Kainate induced theta-frequency oscillatory network activity in the medial septum/diagonal band complex

The medial septum/diagonal band complex (MS/DB) forms part of the septo-hippocampal feedback loop and is thought to have a major functional role in the generation and/or maintenance of the hippocampal theta rhythm in vivo (4 * 15 Hz). Several different mechanistic scenarios may underlie the generation of a theta-frequency EEG pattern, amongst them (1) an external pacemaker-type input (2) theta activity being an emergent property of the septo-hippocampal feedback loop and (3) theta arising in the synaptic network of the MS/DB itself. This investigation tested the latter scenario by using an in vitro slice preparation of the (deafferented) MS/DB. Longitudinal slices (0.45 mm) from 21 day old rats were maintained at 32 deg C in an interface recording chamber perfused with oxygenated ACSF. Following the bath application of the AMPA/kainate receptor agonist kainate (25 *100 nM), extracellular recordings, using ACSF-filled micropipettes, showed rhythmic population activity with a mean peak frequency of ~6 Hz which was most prominent along the midline of the MS/DB. The higher concentrations of kainate were accompanied by corresponding increases in spectral power (amplitude). Subsequently, intracellular recordings were obtained with QX-314 containing electrodes to prevent spiking-activity, and thus allowing IPSPs to be recorded at depolarised membrane potentials. These recordings revealed the presence of rhythmic IPSPs (~6 Hz) in the class of fast-firing cells of oscillating MS/DB slices, presumably arising in the mutually connected interneuronal network of the MS/DB and pacing the oscillation. Moreover, these findings clearly demonstrate that the intrinsic circuitry of the isolated MS/DB complex is sufficient to generate rhythmic theta frequency activity

Kainate induced theta-frequency oscillatory network activity in the medial septum/diagonal band complex

The medial septum/diagonal band complex (MS/DB) forms part of the septo-hippocampal feedback loop and is thought to have a major functional role in the generation and/or maintenance of the hippocampal theta rhythm in vivo (4 * 15 Hz). Several different mechanistic scenarios may underlie the generation of a theta-frequency EEG pattern, amongst them (1) an external pacemaker-type input (2) theta activity being an emergent property of the septo-hippocampal feedback loop and (3) theta arising in the synaptic network of the MS/DB itself. This investigation tested the latter scenario by using an in vitro slice preparation of the (deafferented) MS/DB. Longitudinal slices (0.45 mm) from 21 day old rats were maintained at 32 deg C in an interface recording chamber perfused with oxygenated ACSF. Following the bath application of the AMPA/kainate receptor agonist kainate (25 *100 nM), extracellular recordings, using ACSF-filled micropipettes, showed rhythmic population activity with a mean peak frequency of ~6 Hz which was most prominent along the midline of the MS/DB. The higher concentrations of kainate were accompanied by corresponding increases in spectral power (amplitude). Subsequently, intracellular recordings were obtained with QX-314 containing electrodes to prevent spiking-activity, and thus allowing IPSPs to be recorded at depolarised membrane potentials. These recordings revealed the presence of rhythmic IPSPs (~6 Hz) in the class of fast-firing cells of oscillating MS/DB slices, presumably arising in the mutually connected interneuronal network of the MS/DB and pacing the oscillation. Moreover, these findings clearly demonstrate that the intrinsic circuitry of the isolated MS/DB complex is sufficient to generate rhythmic theta frequency activity

A role for fast rhythmic bursting neurons in cortical gamma oscillations in vitro

Basic cellular and network mechanisms underlying gamma frequency oscillations (30–80 Hz) have been well characterized in the hippocampus and associated structures. In these regions, gamma rhythms are seen as an emergent property of networks of principal cells and fast-spiking interneurons. In contrast, in the neocortex a number of elegant studies have shown that specific types of principal neuron exist that are capable of generating powerful gamma frequency outputs on the basis of their intrinsic conductances alone. These fast rhythmic bursting (FRB) neurons (sometimes referred to as "chattering" cells) are activated by sensory stimuli and generate multiple action potentials per gamma period. Here, we demonstrate that FRB neurons may function by providing a large-scale input to an axon plexus consisting of gap-junctionally connected axons from both FRB neurons and their anatomically similar counterparts regular spiking neurons. The resulting network gamma oscillation shares all of the properties of gamma oscillations generated in the hippocampus but with the additional critical dependence on multiple spiking in FRB cells

GABA-enhanced collective behavior in neuronal axons underlies persistent gamma-frequency oscillations

Gamma (30–80 Hz) oscillations occur in mammalian electroencephalogram in a manner that indicates cognitive relevance. In vitro models of gamma oscillations demonstrate two forms of oscillation: one occurring transiently and driven by discrete afferent input and the second occurring persistently in response to activation of excitatory metabotropic receptors. The mechanism underlying persistent gamma oscillations has been suggested to involve gap-junctional communication between axons of principal neurons, but the precise relationship between this neuronal activity and the gamma oscillation has remained elusive. Here we demonstrate that gamma oscillations coexist with high-frequency oscillations (>90 Hz). High-frequency oscillations can be generated in the axonal plexus even when it is physically isolated from pyramidal cell bodies. They were enhanced in networks by nonsomatic -aminobutyric acid type A (GABAA) receptor activation, were modulated by perisomatic GABAA receptor-mediated synaptic input to principal cells, and provided the phasic input to interneurons required to generate persistent gamma-frequency oscillations. The data suggest that high-frequency oscillations occurred as a consequence of random activity within the axonal plexus. Interneurons provide a mechanism by which this random activity is both amplified and organized into a coherent network rhythm

Cation distribution in manganese cobaltite spinels Co3−xMnxO4 (0 ≤ x ≤ 1) determined by thermal analysis

Thermogravimetric analysis was used in order to study the reduction in air of submicronic powders of Co3−x Mn x O4 spinels, with 0 ≤ x ≤ 1. For x = 0 (i.e. Co3O4), cation reduction occurred in a single step. It involved the CoIII ions at the octahedral sites, which were reduced to Co2+ on producing CoO. For 0 < x ≤ 1, the reduction occurred in two stages at increasing temperature with increasing amounts of manganese. The first step corresponded to the reduction of octahedral CoIII ions and the second was attributed to the reduction of octahedral Mn4+ ions to Mn3+. From the individual weight losses and the electrical neutrality of the lattice, the CoIII and Mn4+ ion concentrations were calculated. The distribution of cobalt and manganese ions present on each crystallographic site of the spinel was determined. In contrast to most previous studies that took into account either CoIII and Mn3+ or Co2+, CoIII and Mn4+ only, our thermal analysis study showed that Co2+/CoIII and Mn3+/Mn4+ pairs occupy the octahedral sites. These results were used to explain the resistivity measurements carried out on dense ceramics prepared from our powders sintered at low temperature (700–750 °C) in a Spark Plasma Sintering apparatus

Genetically altered AMPA-type glutamate receptor kinetics in interneurons disrupt long-range synchrony of gamma oscillation

Gamma oscillations synchronized between distant neuronal populations may be critical for binding together brain regions devoted to common processing tasks. Network modeling predicts that such synchrony depends in part on the fast time course of excitatory postsynaptic potentials (EPSPs) in interneurons, and that even moderate slowing of this time course will disrupt synchrony. We generated mice with slowed interneuron EPSPs by gene targeting, in which the gene encoding the 67-kDa form of glutamic acid decarboxylase (GAD67) was altered to drive expression of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor subunit GluR-B. GluR-B is a determinant of the relatively slow EPSPs in excitatory neurons and is normally expressed at low levels in γ-aminobutyric acid (GABA)ergic interneurons, but at high levels in the GAD-GluR-B mice. In both wild-type and GAD-GluR-B mice, tetanic stimuli evoked gamma oscillations that were indistinguishable in local field potential recordings. Remarkably, however, oscillation synchrony between spatially separated sites was severely disrupted in the mutant, in association with changes in interneuron firing patterns. The congruence between mouse and model suggests that the rapid time course of AMPA receptor-mediated EPSPs in interneurons might serve to allow gamma oscillations to synchronize over distance