Retinal ganglion cells receive inputs from multiple bipolar cells which must be integrated before a decision to fire is made. Theoretical studies have provided clues about how this integration is accomplished but have not directly determined the rules regulating summation of closely timed inputs along single or multiple dendrites. Here we have examined dendritic summation of multiple inputs along On ganglion cell dendrites in whole mount rat retina.
View Article and Find Full Text PDFThe importance of intracortical inhibitory circuits in setting the feature-selective spatial organization of primary sensory cortices remains controversial. To address this issue, we examined the strength of interneuron-to-pyramidal cell connections across the rat anterior piriform cortex (aPC) and found a pronounced gradient of increasing pyramidal cell inhibition along the aPC rostro-caudal axis. This functional heterogeneity could govern aPC spatial activation in response to varying odor identities and features.
View Article and Find Full Text PDFThe role of Ca(2+) in the induction of neural correlates of memory has frequently been described in binary terms despite the fact that many forms of memory are graded in their strength and/or persistence. We find that Ca(2+) dynamics encode the magnitude of sensorimotor adaptation of the electromotor output in a weakly electric fish. The neural correlate of this memory is a synaptically induced Ca(2+)-dependent enhancement of intrinsic excitability of neurons responsible for setting the electromotor output.
View Article and Find Full Text PDFN-Methyl-d-aspartate receptor (NMDAR) activation may promote cell survival or initiate cell death, with the outcome dependent on whether synaptic or extrasynaptic receptors are activated. Similarly, this differential activation has been proposed to govern the direction of plasticity. However, the physiological parameters necessary to activate extrasynaptic NMDARs in brain slices remain unknown.
View Article and Find Full Text PDFN-methyl-d-aspartate receptor (NMDAR) activation can trigger both long- and short-term plasticity, promote cell survival, and initiate cell death. A number of studies suggest that the consequences of NMDAR activation can vary widely depending on whether synaptic or extrasynaptic receptors are activated. Here we have examined the spatial distribution of NMDARs of CA1 pyramidal neurons in acutely dissected hippocampal slices.
View Article and Find Full Text PDFINTRODUCTIONChemical two-photon uncaging is useful for a wide range of applications, including both mapping of receptor location and localized photostimulation of neurons via activation of excitatory glutamate receptors. Experimental preparations could include brain slices, cultured neurons, and, among other possibilities, whole brains in vivo. This protocol documents the utility of chemical two-photon uncaging in examining glutamate receptors of pyramidal neurons in hippocampal slices.
View Article and Find Full Text PDFHippocampal interneuron activity has been linked to epileptogenesis, seizures and the oscillatory synaptic activity detected in behaving rats. Interneurons fire at specific times in the rhythmic cycles that comprise these oscillations; however, the mechanisms controlling these firing patterns remain unclear. We have examined the role of synaptic input in modulating the firing of spontaneously active rat hippocampal interneurons.
View Article and Find Full Text PDFInterneuron kainate receptor (KAR) activation regulates normal network activity and modulates cell excitability. As a result, determining the subcellular distribution of KARs in a cell-specific manner is a necessary step toward understanding their role in network function. We have functionally mapped synaptic and extrasynaptic dendritic KARs on hippocampal oriens interneurons using local photolysis of caged glutamate.
View Article and Find Full Text PDFCalcium (Ca2+) influx through NMDA receptors (NMDARs) is essential for synaptogenesis, experience-dependent synaptic remodeling and plasticity. The NMDAR-mediated rise in postsynaptic Ca2+ activates a network of kinases and phosphatases that promote persistent changes in synaptic strength, such as long-term potentiation (LTP). Here we show that the Ca2+ permeability of neuronal NMDARs is under the control of the cyclic AMP-protein kinase A (cAMP-PKA) signaling cascade.
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