Submitted on February 7, 2007
Accepted on September 6, 2007
Alterations in GABA-A receptor mediated inhibition in adjacent dorsal midline thalamic nuclei in a rat model of chronic limbic epilepsy.
Karthik Rajasekaran1, Jaideep Kapur1, and Edward H Bertram1*
1 Neurology, University of Virginia, Charlottesville, Virginia, United States
* To whom correspondence should be addressed. E-mail: ehb2z{at}virginia.edu.
There is evidence that the dorsal midline thalamus is involved in the seizures of limbic epilepsy. However, little is known about the inhibitory synaptic function in this region. In the present study, inhibitory postsynaptic currents (IPSCs) mediated by GABA-A receptors were recorded from the mediodorsal (MD) and paraventricular (PV) nuclei from control and epileptic animals. In the MD, the sIPSCs for epileptic animals had a lower frequency, prolonged rise time, prolonged decay, but unaltered net charge transfer compared to controls. The mIPSC parameters were unaltered in the epileptic animals. In contrast, in the PV, both sIPSCs and mIPSCs in the epileptic animals were more frequent with larger amplitudes, and there was an increase in the net charge transfer compared to controls. The rise times of the sIPSCs of the PV neurons were significantly prolonged whereas the weighted decay time of the mIPSC was significantly shortened in epileptic animals. These findings suggest that the changes associated with inhibitory synaptic transmission in limbic epilepsy are not uniform across regions in the thalamus that are part of the seizure circuit.
