We examine the properties of the transfer function F T = V m /V LFP between the intracellular membrane potential (V m ) and the local field potential (V LFP ) in cerebral cortex. We first show theoretically that, in the subthreshold regime, the frequency dependence of the extracellular medium and that of the membrane potential have a clear incidence on F T . The calculation of F T from experiments and the matching with theoretical expressions is possible for desynchronized states where individual current sources can be considered as independent. Using a mean-field approximation, we obtain a method to estimate the impedance of the extracellular medium without injecting currents. We examine the transfer function for bipolar (differential) LFPs and compare to simultaneous recordings of V m and V LFP during desynchronized states in rat barrel cortex in vivo. The experimentally derived F T matches the one derived theoretically, only if one assumes that the impedance of the extracellular medium is frequency-dependent, and varies as 1/ √ ω (Warburg impedance) for frequencies between 3 and 500 Hz. This constitutes indirect evidence that the extracellular medium is non-resistive, which has many possible consequences for modeling LFPs.

Circuits in the auditory cortex are highly susceptible to acoustic influences during an early postnatal critical period. The auditory cortex selectively expands neural representations of enriched acoustic stimuli, a process important for human language acquisition. Adults lack this plasticity. Here we show in the murine auditory cortex that juvenile plasticity can be reestablished in adulthood if acoustic stimuli are paired with disruption of ecto-5′-nucleotidase–dependent adenosine production or A1 adenosine receptor signaling in the auditory thalamus. This plasticity occurs at the level of cortical maps and individual neurons in the auditory cortex of awake adult mice and is associated with long-term improvement of tone-discrimination abilities. We conclude that, in adult mice, disrupting adenosine signaling in the thalamus rejuvenates plasticity in the auditory cortex and improves auditory perception.

To reconstruct synaptic background activity, we combined computational models with intracellular recordings in vivo. A new conductance analysis method applied to intracellular recordings in the somatosensory cortex of anesthetized rats revealed mirror changes of excitation and inhibition during the up-and down-states of slow waves, but concerted changes in conductance variances. We then used these measurements to constrain the patterns of random release at excitatory and inhibitory synapses in computational models. We show that measurements of the mean and variance of conductances are sufficient constraints to design models fully consistent with in vivo recordings. r

Roy NC, Bessaih T, Contreras D. Comprehensive mapping of whisker-evoked responses reveals broad, sharply tuned thalamocortical input to layer 4 of barrel cortex. J Neurophysiol 105: 2421-2437, 2011. First published February 16, 2011 doi:10.1152/jn.00939.2010.-Cortical neurons are organized in columns, distinguishable by their physiological properties and input-output organization. Columns are thought to be the fundamental information-processing modules of the cortex. The barrel cortex of rats and mice is an attractive model system for the study of cortical columns, because each column is defined by a layer 4 (L4) structure called a barrel, which can be clearly visualized. A great deal of information has been collected regarding the connectivity of neurons in barrel cortex, but the nature of the input to a given L4 barrel remains unclear. We measured this input by making comprehensive maps of whisker-evoked activity in L4 of rat barrel cortex using recordings of multiunit activity and current source density analysis of local field potential recordings of animals under light isoflurane anesthesia. We found that a large number of whiskers evoked a detectable response in each barrel (mean of 13 suprathreshold, 18 subthreshold) even after cortical activity was abolished by application of muscimol, a GABA A agonist. We confirmed these findings with intracellular recordings and single-unit extracellular recordings in vivo. This constitutes the first direct confirmation of the hypothesis that subcortical mechanisms mediate a substantial multiwhisker input to a given cortical barrel.

Cognitive impairment (CI) is the most frequent non-motor symptom in Parkinson’s disease and is associated with deficits in a number of cognitive functions including working memory. However, the pathophysiology of Parkinson’s disease CI is poorly understood. Beta oscillations have previously been shown to play an important role in cognitive functions including working memory encoding. Decreased dopamine in motor cortico-striato-thalamo-cortical (CSTC) circuits increases the spectral power of beta oscillations and results in Parkinson’s disease motor symptoms. Analogous changes in parallel cognitive CSTC circuits involving the caudate and dorsolateral prefrontal cortex (DLPFC) may contribute to Parkinson’s disease CI. The objective of our study is to evaluate whether changes in beta oscillations in the caudate and DLPFC contribute to CI in Parkinson’s disease patients. To investigate this, we used local field potential recordings during deep brain stimulation surgery in 15 Parkinson’s disease patients. Local field potentials were recorded from DLPFC and caudate at rest and during a working memory task. We examined changes in beta oscillatory power during the working memory task as well as the relationship of beta oscillatory activity to preoperative cognitive status, as determined from neuropsychological testing results. We additionally conducted exploratory analyses on the relationship between cognitive impairment and task-based changes in spectral power in additional frequency bands. Spectral power of beta oscillations decreased in both DLPFC and caudate during working memory encoding and increased in these structures during feedback. Subjects with cognitive impairment had smaller decreases in caudate and DLPFC beta oscillatory power during encoding. In our exploratory analysis, we found that similar differences occurred in alpha frequencies in caudate and theta and alpha in DLPFC. Our findings suggest that oscillatory power changes in cognitive CSTC circuits may contribute to cognitive symptoms in Parkinson’s disease patients. These findings may inform the future development of novel neuromodulatory treatments for Parkinson’s disease CI.