Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2014 Mar 6;12(3):1185–1207. doi: 10.3390/md12031185

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2014 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

PMC Copyright notice

Proposed mechanism for domoic acid induced damage to granule cell dendrodentric contacts with mitral cells in olfactory bulb in rat model for domoic acid epileptic disease. Left: Activation of mitral cells releases glutamate (GLU) into the dendrodentric space. The depolarization of dendritic spine of granule cells relieves magnesium block on NMDA receptor allowing glutamate induced calcium entry and release of GABA. GABA feeds back to hyperpolarize lateral dendrites of mitral cells. Right: Excitotoxic damage of dendritic spines (broken lines) disrupts GABAergic feedback at dendrodentric contacts to promote hyperactivity (bold lines) of mitral cells lack due to loss of inhibition of lateral dendrites.