source] Functions of erg K+ channels in excitable cellsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 1 2004Jürgen R. Schwarz Abstract Ether-à-go-go -related gene (erg) channels are voltage-dependent K+ channels mediating inward-rectifying K+ currents because of their peculiar gating kinetics. These characteristics are essential for repolarization of the cardiac action potential. Inherited and acquired malfunctioning of erg channels may lead to the long QT-syndrome. However, erg currents have also been recorded in many other excitable cells, like smooth muscle fibres of the gastrointestinal tract, neuroblastoma cells or neuroendocrine cells. In these cells erg currents contribute to the maintenance of the resting potential. Changes in the resting potential are related to cell-specific functions like increase in hormone secretion, frequency adaptation or increase in contractility. [source] Feedback inhibition of action potential discharge by endogenous adenosine enhancement of the medium afterhyperpolarizationTHE JOURNAL OF PHYSIOLOGY, Issue 5 2009Ming Ruan Phasic activity in supraoptic nucleus vasopressin neurones is characterized by alternating periods of activity (bursts) and silence. During bursts, activation of a medium afterhyperpolarization induces spike frequency adaptation. Antagonism of A1 adenosine receptors within the supraoptic nucleus decreases spike frequency adaptation and prolongs phasic bursts in vivo, indicating that endogenous adenosine contributes to spike frequency adaptation. Here we used sharp electrode intracellular recordings from supraoptic nucleus neurones in hypothalamic explants to show that endogenous adenosine increases medium afterhyperpolarization amplitude to enhance spike frequency adaptation during phasic bursts. Superfusion of the A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT, 10 ,m) increased intraburst firing rate of phasic neurones (by 2.0 ± 0.7 spikes s,1, P= 0.03) and burst duration (by 141 ± 113 s, P= 0.03). The CPT-induced increase in intraburst firing rate developed over the first few seconds of firing and persisted thereafter. In a separate series of experiments, CPT reduced the amplitude of the medium afterhyperpolarization evoked by a 1 s 20 Hz spike train (by 0.8 ± 0.3 mV, P < 0.001) in supraoptic nucleus neurones; this inhibition was not prevented by 3 mm CsCl (0.8 ± 0.1 mV decrease, P < 0.01) to block the afterdepolarization (which overlaps temporally with the medium afterhyperpolarization). In the presence of apamin to block the medium afterhyperpolarization, CPT did not alter afterdepolarization amplitude. Taken together, these data show that endogenous adenosine enhances medium afterhyperpolarization amplitude to contribute to spike frequency adaptation in phasic supraoptic nucleus neurones. [source] | ||||||||||