Kindling-induced alterations in GABAA receptor-mediated inhibition and neurosteroid activity in the rat piriform cortex.
The piriform cortex makes strong interconnections with limbic structures (amygdala, entorhinal cortex and hippocampus) that are involved in memory processing. These connections have also been implicated in the development of temporal lobe epilepsy. However, little is known about how neurones in this region may change during seizure genesis. Here we tested the hypothesis that in the kindling model of temporal lobe epilepsy GABAA receptor-mediated inhibition is altered in the piriform cortex. To do this we performed whole-cell patch-clamp recordings in piriform cortex brain slices obtained from non-kindled and amygdala-kindled adult rats. We found that kindling coincided with an increase in the amplitude and duration of miniature inhibitory post-synaptic currents (mIPSCs) recorded from non-pyramidal neurones, whereas the mIPSCs occurring on pyramidal (excitatory) cells did not change. Non-stationary noise analysis of mIPSCs occurring on the non-pyramidal neurones showed that inferred unitary conductance of synaptic channels were the same before and after kindling, implying that the channel number increased significantly. Immunocytochemical analysis of the inhibitory innervation showed that it was also unaltered by seizure induction. We also found that the effect of the positive modulator tetrahydrodeoxycorticosterone was reduced on the pyramidal neurones after kindling. In contrast, the potentiating effects of tetrahydrodeoxycorticosterone on non-pyramidal cells were about the same after kindling as in control (sham) rats. These data indicate that amygdala kindling causes a shift in the inhibition 'balance' between the pyramidal and non-pyramidal cells, perhaps leading to the disinhibition of pyramidal cells.
Gavrilovici
Cezar
C
Neuroscience Research Institute, Department of Psychology, Carleton University, Ottawa, Ontario, Canada.
D'Alfonso
Sabrina
S
Dann
Mathew
M
Poulter
Michael O
MO
D000679:Amygdala / Q000503:physiopathology; D000818:Animals; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism*; D003900:Desoxycorticosterone / Q000031:analogs & derivatives* / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D007839:Functional Laterality / Q000502:physiology; D049690:History, Ancient; D007150:Immunohistochemistry / Q000379:methods; D066298:In Vitro Techniques; D007696:Kindling, Neurologic / Q000378:metabolism*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects* / Q000502:physiology / Q000528:radiation effects; D018408:Patch-Clamp Techniques / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000378:metabolism*
D011963:Receptors, GABA-A; D003900:Desoxycorticosterone; C009413:tetrahydrodeoxycorticosterone