Gaba Mediated Long-Term Depression (LTD) in the Rat Medial Vestibular Nuclei
| Autor: | Vito Enrico Pettorossi, Mauro Zampolini, Silvarosa Grassi, Della Torre G |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
GABAB receptor
Receptors N-Methyl-D-Aspartate Synaptic Transmission Pitch Discrimination chemistry.chemical_compound Vestibular nuclei Interneurons Culture Techniques medicine Animals Long-term depression gamma-Aminobutyric Acid Afferent Pathways Brain Mapping integumentary system Chemistry GABAA receptor Neural Inhibition Long-term potentiation General Medicine Vestibular Nuclei Bicuculline Receptors GABA-A Rats Receptors GABA-B nervous system Otorhinolaryngology Anesthesia Saclofen GABAergic Neuroscience medicine.drug |
| Zdroj: | Acta Oto-Laryngologica. 115:164-169 |
| ISSN: | 1651-2251 0001-6489 |
| DOI: | 10.3109/00016489509125218 |
| Popis: | As previously demonstrated, high frequency stimulation (HFS) of the primary vestibular afferents always induces a clear, long lasting depression of the polysynaptic (N2) component of the field potentials recorded in the dorsal portion of the medial vestibular nuclei (MVN). The induction of the HFS effect was mediated by the activation of glutamate NMDA receptors, since it was blocked by AP5. The mechanisms at the basis of such a depression were studied. Our results demonstrate that Gaba, acting on both GabaA and GabaB receptors, is involved in mediating this phenomenon. In fact, HFS applied during Bicuculline and Saclofen perfusion, was no longer able to induce an N2 depression, but provoked a slight potentiation. However, the N2 depression clearly emerged after drug wash-out. Furthermore, Bicuculline and Saclofen fully abolished the N2 depression and highlighted the potentiation, when administered after HFS. The possibility that the N2 depression is the result of a homosynaptic LTD can be excluded on the basis of our results. On the contrary, our findings suggest that the depression is due to an enhancement of the Gaba inhibitory effect due to an HFS dependent increase in gabaergic interneuron activity, which resets vestibular neuron excitability at a lower level. |
| Databáze: | OpenAIRE |
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