Activation of kainate GLU(K5) transmission rescues kindling-induced impairment of LTP in the rat lateral amygdala.
The amygdala is a component of the limbic system that plays a central role in emotional behavior and certain psychiatric diseases. Pathophysiological alterations of neuronal excitability in the amygdala are characteristic features of temporal lobe epilepsy and certain (epilepsy accompanying) psychiatric illnesses such as anxiety and depressive disorders. The role of kainate receptors in the activity of synaptic networks, in brain function, and diseases is still poorly understood. Various kainate receptor subtypes have been shown to contribute to synaptic transmission and modulate presynaptic release of glutamate and gamma-aminobutyric acid (GABA). Several lines of evidence point to the importance of GLU(K5) kainate receptors in epilepsy. In this study we investigated the role of specific GLU(K5) kainate receptor in the lateral nucleus of the amygdala (LA). The cellular mechanisms for emotional learning in the amygdala are believed to be the result of changes in synaptic transmission efficacy, similar to long-term potentiation (LTP). Here, we used both field potential and intracellular recordings in horizontal rat amygdala slices, and showed that LTP in the LA, induced by high-frequency stimulation of afferents running within LA, is impaired 48 h after the last induced seizure. This kindling-induced impairment was reversed by the specific kainate GLU(K5) agonist ATPA. Partial blockade of GABAergic transmission with the specific GABA(A) receptor antagonist SR95531 also significantly facilitated the induction of early LA-LTP, but only partially abolished the kindling-induced impairment of LA-LTP. This study shows that the stimulation of the GLU(K5) kainate receptor subtype rescues the kindling-induced impairment of LA-LTP at least within 48 h after the last seizure. Therefore, GLU(K5) kainate receptor subunits are involved in kindling-induced plasticity changes in the amygdala.
Department of Physiology, Faculty of Medical and Health Science, University of Auckland, Auckland, New Zealand.
Manja
M
Schubert
Doris
D
Albrecht
D000344:Afferent Pathways / Q000502:physiology; D000679:Amygdala / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D000818:Animals; D004558:Electric Stimulation; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D018698:Glutamic Acid / Q000378:metabolism*; D007696:Kindling, Neurologic / Q000187:drug effects / Q000502:physiology*; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009924:Organ Culture Techniques; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000378:metabolism; D018092:Kainic Acid Receptors / Q000819:agonists / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018690:Excitatory Amino Acid Agonists; D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D018698:Glutamic Acid; D011963:Receptors, GABA-A; D018092:Kainic Acid Receptors; D005680:gamma-Aminobutyric Acid