Associating sensory cues with incoming seizures: developing an animal model of auras.

For patients with epilepsy, one of the biggest problems is the unpredictability of the time when the next seizure will occur. Interestingly, some epileptic patients experience a sensory sensation preceding seizures, called aura, which helps them move to safety before a seizure. Here, we describe the development of the first animal model of auras, which could allow for a more detailed study of this phenomenon.

Impaired Spatial Reorientation in the 3xTg-AD Mouse Model of Alzheimer's Disease.

In early Alzheimer's disease (AD) spatial navigation is impaired; however, the precise cause of this impairment is unclear. Recent evidence suggests that getting lost is one of the first impairments to emerge in AD. It is possible that getting lost represents a failure to use distal cues to get oriented in space.

Age-dependent behavioral and biochemical characterization of single APP knock-in mouse (APP) model of Alzheimer's disease.

Saito et al developed a novel amyloid precursor protein (APP) knock-in mouse model (APP) for Alzheimer's disease (AD) to overcome the problem of overexpression of APP in available transgenic mouse models. However, this new mouse model for AD is not fully characterized age-dependently with respect to behavioral and biochemical changes. Therefore, in the present study, we performed an age-dependent behavioral and biochemical characterization of this newly developed mouse model.

Involvement of fast-spiking cells in ictal sequences during spontaneous seizures in rats with chronic temporal lobe epilepsy.

See Lenck-Santini (doi:10.1093/awx205) for a scientific commentary on this article. Epileptic seizures represent altered neuronal network dynamics, but the temporal evolution and cellular substrates of the neuronal activity patterns associated with spontaneous seizures are not fully understood.

Manganese-Enhanced Magnetic Resonance Imaging and Studies of Rat Behavior: Transient Motor Deficit in Skilled Reaching, Rears, and Activity in Rats After a Single Dose of MnCl.

Manganese-enhanced magnetic resonance imaging (MEMRI) has been suggested to be a useful tool to visualize and map behavior-relevant neural populations at large scale in freely behaving rodents. A primary concern in MEMRI applications is Mn toxicity. Although a few studies have specifically examined toxicity on gross motor behavior, Mn toxicity on skilled motor behavior was not explored.

Postnatal development of Homer1a in the rat hippocampus.

Homer1a (H1a) is an immediate early gene involved in multiple forms of synaptic plasticity. It exhibits a postnatal increase in the rat forebrain (Brakeman et al. (1997) Nature 386:284-288) and reduces the density and size of dendritic spines in hippocampal neurons (Sala et al.

Cell type-specific changes in spontaneous and minimally evoked excitatory synaptic activity in hippocampal CA1 interneurons of kainate-treated rats.

The epileptiform activity in the kainic acid (KA) model of epilepsy arises from complex changes in excitation and inhibition. To assess the involvement of excitatory drive onto inhibitory interneurons in this epileptiform activity, we examined changes in spontaneous and minimally evoked excitatory post-synaptic currents (sEPSCs and eEPSCs) in CA1 interneurons in stratum oriens/alveus (O/A) and stratum radiatum (RAD) in rat hippocampal slices after KA treatment. The frequency and amplitude of sEPSCs and the amplitude of eEPSCs were unchanged in O/A interneurons, but the EPSC kinetics were significantly slower.

Synapse-specific mGluR1-dependent long-term potentiation in interneurones regulates mouse hippocampal inhibition.

Hippocampal CA1 inhibitory interneurones control the excitability and synchronization of pyramidal cells, and participate in hippocampal synaptic plasticity. Pairing theta-burst stimulation (TBS) with postsynaptic depolarization, we induced long-term potentiation (LTP) of putative single-fibre excitatory postsynaptic currents (EPSCs) in stratum oriens/alveus (O/A) interneurones of mouse hippocampal slices. LTP induction was absent in metabotropic glutamate receptor 1 (mGluR1) knockout mice, was correlated with the postsynaptic presence of mGluR1a, and required a postsynaptic Ca2+ rise.