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Repeated administration of imipramine attenuates glutamatergic transmission in rat frontal cortex
K Tokarski1, B Bobula, J Wabno
1Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.
Abstract:
The effects of repeated administration of a tricyclic antidepressant, imipramine, lasting 14 days (10 mg/kg p.o., twice daily), were studied ex vivo in rat frontal cortex slices prepared 48 h after last dose of the drug. In slices prepared from imipramine-treated animals the mean frequency, and to a lesser degree the mean amplitude, of spontaneous excitatory postsynaptic currents recorded from layer II/III pyramidal neurons, were decreased. These effects were accompanied by a reduction of the initial slope ratio of pharmacologically isolated N-methyl-D-aspartate to AMPA/kainate receptor-mediated stimulation-evoked excitatory postsynaptic currents. Imipramine treatment also resulted in a decrease of extracellular field potentials evoked in layer II/III by stimulation of underlying sites in layer V. These results indicate that chronic treatment with imipramine results in an attenuation of the release of glutamate and an alteration in the postsynaptic reactivity of ionotropic glutamate receptors in rat cerebral cortex.
Insights
Chronic imipramine treatment in rats reduced excitatory postsynaptic currents and altered glutamate receptor function in the frontal cortex. This suggests imipramine affects neuronal communication and glutamate signaling in the brain.
Area of Science:
- Neuroscience
- Pharmacology
- Molecular Biology
Background:
- Tricyclic antidepressants like imipramine are widely used for treating depression.
- The precise neurobiological mechanisms underlying imipramine's long-term effects on neuronal excitability remain incompletely understood.
Purpose of the Study:
- To investigate the ex vivo effects of chronic imipramine administration on synaptic transmission and glutamate receptor function in rat frontal cortex.
- To elucidate the impact of imipramine on excitatory postsynaptic currents and receptor-mediated signaling.
Main Methods:
- Repeated oral administration of imipramine (10 mg/kg, twice daily for 14 days) to rats.
- Ex vivo electrophysiological recordings from rat frontal cortex slices 48 hours after the last drug dose.
- Measurement of spontaneous excitatory postsynaptic currents (sEPSCs) and stimulation-evoked postsynaptic potentials in pyramidal neurons.
Main Results:
- Chronic imipramine treatment significantly decreased the frequency and amplitude of spontaneous excitatory postsynaptic currents in layer II/III pyramidal neurons.
- A reduction in the ratio of N-methyl-D-aspartate (NMDA) to AMPA/kainate receptor-mediated currents was observed.
- Imipramine administration led to decreased extracellular field potentials, indicating attenuated glutamate release and altered postsynaptic receptor sensitivity.
Conclusions:
- Chronic imipramine treatment results in a significant attenuation of glutamate release in the rat cerebral cortex.
- Imipramine alters the postsynaptic reactivity of ionotropic glutamate receptors, impacting neuronal excitability.
- These findings provide insights into the neurochemical adaptations associated with long-term antidepressant treatment.
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