Sat, 26 Jul 2008 08:41:10 BST CiteULike: awooga Cooper http://www.citeulike.org/user/awooga/author/Cooper CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/awooga/article/2586231 <i>Proceedings of the National Academy of Sciences, Vol. 101, No. 41. (12 October 2004), pp. 14943-14948.</i><br /><br />Modifications in the strengths of synapses are thought to underlie memory, learning, and development of cortical circuits. Many cellular mechanisms of synaptic plasticity have been investigated in which differential elevations of postsynaptic calcium concentrations play a key role in determining the direction and magnitude of synaptic changes. We have previously described a model of plasticity that uses calcium currents mediated by N-methyl-D-aspartate receptors as the associative signal for Hebbian learning. However, this model is not completely stable. Here, we propose a mechanism of stabilization through homeostatic regulation of intracellular calcium levels. With this model, synapses are stable and exhibit properties such as those observed in metaplasticity and synaptic scaling. In addition, the model displays synaptic competition, allowing structures to emerge in the synaptic space that reflect the statistical properties of the inputs. Therefore, the combination of a fast calcium-dependent learning and a slow stabilization mechanism can account for both the formation of selective receptive fields and the maintenance of neural circuits in a state of equilibrium. 10.1073/pnas.0405555101 Synaptic homeostasis and input selectivity follow from a calcium-dependent plasticity model Luk Yeung Harel Shouval Brian Blais Leon Cooper doi:10.1073/pnas.0405555101 Proceedings of the National Academy of Sciences, Vol. 101, No. 41. (12 October 2004), pp. 14943-14948. 2008-03-25T15:19:22-00:00 2004 Proceedings of the National Academy of Sciences 101 41 14943 14948 no-tag http://www.citeulike.org/user/awooga/article/2567765 <i>Proc Natl Acad Sci U S A, Vol. 99, No. 16. (6 August 2002), pp. 10831-10836.</i><br /><br />Synapses in the brain are bidirectionally modifiable, but the routes of induction are diverse. In various experimental paradigms, N-methyl-d-aspartate receptor-dependent long-term depression and long-term potentiation have been induced selectively by varying the membrane potential of the postsynaptic neurons during presynaptic stimulation of a constant frequency, the rate of presynaptic stimulation, and the timing of pre- and postsynaptic action potentials. In this paper, we present a mathematical embodiment of bidirectional synaptic plasticity that is able to explain diverse induction protocols with a fixed set of parameters. The key assumptions and consequences of the model can be tested experimentally; further, the model provides the foundation for a unified theory of N-methyl-d-aspartate receptor-dependent synaptic plasticity. A unified model of NMDA receptor-dependent bidirectional synaptic plasticity. HZ Shouval MF Bear LN Cooper doi:10.1073/pnas.152343099 Proc Natl Acad Sci U S A, Vol. 99, No. 16. (6 August 2002), pp. 10831-10836. 2008-03-20T17:42:30-00:00 2002 Proc Natl Acad Sci U S A 0027-8424 99 16 10831 10836 no-tag http://www.citeulike.org/user/awooga/article/1191372 <i>Science, Vol. 281, No. 5378. (7 August 1998), pp. 838-842.</i><br /><br />Dopaminergic neurons exert a major modulatory effect on the forebrain. Dopamine and adenosine 3',5'-monophosphate-regulated phosphoprotein (32 kilodaltons) (DARPP-32), which is enriched in all neurons that receive a dopaminergic input, is converted in response to dopamine into a potent protein phosphatase inhibitor. Mice generated to contain a targeted disruption of the DARPP-32 gene showed profound deficits in their molecular, electrophysiological, and behavioral responses to dopamine, drugs of abuse, and antipsychotic medication. The results show that DARPP-32 plays a central role in regulating the efficacy of dopaminergic neurotransmission. DARPP-32: regulator of the efficacy of dopaminergic neurotransmission. AA Fienberg N Hiroi PG Mermelstein W Song GL Snyder A Nishi A Cheramy JP O'Callaghan DB Miller DG Cole R Corbett CN Haile DC Cooper SP Onn AA Grace CC Ouimet FJ White SE Hyman DJ Surmeier J Girault EJ Nestler P Greengard Science, Vol. 281, No. 5378. (7 August 1998), pp. 838-842. 2007-03-28T12:07:43-00:00 1998 Science 0036-8075 281 5378 838 842 darpp-32 dopamine plasticity http://www.citeulike.org/user/awooga/article/915416 <i>Neurosci Res, Vol. 48, No. 2. (February 2004), pp. 221-227.</i><br /><br />We have introduced an in-situ preparation to induce motor unit activity by stimulating a sensory-CNS circuit, using the third instar larvae of Drosophila melanogaster. Discrete identifiable motor units that are well defined in anatomic and physiologic function can be recruited selectively and driven depending on the sensory stimulus intensity, duration, and frequency. Since the peripheral nervous system is bilaterally symmetric to coordinate bilateral symmetric segmental musculature patterns, fictive forms of locomotion are able to be induced. Monitoring the excitatory postsynaptic potentials (EPSP) on the prominent ventral longitudinal body wall muscles, such as m6 and m12, provides additional insight into how the selective motor units might be recruited within intact animals. We also introduce the actions of the neuromodulators (serotonin, octopamine (OA) and dopamine (DA)) on the inducible patterns of activity within the sensory-motor circuit. The powerful genetic manipulation in Drosophila opens many avenues for further investigations into the circuitry and cellular aspects of pattern generation and developmental issues of circuitry formation and maintenance in the model organism. Modulation of sensory-CNS-motor circuits by serotonin, octopamine, and dopamine in semi-intact Drosophila larva. S Dasari RL Cooper Neurosci Res, Vol. 48, No. 2. (February 2004), pp. 221-227. 2006-10-27T16:39:02-00:00 2004 Neurosci Res 0168-0102 48 2 221 227 drosophila neuromodulation technical-note