It has commonly been assumed that the many separate areas of the visual system perform modular analyses, each restricted to a single attribute of the image. A recent paper advocates a radically different approach, where all areas in the hierarchy analyse all attributes of the image to extract perceptually relevant decisions. (+info)
Somatic recording of GABAergic autoreceptor current in cerebellar stellate and basket cells.
Patch-clamp recordings were performed from stellate and basket cells in rat cerebellar slices. Under somatic voltage clamp, short depolarizing pulses were applied to elicit action potentials in the axon. After the action potential, a bicuculline- and Cd2+-sensitive current transient was observed. A similar response was obtained when eliciting axonal firing by extracellular stimulation. With an isotonic internal Cl- solution, the peak amplitude of this current varied linearly with the holding potential, yielding an extrapolated reversal potential of -20 to 0 mV. Unlike synaptic or autaptic GABAergic currents obtained in the same preparation, the current transient had a slow rise-time and a low variability between trials. This current was blocked when 10 mM BAPTA was included in the recording solution. In some experiments, the current transient elicited axonal action potentials. The current transient was reliably observed in animals aged 12-15 d, with a mean amplitude of 82 pA at -70 mV, but was small and rare in the age group 29-49 d. Numerical simulations could account for all properties of the current transient by assuming that an action potential activates a distributed GABAergic conductance in the axon. The actual conductance is probably restricted to release sites, with an estimated mean presynaptic current response of 10 pA per site (-70 mV, age 12-15 d). We conclude that in developing rats, stellate and basket cell axons have a high density of GABAergic autoreceptors and that a sizable fraction of the corresponding current can be measured from the soma. (+info)
Competitive mechanisms subserve attention in macaque areas V2 and V4.
It is well established that attention modulates visual processing in extrastriate cortex. However, the underlying neural mechanisms are unknown. A consistent observation is that attention has its greatest impact on neuronal responses when multiple stimuli appear together within a cell's receptive field. One way to explain this is to assume that multiple stimuli activate competing populations of neurons and that attention biases this competition in favor of the attended stimulus. In the absence of competing stimuli, there is no competition to be resolved. Accordingly, attention has a more limited effect on the neuronal response to a single stimulus. To test this interpretation, we measured the responses of neurons in macaque areas V2 and V4 using a behavioral paradigm that allowed us to isolate automatic sensory processing mechanisms from attentional effects. First, we measured each cell's response to a single stimulus presented alone inside the receptive field or paired with a second receptive field stimulus, while the monkey attended to a location outside the receptive field. Adding the second stimulus typically caused the neuron's response to move toward the response that was elicited by the second stimulus alone. Then, we directed the monkey's attention to one element of the pair. This drove the neuron's response toward the response elicited when the attended stimulus appeared alone. These findings are consistent with the idea that attention biases competitive interactions among neurons, causing them to respond primarily to the attended stimulus. A quantitative neural model of attention is proposed to account for these results. (+info)
Voltage-dependent properties of dendrites that eliminate location-dependent variability of synaptic input.
We examined the hypothesis that voltage-dependent properties of dendrites allow for the accurate transfer of synaptic information to the soma independent of synapse location. This hypothesis is motivated by experimental evidence that dendrites contain a complex array of voltage-gated channels. How these channels affect synaptic integration is unknown. One hypothesized role for dendritic voltage-gated channels is to counteract passive cable properties, rendering all synapses electrotonically equidistant from the soma. With dendrites modeled as passive cables, the effect a synapse exerts at the soma depends on dendritic location (referred to as location-dependent variability of the synaptic input). In this theoretical study we used a simplified three-compartment model of a neuron to determine the dendritic voltage-dependent properties required for accurate transfer of synaptic information to the soma independent of synapse location. A dendrite that eliminates location-dependent variability requires three components: 1) a steady-state, voltage-dependent inward current that together with the passive leak current provides a net outward current and a zero slope conductance at depolarized potentials, 2) a fast, transient, inward current that compensates for dendritic membrane capacitance, and 3) both alpha amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid- and N-methyl-D-aspartate-like synaptic conductances that together permit synapses to behave as ideal current sources. These components are consistent with the known properties of dendrites. In addition, these results indicate that a dendrite designed to eliminate location-dependent variability also actively back-propagates somatic action potentials. (+info)
Simultaneous measurement of evoked release and [Ca2+]i in a crayfish release bouton reveals high affinity of release to Ca2+.
The opener neuromuscular junction of crayfish was used to determine the affinity of the putative Ca2+ receptor(s) responsible for evoked release. Evoked, asynchronous release, and steady-state intracellular Ca2+ concentration, [Ca2+]ss, were measured concomitantly in single release boutons. It was found that, as expected, asynchronous release is highly correlated with [Ca2+]ss. Surprisingly, evoked release was also found to be highly correlated with [Ca2+]ss. The quantal content (m) and the rate of asynchronous release (S) showed sigmoidal dependence on [Ca2+]ss. The slope log m/log [Ca2+]ss varied between 1.6 and 3.3; the higher slope observed at the lower [Ca2+]o. The slope log S/log [Ca2+]ss varied between 3 and 4 and was independent of [Ca2+]o. These results are consistent with the assumption that evoked release is controlled by the sum of [Ca2+]ss and the local elevation of Ca2+ concentration near the release sites resulting from Ca2+ influx through voltage-gated Ca2+ channels (Y). On the basis of the above, we were able to estimate Y. We found Y to be significantly <10 microM even for [Ca2+]o = 13.5 mM. The dissociation constant (Kd) of the Ca2+ receptor(s) associated with evoked release was calculated to be in the range of 4-5 microM. This value of Kd is similar to that found previously for asynchronous release. (+info)
Small conductance potassium channels cause an activity-dependent spike frequency adaptation and make the transfer function of neurons logarithmic.
We made a computational model of a single neuron to study the effect of the small conductance (SK) Ca2+-dependent K+ channel on spike frequency adaptation. The model neuron comprised a Na+ conductance, a Ca2+ conductance, and two Ca2+-independent K+ conductances, as well as a small and a large (BK) Ca2+-activated K+ conductance, a Ca2+ pump, and mechanisms for Ca2+ buffering and diffusion. Sustained current injection that simulated synaptic input resulted in a train of action potentials (APs) which in the absence of the SK conductance showed very little adaptation with time. The transfer function of the neuron was nearly linear, i.e., both asymptotic spike rate as well as the intracellular free Ca2+ concentration ([Ca2+]i) were approximately linear functions of the input current. Adding an SK conductance with a steep nonlinear dependence on [Ca2+]i (. Pflugers Arch. 422:223-232; Kohler, Hirschberg, Bond, Kinzie, Marrion, Maylie, and Adelman. 1996. Science. 273:1709-1714) caused a marked time-dependent spike frequency adaptation and changed the transfer function of the neuron from linear to logarithmic. Moreover, the input range the neuron responded to with regular spiking increased by a factor of 2.2. These results can be explained by a shunt of the cell resistance caused by the activation of the SK conductance. It might turn out that the logarithmic relationships between the stimuli of some modalities (e.g., sound or light) and the perception of the stimulus intensity (Fechner's law) have a cellular basis in the involvement of SK conductances in the processing of these stimuli. (+info)
Transient potassium currents regulate the discharge patterns of dorsal cochlear nucleus pyramidal cells.
Pyramidal cells in the dorsal cochlear nucleus (DCN) show three distinct temporal discharge patterns in response to sound: "pauser," "buildup," and "chopper." Similar discharge patterns are seen in vitro and depend on the voltage from which the cell is depolarized. It has been proposed that an inactivating A-type K+ current (IKI) might play a critical role in generating the three different patterns. In this study we examined the characteristics of transient currents in DCN pyramidal cells to evaluate this hypothesis. Morphologically identified pyramidal cells in rat brain slices (P11-P17) exhibited the three voltage-dependent discharge patterns. Two inactivating currents were present in outside-out patches from pyramidal cells: a rapidly inactivating (IKIF, tau approximately 11 msec) current insensitive to block by tetraethylammonium (TEA) and variably blocked by 4-aminopyridine (4-AP) with half-inactivation near -85 mV, and a slowly inactivating TEA- and 4-AP-sensitive current (IKIS, tau approximately 145 msec) with half-inactivation near -35 mV. Recovery from inactivation at 34 degrees C was described by a single exponential with a time constant of 10-30 msec, similar to the rate at which first spike latency increases with the duration of a hyperpolarizing prepulse. Acutely isolated cells also possessed a rapidly activating (<1 msec at 22 degrees C) transient current that activated near -45 mV and showed half-inactivation near -80 mV. A model demonstrated that the deinactivation of IKIF was correlated with the discharge patterns. Overall, the properties of the fast inactivating K+ current were consistent with their proposed role in shaping the discharge pattern of DCN pyramidal cells. (+info)
Passive electrotonic properties of rat hippocampal CA3 interneurones.
1. The linear membrane responses of CA3 interneurones were determined with the use of whole-cell patch recording methods. The mean input resistance (RN) for all cells in this study was 526 +/- 16 MOmega and the slowest membrane time constant (tau0) was 73 +/- 3 ms. 2. The three-dimensional morphology of 63 biocytin-labelled neurones was used to construct compartmental models. Specific membrane resistivity (Rm) and specific membrane capacitance (Cm) were estimated by fitting the linear membrane response. Acceptable fits were obtained for 24 CA3 interneurones. The mean Rm was 61.9 +/- 34.2 Omega cm2 and the mean Cm was 0.9 +/- 0.3 microF cm-2. Intracellular resistance (Ri) could not be resolved in this study. 3. Examination of voltage attenuation revealed a significantly low synaptic efficiency from most dendritic synaptic input locations to the soma. 4. Simulations of excitatory postsynaptic potentials (EPSPs) were analysed at both the site of synaptic input and at the soma. There was little variability in the depolarization at the soma from synaptic inputs placed at different locations along the dendritic tree. The EPSP amplitude at the site of synaptic input was progressively larger with distance from the soma, consistent with a progressive increase in input impedance. 5. The 'iso-efficiency' of spatially different synaptic inputs arose from two opposing factors: an increase in EPSP amplitude at the synapse with distance from the soma was opposed by a nearly equivalent increase in voltage attenuation. These simulations suggest that, in these particular neurones, the amplitude of EPSPs measured at the soma will not be significantly affected by the location of synaptic inputs. (+info)