By Antonio Rodriguez-Moreno, Talvinder S. Sihra
This quantity severely examines the practical activities of the kainate‑type glutamate receptors (KARs). Following on from the bigger physique of labor at the NMDA‑ and AMPA-type ionotropic glutamate receptors (GluRs), reports with KARs have continuously thrown up exceptions to basic ideas approximately synaptic modulation. members herein supply an perception to the idiosyncracies that now virtually typify the KAR box. The interesting insights supplied during this quantity serve to inspire looking out mechanistic questions.
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Additional resources for Kainate Receptors: Novel Signaling Insights
GLUK1 receptor antagonists and hippocampal mossy fiber function. Int Rev Neurobiol 2009; 85:13-27. 2. Huettner JE. Kainate receptors and synaptic transmission. Prog Neurobiol 2003; 70:387-407. 3. Collingridge GL, Olsen RW, Peters J et al. A nomenclature for ligand-gated ion channels. Neuropharm 2009; 56:2-5. 4. Egebjerg J, Bettler B, Hermans-Borgmeyer I et al. Cloning of a cDNA for a glutamate receptor subunit activated by kainate but not by AMPA. Nature 1991; 351:745-748. 5. Schiffer HH, Swanson GT, Heinemann SF.
2). In addition, in “presynaptically” silent neurons, UBP 302 induces the appearance of synaptic responses to the first stimulus suggesting that endogenous activation of GluK1 contributes to synapses silencing (Fig. 3). Silent synapses represent a common feature of the developing brain. 74 It is known that presynaptic receptors are usually activated by spillover of the neurotransmitter from axon terminals. One fundamental question to be addressed is how presynaptic GluK1 receptors can be activated if the main neurotransmitter released from MFs is GABA.
The decrease in amplitude of GPSCs, which persists without decrement for periods of time variable from 40 to 60 min, reaches its maximum when in the case of positive pairing antidromic spikes follow MF stimulation with a delay of 15 ms (coincident with the peak of the synaptic potentials) or when, in the case of negative pairing, it precedes MF activation by 50 ms. These effects, which require for their induction a rise of calcium in the postsynaptic cell via voltage-dependent calcium channels, are associated with a significant decrease in successes rate, in the inverse squared value of the coefficient of variation of responses amplitude and a significant increase in paired pulse ratio, suggesting a presynaptic site of expression.