Adaptive Filtering Enhances Information Transmission in Visual Cortex

Sensory neuroscience seeks to understand how the brain encodes natural environments. However, neural coding has largely been studied using simplified stimuli. In order to assess whether the brain's coding strategy depend on the stimulus ensemble, we apply a new information-theoretic method that allows unbiased calculation of neural filters (receptive fields) from responses to natural scenes or other complex signals with strong multipoint correlations. In the cat primary visual cortex we compare responses to natural inputs with those to noise inputs matched for luminance and contrast. We find that neural filters adaptively change with the input ensemble so as to increase the information carried by the neural response about the filtered stimulus. Adaptation affects the spatial frequency composition of the filter, enhancing sensitivity to under-represented frequencies in agreement with optimal encoding arguments. Adaptation occurs over 40 s to many minutes, longer than most previously reported forms of adaptation.Comment: 20 pages, 11 figures, includes supplementary informatio

Slow GABAA mediated synaptic transmission in rat visual cortex

<p>Abstract</p> <p>Background</p> <p>Previous reports of inhibition in the neocortex suggest that inhibition is mediated predominantly through GABA_Areceptors exhibiting fast kinetics. Within the hippocampus, it has been shown that GABA_Aresponses can take the form of either fast or slow response kinetics. Our findings indicate, for the first time, that the neocortex displays synaptic responses with slow GABA_Areceptor mediated inhibitory postsynaptic currents (IPSCs). These IPSCs are kinetically and pharmacologically similar to responses found in the hippocampus, although the anatomical specificity of evoked responses is unique from hippocampus. Spontaneous slow GABA_AIPSCs were recorded from both pyramidal and inhibitory neurons in rat visual cortex.</p> <p>Results</p> <p>GABA_Aslow IPSCs were significantly different from fast responses with respect to rise times and decay time constants, but not amplitudes. Spontaneously occurring GABA_Aslow IPSCs were nearly 100 times less frequent than fast sIPSCs and both were completely abolished by the chloride channel blocker, picrotoxin. The GABA_Asubunit-specific antagonist, furosemide, depressed spontaneous and evoked GABA_Afast IPSCs, but not slow GABA_A-mediated IPSCs. Anatomical specificity was evident using minimal stimulation: IPSCs with slow kinetics were evoked predominantly through stimulation of layer 1/2 apical dendritic zones of layer 4 pyramidal neurons and across their basal dendrites, while GABA_Afast IPSCs were evoked through stimulation throughout the dendritic arborization. Many evoked IPSCs were also composed of a combination of fast and slow IPSC components.</p> <p>Conclusion</p> <p>GABA_Aslow IPSCs displayed durations that were approximately 4 fold longer than typical GABA_Afast IPSCs, but shorter than GABA_B-mediated inhibition. The anatomical and pharmacological specificity of evoked slow IPSCs suggests a unique origin of synaptic input. Incorporating GABA_Aslow IPSCs into computational models of cortical function will help improve our understanding of cortical information processing.</p

Statistical summary of anatomically classified evoked synaptic responses

<p><b>Copyright information:</b></p><p>Taken from "Slow GABAmediated synaptic transmission in rat visual cortex"</p><p>http://www.biomedcentral.com/1471-2202/9/8</p><p>BMC Neuroscience 2008;9():8-8.</p><p>Published online 16 Jan 2008</p><p>PMCID:PMC2245967.</p><p></p> A) Representative IPSC trace averages (n = 10 repeats) are shown based on the location of stimulating electrode placement: distal apical (top and second from top), proximal apical (third from top) and basal (bottom). B) Box plots show the first and third quartiles around the median with the notch signifying 95% of the median for each sample population (distal apical, n = 18; proximal apical, n = 21; basal, n = 22) and dashed lines indicate the whiskers (1.5× inter-quartile range) and crosses indicate outliers. Rise time estimates are shown summarized by the box plot for distal (median = 4.6 ms), proximal (median = 2.6 ms) and basal (median = 3.8 ms) responses. C) Decay time (τ) estimates from the double-exponential fits to the IPSCs evoked from stimulation distally (median = 22 ms), proximally (median = 14 ms) or basally (median = 21 ms). D) Population summary of the total duration (rise time + decay time (τ)) estimates are shown for responses evoked distally (median = 27 ms), proximally (median = 17.7 ms) and basally (median = 24 ms). Proximal stimulation produced short duration IPSCs, while distal and basal IPSCs contained a mixture of slow and fast IPSCs with greater range and variability (quartile difference (third-first) = 12 ms, 9 ms and 24 ms for distal, proximal and basal respectively)

Evoked IPSCs do not inhibit the occurrence of spontaneous IPSCs Representative IPSC recording of a pyramidal cell evoked through stimulation of the input fibers within the distal apical dendrites

<p><b>Copyright information:</b></p><p>Taken from "Slow GABAmediated synaptic transmission in rat visual cortex"</p><p>http://www.biomedcentral.com/1471-2202/9/8</p><p>BMC Neuroscience 2008;9():8-8.</p><p>Published online 16 Jan 2008</p><p>PMCID:PMC2245967.</p><p></p> Slow IPSCs were evoked with 1 s separation (30 consecutive repeats). Fast spontaneous IPSCs occurred immediately before, during or following evoked ISPC stimulation. Arrows indicate specific spontaneous fast and slow events. The kinetics of the slow spontaneous events was consistent with the evoked responses. Vertical arrow marks the electrically evoked response

Population analysis (μ indicates geometric mean) of spontaneous isolated IPSC kinetics

<p><b>Copyright information:</b></p><p>Taken from "Slow GABAmediated synaptic transmission in rat visual cortex"</p><p>http://www.biomedcentral.com/1471-2202/9/8</p><p>BMC Neuroscience 2008;9():8-8.</p><p>Published online 16 Jan 2008</p><p>PMCID:PMC2245967.</p><p></p> The population of spontaneous isolated IPSCs was divided into two sub-populations based on the bimodal clustering in the correlation scatter plot of rise and decay time (τ) (see Figure 2A). A) Representative current recording of a pyramidal neuron. Asterisk indicates the identified slow IPSC event and the vertical arrows indicate the randomly selected events. B) Population histograms and Gaussian fits of the decay time constant (τ) estimates for fast (open, solid, μ = 10 ms) and slow (gray, dashed, μ = 36 ms) event sub-populations are shown plotted on the same axis. Inset plot shows cumulative distribution for the fast and slow populations (solid and dashed lines respectively). C) Population histograms of rise times for both fast (open, n = 714) and slow (gray, n = 240) events. Solid and dashed curves (fast and slow respectively) represent Gaussian fits to the distributions on a log scale (μ = 1.3 ms and 9.0 ms respectively, p < 0.01). D) Duration estimates (rise time + decay time (τ) or rise time + decay time (τ) for cases wher

Facilitation of neocortical presynaptic terminal development by NMDA receptor activation

<p>Abstract</p> <p>Background</p> <p>Neocortical circuits are established through the formation of synapses between cortical neurons, but the molecular mechanisms of synapse formation are only beginning to be understood. The mechanisms that control synaptic vesicle (SV) and active zone (AZ) protein assembly at developing presynaptic terminals have not yet been defined. Similarly, the role of glutamate receptor activation in control of presynaptic development remains unclear.</p> <p>Results</p> <p>Here, we use confocal imaging to demonstrate that NMDA receptor (NMDAR) activation regulates accumulation of multiple SV and AZ proteins at nascent presynaptic terminals of visual cortical neurons. NMDAR-dependent regulation of presynaptic assembly occurs even at synapses that lack postsynaptic NMDARs. We also provide evidence that this control of presynaptic terminal development is independent of glia.</p> <p>Conclusions</p> <p>Based on these data, we propose a novel NMDAR-dependent mechanism for control of presynaptic terminal development in excitatory neocortical neurons. Control of presynaptic development by NMDARs could ultimately contribute to activity-dependent development of cortical receptive fields.</p

Effects of furosemide on evoked IPSCs based on anatomical origins of stimulation

<p><b>Copyright information:</b></p><p>Taken from "Slow GABAmediated synaptic transmission in rat visual cortex"</p><p>BMC Neuroscience 2008;9():8-8.</p><p>Published online 16 Jan 2008</p><p>PMCID:PMC2245967.</p><p></p> Controls vs. furosemide treated (1 mM) conditions are shown in box plot form. Furosemide responses are shown in gray and control groups as open boxes. Evoked IPSC response amplitude, rise time and decay time constants are shown for stimulation of the basal (basal, n = 9), proximal apical (apical, n = 12) and distal apical (distal, n = 8) dendritic regions. Significance (p < 0.01) is indicated by ** (MANOVA and ANOVA factorial, see Table 4). Boxes span the first and third quartiles with medians indicated by thick center line and notch. A) Evoked IPSC amplitudes were reduced in the presence of furosemide compared to control for the stimulation sites in the region of the basal and proximal apical dendrites, but not the distal apical dendrites (see Table 3 for quantification). B) Rise time estimates were greater in the presence of furosemide for stimulation sites near the basal and proximal apical dendrites but not the distal apical dendrites. C) On average, the decay time constants (τ) for evoked IPSCs were significantly greater with furosemide treatment than control conditions for stimulation sites near the basal dendrites. Decay time constants were not significantly different for responses evoked through stimulation of the distal apical dendrites in the presence of furosemide compared to control