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 PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Stutzmann, G. E. Articles by LeDoux, J. E. Search for Related Content PubMed PubMed Citation Articles by Stutzmann, G. E. Articles by LeDoux, J. E. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB GLUTAMIC ACID HYDROCHLORIDE

 Previous Article  |  Next Article 

The Journal of Neuroscience, 1999:RC8:1-4

RAPID COMMUNICATION
GABAergic Antagonists Block the Inhibitory Effects of Serotonin in the Lateral Amygdala: A Mechanism for Modulation of Sensory Inputs Related to Fear Conditioning

Grace E. Stutzmann and Joseph E. LeDoux

Center for Neural Science, New York University, New York, New York 10003

Neurons in the lateral amygdala (LA) receive glutamatergic sensory input from the auditory thalamus and auditory cortex, and these inputs can be modulated by serotonin (5-HT). In the present study, we examined whether serotonergic inhibition of glutamatatergic excitation in the LA occurs via activation of GABAergic interneurons. Single-unit extracellular activity in the LA was recorded in response to iontophoretically applied glutamate. Concurrent application of 5-HT reduced the number of glutamate-evoked action potentials in the majority of neurons tested. GABA antagonists were then iontophoresed with both glutamate and 5-HT. Of the neurons that were inhibited by 5-HT, concurrent application of the GABA antagonists significantly reversed this effect. Application of the GABA antagonists alone had little or no effect on basal neuronal activity. We conclude that the 5-HT-induced inhibition of glutamatergic activity occurs in part through activation of serotonergic receptors on GABAergic interneurons.

Key words: electrophysiology; iontophoresis; rat; glutamate; anxiety; sensory modulation

---

Copyright © 1999 Society for Neuroscience  0270-6474/99/$05.00/0

This article has been cited by other articles:

				R. A. Ruden Encoding States: A Model for the Origin and Treatment of Complex Psychogenic Pain Traumatology, March 1, 2008; 14(1): 119 - 126. [Abstract] [PDF]

				R. NORBURY, C. E. MACKAY, P. J. COWEN, G. M. GOODWIN, and C. J. HARMER Short-term antidepressant treatment and facial processing: Functional magnetic resonance imaging study The British Journal of Psychiatry, June 1, 2007; 190(6): 531 - 532. [Abstract] [Full Text] [PDF]

				R. A. Ruden A Model for Disrupting an Encoded Traumatic Memory Traumatology, March 1, 2007; 13(1): 71 - 75. [Abstract] [PDF]

				C.-H. Lin, S. Hansen, Z. Wang, D. R. Storm, S. J. Tapscott, and J. M. Olson The dosage of the neuroD2 transcription factor regulates amygdala development and emotional learning PNAS, October 11, 2005; 102(41): 14877 - 14882. [Abstract] [Full Text] [PDF]

				R. A. Ruden A Neurological Basis for the Observed Peripheral Sensory Modulation of Emotional Responses Traumatology, September 1, 2005; 11(3): 145 - 158. [Abstract] [PDF]

				J. M. Gorman, J. M. Kent, G. M. Sullivan, and J. D. Coplan Neuroanatomical Hypothesis of Panic Disorder, Revised Focus, July 1, 2004; 2(3): 426 - 439. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help