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Sci. STKE, 24 April 2007
Vol. 2007, Issue 383, p. tw143
[DOI: 10.1126/stke.3832007tw143]

EDITORS' CHOICE

Neuroscience Adjusting Synaptic Plasticity

L. Bryan Ray

Science, Science’s STKE, AAAS, Washington, DC 20005, USA

Researchers are beginning to dissect the complex signaling events that underlie sophisticated functions in the mammalian brain. One example occurs in the dorsal cochlear nucleus (DCN), where auditory sensations are combined with somatosensory input, which may allow orientation of the head with respect to sounds an animal is hearing. Nonauditory signals are transmitted from parallel fibers either directly to the principal neurons of the DCN, known as fusiform cells, or to so-called "cartwheel" interneurons, which then innervate and inhibit fusiform cells. At synapses where the parallel fibers talk to the fusiform cells, an increase in synaptic strength (long-term potentiation, LTP) occurs when an action potential in the postsynaptic cell follows that in the presynaptic neuron. Tzounopoulos et al. wanted to explain why just the opposite (long-term depression, LTD) occurred at the synapses between parallel fibers and the cartwheel interneurons. In electrophysiological studies of mouse brain slices in culture, the authors used a range of pharmacological manipulations along with histological analyses to show that distinct use of two signaling pathways in the different cells could account for the differences in effects on synaptic plasticity. Postsynaptic LTP in the fusiform cells required signaling through Ca2+/calmodulin-dependent protein kinase II, whereas LTD in the interneurons resulted from an additional presynaptically mediated effect of retrograde signaling by endocannabinoids. Distinct subcellular localization of presynaptic endocannabinoid receptors was largely responsible for the differences in cellular learning responses, and it appeared to be the balance of presynaptic and postsynaptic effects that determined the overall cellular response. Furthermore, the polarity of the plasticity (strengthening or weakening) in cartwheel cells depended on the frequency of neuronal stimulation. The authors explain how these mechanisms may allow cells to change the rules through which they and, in turn, the networks in which they participate respond to stimuli. Understanding these properties may eventually help explain how the brain manages, for example, to filter out predictable consequences of the animal’s movement in response to auditory signals or to suppress responses to self-generated sounds.

T. Tzounopoulos, M. E. Rubio, J. E. Keen, L. O. Trussell, Coactivation of pre- and postsynaptic signaling mechanisms determines cell-specific spike-timing-dependent plasticity. Neuron 54, 291-301 (2007). [Online Journal]

Citation: L. B. Ray, Adjusting Synaptic Plasticity. Sci. STKE 2007, tw143 (2007).


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