Disambiguating Different Covariation Types

Covariations in neuronal latency or excitability can lead to peaks in spike train covariograms that may be very similar to those caused by spike timing synchronization (see companion article). Two quantitative methods are described here. The first is a method to estimate the excitability component of a covariogram, based on trial-by-trial estimates of excitability. Once estimated, this component may be subtracted from the covariogram, leaving only other types of contributions. The other is a method to determine whether the covariogram could potentially have been caused by latency covariations

Correlations Without Synchrony

Peaks in spike train correlograms are usually taken as indicative of spike timing synchronization between neurons. Strictly speaking, however, a peak merely indicates that the two spike trains were not independent. Two biologically plausible ways of departing from independence that are capable of generating peaks very similar to spike timing peaks are described here: covariations over trials in response latency and covariations over trials in neuronal excitability. Since peaks due to these interactions can be similar to spike timing peaks, interpreting a correlogram may be a problem with ambiguous solutions. What peak shapes do latency or excitability interactions generate? When are they similar to spike timing peaks? When can they be ruled out from having caused an observed correlogram peak? These are the questions addressed here. The previous article in this issue proposes quantitative methods to tell cases apart when latency or excitability covariations cannot be ruled out

A Model of Feedback to the Lateral Geniculate Nucleus

Simplified models of the lateral geniculate nucles (LGN) and striate cortex illustrate the possibility that feedback to the LGN may be used for robust, low-level pattern analysis. The information fed back to the LGN is rebroadcast to cortex using the LGN's full fan-out, so the cortex-LGN-cortex pathway mediates extensive cortico-cortical communication while keeping the number of necessary connections small

Causal contribution and dynamical encoding in the striatum during evidence accumulation.

A broad range of decision-making processes involve gradual accumulation of evidence over time, but the neural circuits responsible for this computation are not yet established. Recent data indicate that cortical regions that are prominently associated with accumulating evidence, such as the posterior parietal cortex and the frontal orienting fields, may not be directly involved in this computation. Which, then, are the regions involved? Regions that are directly involved in evidence accumulation should directly influence the accumulation-based decision-making behavior, have a graded neural encoding of accumulated evidence and contribute throughout the accumulation process. Here, we investigated the role of the anterior dorsal striatum (ADS) in a rodent auditory evidence accumulation task using a combination of behavioral, pharmacological, optogenetic, electrophysiological and computational approaches. We find that the ADS is the first brain region known to satisfy the three criteria. Thus, the ADS may be the first identified node in the network responsible for evidence accumulation

Sequence reproduction, single trial learning, and mimicry based on a mammalian-like distributed code for time

Animals learn tasks requiring a sequence of actions over time. Waiting a given time before taking an action is a simple example. Mimicry is a complex example, e.g. in humans, humming a brief tune you have just heard. Re-experiencing a sensory pattern mentally must involve reproducing a sequence of neural activities over time. In mammals, neurons in prefrontal cortex have time-dependent firing rates that vary smoothly and slowly in a stereotyped fashion. We show through modeling that a Many are Equal computation can use such slowly-varying activities to identify each timepoint in a sequence by the population pattern of activity at the timepoint. The MAE operation implemented here is facilitated by a common inhibitory conductivity due to a theta rhythm. Sequences of analog values of discrete events, exemplified by a brief tune having notes of different durations and intensities, can be learned in a single trial through STDP. An action sequence can be played back sped up, slowed down, or reversed by modulating the system that generates the slowly changing stereotyped activities. Synaptic adaptation and cellular post-hyperpolarization rebound contribute to robustness. An ability to mimic a sequence only seconds after observing it requires the STDP to be effective within seconds.Comment: 18 page

Coarse--graining, fixed points, and scaling in a large population of neurons

We develop a phenomenological coarse--graining procedure for activity in a large network of neurons, and apply this to recordings from a population of 1000+ cells in the hippocampus. Distributions of coarse--grained variables seem to approach a fixed non--Gaussian form, and we see evidence of scaling in both static and dynamic quantities. These results suggest that the collective behavior of the network is described by a non--trivial fixed point

A Cortical Substrate for Memory-Guided Orienting in the Rat

SummaryAnatomical, stimulation, and lesion data have suggested a homology between the rat frontal orienting fields (FOF) (centered at +2 AP, ±1.3 ML mm from Bregma) and primate frontal cortices such as the frontal or supplementary eye fields. We investigated the functional role of the FOF using rats trained to perform a memory-guided orienting task, in which there was a delay period between the end of a sensory stimulus instructing orienting direction and the time of the allowed motor response. Unilateral inactivation of the FOF resulted in impaired contralateral responses. Extracellular recordings of single units revealed that 37% of FOF neurons had delay period firing rates that predicted the direction of the rats' later orienting motion. Our data provide the first electrophysiological and pharmacological evidence supporting the existence in the rat, as in the primate, of a frontal cortical area involved in the preparation and/or planning of orienting responses

Minimal Impairment in a Rat Model of Duration Discrimination Following Excitotoxic Lesions of Primary Auditory and Prefrontal Cortices

We present a behavioral paradigm for the study of duration perception in the rat, and report the result of neurotoxic lesions that have the goal of identifying sites that mediate duration perception. Using a two-alternative forced-choice paradigm, rats were either trained to discriminate durations of pure tones (range = [200,500] ms; boundary = 316 ms; Weber fraction after training = 0.24 ± 0.04), or were trained to discriminate frequencies of pure tones (range = [8,16] kHz; boundary = 11.3 kHz; Weber = 0.16 ± 0.11); the latter task is a control for non-timing-specific aspects of the former. Both groups discriminate the same class of sensory stimuli, use the same motions to indicate decisions, have identical trial structures, and are trained to psychophysical threshold; the tasks are thus matched in a number of sensorimotor and cognitive demands. We made neurotoxic lesions of candidate timing-perception areas in the cerebral cortex of both groups. Following extensive bilateral lesions of the auditory cortex, the performance of the frequency discrimination group was significantly more impaired than that of the duration discrimination group. We also found that extensive bilateral lesions of the medial prefrontal cortex resulted in little to no impairment of both groups. The behavioral framework presented here provides an audition-based approach to study the neural mechanisms of time estimation and memory for durations