Epileptiform activity in the nucleus accumbens induced by GABA A receptor antagonists in rat forebrain slices is of cortical origin
| Autor: | Michael G. Lacey, Buckby Le |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Male
medicine.medical_specialty Glutamic Acid Neurotransmission Nucleus accumbens Receptors N-Methyl-D-Aspartate Synaptic Transmission Nucleus Accumbens GABA Antagonists chemistry.chemical_compound Piriform cortex Internal medicine Neural Pathways medicine Animals Cerebral Decortication GABA-A Receptor Antagonists Receptors AMPA Rats Wistar Cerebral Cortex Neurons Epilepsy GABAA receptor musculoskeletal neural and ocular physiology General Neuroscience Excitatory Postsynaptic Potentials Neural Inhibition Receptors GABA-A Electric Stimulation Rats medicine.anatomical_structure Endocrinology nervous system chemistry Cerebral cortex CNQX Excitatory postsynaptic potential Excitatory Amino Acid Antagonists Neuroscience psychological phenomena and processes Picrotoxin |
| Zdroj: | Experimental Brain Research. 141:146-152 |
| ISSN: | 0014-4819 |
| Popis: | Extracellularly recorded field potentials, evoked by stimulation of cortico-nucleus accumbens border, were recorded in the nucleus accumbens (NAcc) in horizontal slices of rat ventral forebrain. The field excitatory postsynaptic potential (EPSP) event (N2) was calcium dependent, blocked by tetrodotoxin (1 microM), and reduced by over 70% by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM), the antagonist of AMPA-type glutamate receptors. The EPSP amplitude was enhanced by either of the GABA(A) receptor antagonists, picrotoxin (10 microM; by 252+/-33%, n=18) and bicuculline methiodide (20 microM; by 216+/-34%, n=4). Additionally, picrotoxin (3-50 microM) and bicuculline methiodide (20 microM) promoted epileptiform activity within the NAcc, manifest as the emergence of additional late components, N3, N4 and N5, in the evoked synaptic waveform. In slices with the frontal cortex removed, picrotoxin (10-50 microM) and bicuculline methiodide (20 microM) were unable to promote epileptiform activity within the NAcc, although a smaller increase in the peak amplitude of the field EPSP (163+/-18%, n=6) was observed at the highest concentrations of picrotoxin (50 microM). Histological examination of the slice demonstrated that in such decorticated slices, the piriform cortex (PC) had been removed. We propose that stimulation of the cortico-NAcc border not only evokes an orthodromic EPSP in the NAcc, but also causes antidromic activation of cortical tissue. Disinhibition by GABA(A) antagonists of circuits intrinsic to the cortex, possibly the piriform cortex, is the principal cause of the facilitation of the EPSP and of regenerative epileptiform activity in NAcc evoked by stimulation of cortical input. |
| Databáze: | OpenAIRE |
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