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Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
Published on: August 15, 2017
Requirement of protein synthesis for group I mGluR-mediated induction of epileptiform discharges
L R Merlin1, P J Bergold, R K Wong
1Department of Neurology, State University of New York Health Science Center at Brooklyn, Brooklyn, New York 11203, USA.
Abstract:
Picrotoxin (50 microM) elicited rhythmic synchronized bursting in CA3 pyramidal cells in guinea pig hippocampal slices. Addition of the selective group I metabotropic glutamate receptor (mGluR) agonist (S)-3,5-dihydroxyphenylglycine (25 microM) elicited an increase in burst frequency. This was soon followed by a slowly progressive increase in burst duration (BD), converting the brief 250-520 ms picrotoxin-induced synchronized bursts into prolonged discharges of 1-5 s in duration. BD was significantly increased within 60 min and reached a maximum after 2-2.5 h of agonist exposure. The protein synthesis inhibitors anisomycin (15 microM) or cycloheximide (25 microM) significantly impeded the mGluR-mediated development of the prolonged bursts; 90-120 min of agonist application failed to elicit the expected burst prolongation. By contrast, the mGluR-mediated enhancement of burst frequency progressed unimpeded. Furthermore, protein synthesis inhibitors had no significant effect on the frequency or duration of fully developed mGluR-induced prolonged discharges. These results suggest that the group I mGluR-mediated prolongation of synchronized bursts has a protein synthesis-dependent mechanism.
Insights
Group I metabotropic glutamate receptors (mGluRs) prolong synchronized bursts in CA3 pyramidal cells. This effect requires new protein synthesis, suggesting a molecular mechanism for long-term changes in neuronal excitability.
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Synaptic Plasticity
Background:
- Picrotoxin induces synchronized bursting in CA3 pyramidal cells.
- Group I metabotropic glutamate receptors (mGluRs) modulate neuronal excitability.
Purpose of the Study:
- To investigate the mechanism underlying the prolongation of picrotoxin-induced synchronized bursts by group I mGluR activation.
- To determine if protein synthesis is required for mGluR-mediated burst prolongation.
Main Methods:
- Hippocampal slices from guinea pigs were used.
- Picrotoxin induced synchronized bursting in CA3 pyramidal cells.
- Group I mGluR agonist (S)-3,5-dihydroxyphenylglycine was applied.
- Protein synthesis inhibitors (anisomycin, cycloheximide) were used to test for dependence on protein synthesis.
Main Results:
- Group I mGluR activation increased burst frequency and prolonged burst duration (BD).
- The development of prolonged bursts was significantly impeded by protein synthesis inhibitors.
- Burst frequency enhancement by mGluRs was not affected by protein synthesis inhibitors.
- Protein synthesis inhibitors did not affect fully developed prolonged bursts.
Conclusions:
- Group I mGluR-mediated prolongation of synchronized bursts in CA3 pyramidal cells is dependent on protein synthesis.
- This suggests a molecular mechanism involving protein synthesis for long-term changes in neuronal excitability.
