QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Belousov, A. B. Articles by Denisova, J. V. Search for Related Content PubMed PubMed Citation Articles by Belousov, A. B. Articles by Denisova, J. V.

 Previous Article  |  Next Article 

The Journal of Neuroscience, March 15, 2001, 21(6):2015-2027

Acetylcholine Becomes the Major Excitatory Neurotransmitter in the Hypothalamus In Vitro in the Absence of Glutamate Excitation

Andrei B. Belousov¹, Bruce F. O'Hara², and Janna V. Denisova¹

¹ Department of Cell and Molecular Biology, Tulane University, New Orleans, Louisiana 70118, and ² Department of Biological Sciences, Stanford University, Stanford, California 94305

Glutamate and GABA are two major fast neurotransmitters (excitatory and inhibitory, respectively) in the CNS, including the hypothalamus. They play a key role in the control of excitation/inhibition balance and determine the activity and excitability of neurons in many neuronal circuits. Using neuronal cultures, whole-cell recording, Ca²⁺ imaging, and Northern blots, we studied the compensatory regulation of neuronal activity during a prolonged decrease in glutamate excitation. We report here that after a chronic (6-17 d) blockade of ionotropic glutamate receptors, neurons in hypothalamic cultures revealed excitatory electrical and Ca²⁺ synaptic activity, which was not elicited in the control cultures that were not subjected to glutamate blockade. This activity was suppressed with acetylcholine (ACh) receptor antagonists and was potentiated by eserine, an inhibitor of acetylcholinesterase, suggesting its cholinergic nature. The upregulation of ACh receptors and the contribution of ACh to the control of the excitation/inhibition balance in cultures after a prolonged decrease in glutamate activity were also demonstrated. Enhanced ACh transmission was also found in chronically blocked cerebellar but not cortical cultures, suggesting the region-specific character of glutamate-ACh interactions in the brain. We believe that in the absence of glutamate excitation in the hypothalamus in vitro, ACh, a neurotransmitter normally exhibiting only weak activity in the hypothalamus, becomes the major excitatory neurotransmitter and supports the excitation/inhibition balance. The increase in excitatory ACh transmission during a decrease in glutamate excitation may represent a novel form of neuronal plasticity that regulates activity and excitability of neurons during the glutamate/GABA imbalance.

Key words: acetylcholine; glutamate; GABA; hypothalamus; plasticity; excitation/inhibition balance

---

Copyright © 2001 Society for Neuroscience  0270-6474/01/2162015-13$05.00/0

This article has been cited by other articles:

				X. Liu, I. R. Popescu, J. V. Denisova, R. L. Neve, R. A. Corriveau, and A. B. Belousov Regulation of Cholinergic Phenotype in Developing Neurons J Neurophysiol, May 1, 2008; 99(5): 2443 - 2455. [Abstract] [Full Text] [PDF]

				J. C. de Rivero Vaccari, R. A. Corriveau, and A. B. Belousov Gap Junctions Are Required for NMDA Receptor Dependent Cell Death in Developing Neurons J Neurophysiol, November 1, 2007; 98(5): 2878 - 2886. [Abstract] [Full Text] [PDF]

				L.-E. Trudeau and R. Gutierrez On Cotransmission & Neurotransmitter Phenotype Plasticity Mol. Interv., June 1, 2007; 7(3): 138 - 146. [Abstract] [Full Text] [PDF]

				A. B. Belousov, N. D. Hunt, R. P. Raju, and J. V. Denisova Calcium-Dependent Regulation of Cholinergic Cell Phenotype in the Hypothalamus In Vitro J Neurophysiol, September 1, 2002; 88(3): 1352 - 1362. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help