| A “Sample-and-Hold” Pulse-Counting Integrator as a Mechanism for Graded Memory Underlying Sensorimotor Adaptation Neuron, Volume 49, Issue 4, 16 February 2006, Pages 577-588 Jörg Oestreich, Nikolai C. Dembrow, Andrew A. George and Harold H. Zakon Summary The mechanisms behind the induction of cellular correlates of memory by sensory input and their contribution to meaningful behavioral changes are largely unknown. We previously reported a graded memory in the form of sensorimotor adaptation in the electromotor output of electric fish. Here we show that the mechanism for this adaptation is a synaptically induced long-lasting shift in intrinsic neuronal excitability. This mechanism rapidly integrates hundreds of spikes in a second, or gradually integrates the same number of spikes delivered over tens of minutes. Thus, this mechanism appears immune to frequency-dependent fluctuations in input and operates as a simple pulse counter over a wide range of time scales, enabling it to transduce graded sensory information into a graded memory and a corresponding change in the behavioral output. This adaptation is based on an NMDA receptor-mediated change in intrinsic excitability of the postsynaptic neurons involving the Ca-dependent activation of TRP channels. Summary | Full Text | PDF (415 kb) |
| Activation of Kinetically Distinct Synaptic Conductances on Inhibitory Interneurons by Electrotonically Overlapping Afferents Neuron, Volume 35, Issue 1, 3 July 2002, Pages 161-171 Harrison C. Walker, J.Josh Lawrence and Chris J. McBain Summary Mossy fiber (MF) and CA3 collateral (CL) axons activate common interneurons via synapses comprised of different AMPA receptors to provide feedforward and feedback inhibitory control of the CA3 hippocampal network. Because synapses potentially occur over variable electrotonic distances that distort somatically recorded synaptic currents, it is not known whether the underlying afferent-specific synaptic conductances are associated with different time courses. Using a somatic voltage jump technique to alter the driving force at the site of the synapse, we demonstrate that MF and CL synapses overlap in electrotonic location yet differ in conductance time course. Thus, afferent-specific conductance time courses allow single interneurons to differentially integrate feedforward and feedback information without the need to segregate distinct AMPA receptor subunits to different electrotonic domains. Summary | Full Text | PDF (411 kb) |
| The AMPA Receptor Subunits GluR-A and GluR-B Reciprocally Modulate Spinal Synaptic Plasticity and Inflammatory Pain Neuron, Volume 44, Issue 4, 18 November 2004, Pages 637-650 Bettina Hartmann, Seifollah Ahmadi, Paul A. Heppenstall, Gary R. Lewin, Claus Schott, Thilo Borchardt, Peter H. Seeburg, Hanns Ulrich Zeilhofer, Rolf Sprengel and Rohini Kuner Summary Ca-permeable AMPA receptors are densely expressed in the spinal dorsal horn, but their functional significance in pain processing is not understood. By disrupting the genes encoding GluR-A or GluR-B, we generated mice exhibiting increased or decreased numbers of Ca-permeable AMPA receptors, respectively. Here, we demonstrate that AMPA receptors are critical determinants of nociceptive plasticity and inflammatory pain. A reduction in the number of Ca-permeable AMPA receptors and density of AMPA channel currents in spinal neurons of GluR-A-deficient mice is accompanied by a loss of nociceptive plasticity in vitro and a reduction in acute inflammatory hyperalgesia in vivo. In contrast, an increase in spinal Ca-permeable AMPA receptors in GluR-B-deficient mice facilitated nociceptive plasticity and enhanced long-lasting inflammatory hyperalgesia. Thus, AMPA receptors are not mere determinants of fast synaptic transmission underlying basal pain sensitivity as previously thought, but are critically involved in activity-dependent changes in synaptic processing of nociceptive inputs. Summary | Full Text | PDF (862 kb) |
Copyright © 1996 The Biophysical Society. All rights reserved.
Biophysical Journal, Volume 70, Issue 6, 2513-2526, 1 June 1996
doi:10.1016/S0006-3495(96)79823-5
Research Article
Y. Kashimori, M. Goto and T. Kambara
To clarify the microscopic mechanisms by which P- and T-receptors encode amplitude modulation and zero crossing time of jamming signals, we present a model of P- and T-receptors based on their physiological and anatomical properties. The model consists of a receptor cell, supporting cells, and an afferent nerve fiber. The basal membrane of the receptor cell includes voltage-sensitive Ca2+ channels, Ca(2+)-activated K+ channels, and leak channels of Na+, K+, and Cl-. The driving force of potential change under stimulation is generated by the voltage-sensitive Ca2+ channels, and the suppressing force of the change is generated by Ca(2+)-activated K+ channels. It has been shown that in T-receptor cells the driving force is much stronger than the suppressing force, whereas in P-receptor cells the driving force is comparable with the suppressing force. The difference in various kinds of response properties between P- and T-receptors have been consistently explained based on the difference in the relative strengths of the driving and suppressing forces between P- and T-receptor cells. The response properties considered are encoding function, probability of firing of afferent nerve, pattern of damped oscillation, shape of tuning curves, values of the optimum frequency, and response latency.