Ih tunes theta/gamma oscillations and cross-frequency coupling in an in silico CA3 model.

Ih channels are uniquely positioned to act as neuromodulatory control points for tuning hippocampal theta (4-12 Hz) and gamma (25 Hz) oscillations, oscillations which are thought to have importance for organization of information flow. contributes to neuronal membrane resonance and resting membrane potential, and is modulated by second messengers. We investigated oscillatory control using a multiscale computer model of hippocampal CA3, where each cell class (pyramidal, basket, and oriens-lacunosum moleculare cells), contained type-appropriate isoforms of .

Ketamine disrupts θ modulation of γ in a computer model of hippocampus.

Abnormalities in oscillations have been suggested to play a role in schizophrenia. We studied theta-modulated gamma oscillations in a computer model of hippocampal CA3 in vivo with and without simulated application of ketamine, an NMDA receptor antagonist and psychotomimetic. Networks of 1200 multicompartment neurons [pyramidal, basket, and oriens-lacunosum moleculare (OLM) cells] generated theta and gamma oscillations from intrinsic network dynamics: basket cells primarily generated gamma and amplified theta, while OLM cells strongly contributed to theta.

Synaptic noise and physiological coupling generate high-frequency oscillations in a hippocampal computational model.

There is great interest in the role of coherent oscillations in the brain. In some cases, high-frequency oscillations (HFOs) are integral to normal brain function, whereas at other times they are implicated as markers of epileptic tissue. Mechanisms underlying HFO generation, especially in abnormal tissue, are not well understood.

Ketamine modulates theta and gamma oscillations.

Ketamine, an N-methyl-D-aspartate (NMDA) receptor glutamatergic antagonist, has been studied as a model of schizophrenia when applied in subanesthetic doses. In EEG studies, ketamine affects sensory gating and alters the oscillatory characteristics of neuronal signals in a complex manner. We investigated the effects of ketamine on in vivo recordings from the CA3 region of mouse hippocampus referenced to the ipsilateral frontal sinus using a paired-click auditory gating paradigm.

Sensitivity to motion features in point light displays of biological motion.

Psychophysical experiments are described that measure the sensitivity to motion features in point light displays of biological motion. Three motion features were investigated: the relative motion of the thighs, the relative motion of the thigh and leg, and the velocity profile of the leg. The perceptual threshold for discriminating a change in each motion feature was compared in upright and inverted point light displays.

NMDA/AMPA ratio impacts state transitions and entrainment to oscillations in a computational model of the nucleus accumbens medium spiny projection neuron.

We describe a computational model of the principal cell in the nucleus accumbens (NAcb), the medium spiny projection (MSP) neuron. The model neuron, constructed in NEURON, includes all of the known ionic currents in these cells and receives synaptic input from simulated spike trains via NMDA, AMPA, and GABAA receptors. After tuning the model by adjusting maximal current conductances in each compartment, the model cell closely matched whole-cell recordings from an adult rat NAcb slice preparation.

Quantitative morphometry of hippocampal pyramidal cells: differences between anatomical classes and reconstructing laboratories.

The dendritic trees of hippocampal pyramidal cells play important roles in the establishment and regulation of network connectivity, synaptic plasticity, and firing dynamics. Several laboratories routinely reconstruct CA3 and CA1 dendrites to correlate their three-dimensional structure with biophysical, electrophysiological, and anatomical observables. To integrate and assess the consistency of the quantitative data available to the scientific community, we exhaustively analyzed 143 completely reconstructed neurons intracellularly filled and digitized in five different laboratories from 10 experimental conditions.

A new bursting model of CA3 pyramidal cell physiology suggests multiple locations for spike initiation.

We introduce a novel computational model of hippocampal pyramidal cells physiology based on an up-to-date, detailed description of passive and active biophysical properties and real dendritic morphology. This model constitutes a modification of a previous (1995) model which included complex calcium dynamics and Na(+), K(+), and Ca(2+) currents. Changes reflect recently acquired experimental knowledge regarding the types and spatial distributions of these currents.