Abstracts

SIMILAR ACTIVATION OF GIN INHIBITORY CELLS YIELDS DIFFERENT DOWNSTREAM EFFECTS ON EXCITATORY CELLS

Abstract number : 3.352
Submission category : 13. Neuropathology of Epilepsy
Year : 2009
Submission ID : 10431
Source : www.aesnet.org
Presentation date : 12/4/2009 12:00:00 AM
Published date : Aug 26, 2009, 08:12 AM

Authors :
Erika Fanselow and A. Kinnischtzke

Rationale: It has been proposed that increased cortical activity, including seizures, could increase the activity of GFP-expressing interneurons (GIN), which could, in turn, bring levels of cortical excitation under control. However, it is not well understood how GIN cells behave when activated by ambient conditions, or how they influence their downstream excitatory targets during such activation. Methods: We activated GIN cells in a slice preparation from mouse somatosensory cortex using two methods: 1) bath application of the mGluR1 agonist, (S)-3,5-dihydroxyphenylglycine hydrate (DHPG; 5 uM), and 2) bath application of carbachol (10 uM). Whole cell recordings were made from GIN and RS cells during agonist application. Cells were polarized in order to isolate inhibitory postsynaptic potentials (IPSPs). Results: Both activating conditions (DHPG and carbachol) caused GIN cells to fire rhythmically, but the rhythmicity was stronger during carbachol application than during DHPG. During carbachol application, the IPSPs we observed were significantly larger and more frequent than during GIN cell activation by DHPG. Furthermore, the IPSPs observed during carbachol application showed power in the theta frequency range, whereas no such theta-frequency power was observed during DHPG application. Conclusions: We conclude that during application of carbachol to cortical slices, the IPSP content is higher and more rhythmic than during DHPG application. This may be due to the differential activation and synchronous firing of GIN inhibitory neurons. Thus, the method of activation of a given inhibitory cell population may affect its influence on downstream excitatory neurons.
Neuropathology of Epilepsy