Short-term inhibition of GABAergic IPSCs induced by association of pre- and postsynaptic activation in the neonatal hippocampus

Autor: Megumi Taketo, Hiroko Matsuda
Rok vydání: 2016
Předmět:
0301 basic medicine
Male
Patch-Clamp Techniques
Postsynaptic Current
Polyunsaturated Alkamides
Presynaptic Terminals
Arachidonic Acids
Biology
In Vitro Techniques
Inhibitory postsynaptic potential
Hippocampus
Statistics
Nonparametric
03 medical and health sciences
Cellular and Molecular Neuroscience
0302 clinical medicine
Piperidines
Postsynaptic potential
Muscarinic acetylcholine receptor
Animals
Excitatory Amino Acid Agents
GABAergic Neurons
Pharmacology
Post-tetanic potentiation
Pyramidal Cells
Neural Inhibition
Rats
030104 developmental biology
nervous system
Animals
Newborn
Inhibitory Postsynaptic Potentials
Metabotropic glutamate receptor
Excitatory postsynaptic potential
Biophysics
Potassium
NMDA receptor
Pyrazoles
Calcium
Female
Neuroscience
030217 neurology & neurosurgery
Endocannabinoids
Zdroj: Neuropharmacology. 121
ISSN: 1873-7064
Popis: Activity–dependent plasticity including short and long-term depression accompanied by a reduction in transmitter release probability has been demonstrated in both inhibitory and excitatory synapses. In the neonatal hippocampus, repetitive postsynaptic depolarization is followed by presynaptic alterations of the efficacy of GABAAergic transmission. Both facilitation and inhibition have been observed, but the mechanisms underlying this plasticity have not yet been elucidated. In the present experiment, repetitive postsynaptic depolarization by itself did not cause marked alterations of spontaneous inhibitory postsynaptic currents (sIPSCs). Activation of presynaptic neurons by increasing extracellular K+ concentration ([K+]o) temporarily induced facilitation of sIPSCs, but successive repetitive depolarizations transiently reduced the current frequency. This newly discovered inhibition was expressed presynaptically, could not be induced by postsynaptic depolarization alone, and was facilitated by the activation of NMDA receptors. IPSC inhibition was suppressed using the antagonists of metabotropic glutamate receptors (mGluRs) or muscarinic ACh receptors (mAChRs). Furthermore, transient inhibition was reduced by an antagonist of the type 1 cannabinoid receptor (CB1 receptor). The effect of CB1 receptor agonist on the sIPSCs was potentiated by [K+]o elevation, implying a role for the [K+]o elevation other than the release of transmitters. These results show that weak postsynaptic activation, when combined with presynaptic activation, leads to an inhibition of GABAergic synapses in the neonatal hippocampus. This inhibition is mediated by a mechanism involving mGluRs, mAChRs, and CB1 receptors, and potentiated by NMDA receptor activation.
Databáze: OpenAIRE
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