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

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

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

Developmental up-regulation of vesicular glutamate transporter-1 promotes neocortical presynaptic terminal development.

Presynaptic terminal formation is a complex process that requires assembly of proteins responsible for synaptic transmission at sites of axo-dendritic contact. Accumulation of presynaptic proteins at developing terminals is facilitated by glutamate receptor activation. Glutamate is loaded into synaptic vesicles for release via the vesicular glutamate transporters VGLUT1 and VGLUT2. During postnatal development there is a switch from predominantly VGLUT2 expression to high VGLUT1 and low VGLUT2, raising the question of whether the developmental increase in VGLUT1 is important for presynaptic development. Here, we addressed this question using confocal microscopy and quantitative immunocytochemistry in primary cultures of rat neocortical neurons. First, in order to understand the extent to which the developmental switch from VGLUT2 to VGLUT1 occurs through an increase in VGLUT1 at individual presynaptic terminals or through addition of VGLUT1-positive presynaptic terminals, we examined the spatio-temporal dynamics of VGLUT1 and VGLUT2 expression. Between 5 and 12 days in culture, the percentage of presynaptic terminals that expressed VGLUT1 increased during synapse formation, as did expression of VGLUT1 at individual terminals. A subset of VGLUT1-positive terminals also expressed VGLUT2, which decreased at these terminals. At individual terminals, the increase in VGLUT1 correlated with greater accumulation of other synaptic vesicle proteins, such as synapsin and synaptophysin. When the developmental increase in VGLUT1 was prevented using VGLUT1-shRNA, the density of presynaptic terminals and accumulation of synapsin and synaptophysin at terminals were decreased. Since VGLUT1 knock-down was limited to a small number of neurons, the observed effects were cell-autonomous and independent of changes in overall network activity. These results demonstrate that up-regulation of VGLUT1 is important for development of presynaptic terminals in the cortex