Properties of GABAergic Neurons Containing Calcium-Permeable Kainate and AMPA-Receptors.

Calcium-permeable kainate and AMPA receptors (CP-KARs and CP-AMPARs), as well as NMDARs, play a pivotal role in plasticity and in regulating neurotransmitter release. Here we visualized in the mature hippocampal neuroglial cultures the neurons expressing CP-AMPARs and CP-KARs. These neurons were visualized by a characteristic fast sustained [Ca] increase in response to the agonist of these receptors, domoic acid (DoA), and a selective agonist of GluK1-containing KARs, ATPA.

Dopamine controls neuronal spontaneous calcium oscillations via astrocytic signal.

Dopamine is a neuromodulator and neurotransmitter responsible for a number of physiological processes. Dysfunctions of the dopamine metabolism and signalling are associated with neurological and psychiatric diseases. Here we report that in primary co-culture of neurons and astrocytes dopamine-induces calcium signal in astrocytes and suppress spontaneous synchronous calcium oscillations (SSCO) in neurons.

Activation of alpha-2 adrenergic receptors stimulates GABA release by astrocytes.

Norepinephrine is one of the key neurotransmitters in the hippocampus, but its role in the functioning of the neuroglial networks remains unclear. Here we show that norepinephrine suppresses NH Cl-induced oscillations of the intracellular Ca concentration ([Ca ] ) in hippocampal neurons. We found that the inhibitory effect of norepinephrine against ammonium-induced [Ca ] oscillations is mediated by activation of alpha-2 adrenergic receptors.

Domoic acid suppresses hyperexcitation in the network due to activation of kainate receptors of GABAergic neurons.

Kainate receptors play an important role in the brain. They contribute to postsynaptic depolarization, modulate the release of neurotransmitters such as GABA and glutamate, affect the development of the neuronal network. At the same time, their functions depend not only on the type of neuron expressing them but also on their localization (pre- or postsynaptic).

Fast changes of NMDA and AMPA receptor activity under acute hyperammonemia in vitro.

It was established in experiments on cell cultures of neurons and astrocytes that ammonium ions at concentrations of 4-8 mM cause hyperexcitation of the neuronal network, as a result of which there is a disturbance of calcium homeostasis, which can lead to the death of neurons. In the present study, we investigated the effect of toxic doses of ammonium (8 mM NHCl) on the activity of NMDA and AMPA receptors and the role of these receptors in spontaneous synchronous activity (SSA). In a control experiment in the absence of NHCl, SSA is not suppressed by NMDA receptor inhibitors, but is suppressed by AMPA receptor antagonists.

To Break or to Brake Neuronal Network Accelerated by Ammonium Ions?

Purpose: The aim of present study was to investigate the effects of ammonium ions on in vitro neuronal network activity and to search alternative methods of acute ammonia neurotoxicity prevention.

Methods: Rat hippocampal neuronal and astrocytes co-cultures in vitro, fluorescent microscopy and perforated patch clamp were used to monitor the changes in intracellular Ca2+- and membrane potential produced by ammonium ions and various modulators in the cells implicated in neural networks.

Results: Low concentrations of NH4Cl (0.