Tufted cell dendrodendritic inhibition in the olfactory bulb is dependent on NMDA receptor activity

J. M. Christie, N. E. Schoppa, Gary Westbrook

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Mitral and tufted cells constitute the primary output cells of the olfactory bulb. While tufted cells are often considered as "displaced" mitral cells, their actual role in olfactory bulb processing has been little explored. We examined dendrodendritic inhibition between tufted cells and interneurons using whole cell voltage-clamp recording. Dendrodendritic inhibitory postsynaptic currents (IPSCs) generated by depolarizing voltage steps in tufted cells were completely blocked by the N-methyl-D-aspartate (NMDA) receptor antagonist D,L-2-amino-5-phosphonopentanoic acid (D,L-AP5), whereas the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist 2-3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f] quinoxaline-7-sulfonamide (NBQX) had no effect. Tufted cells in the external plexiform layer (EPL) and in the periglomerular region (PGR) showed similar behavior. These results indicate that NMDA receptor-mediated excitation of interneurons drives inhibition of tufted cells at dendrodendritic synapses as it does in mitral cells. However, the spatial extent of lateral inhibition in tufted cells was much more limited than in mitral cells. We suggest that the sphere of influence of tufted cells, while qualitatively similar to mitral cells, is centered on only one or a few glomeruli.

Original languageEnglish (US)
Pages (from-to)169-173
Number of pages5
JournalJournal of Neurophysiology
Volume85
Issue number1
StatePublished - 2001

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Olfactory Bulb
N-Methyl-D-Aspartate Receptors
Interneurons
2-Amino-5-phosphonovalerate
Quinoxalines
Inhibitory Postsynaptic Potentials
AMPA Receptors
Sulfonamides
Synapses

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

Tufted cell dendrodendritic inhibition in the olfactory bulb is dependent on NMDA receptor activity. / Christie, J. M.; Schoppa, N. E.; Westbrook, Gary.

In: Journal of Neurophysiology, Vol. 85, No. 1, 2001, p. 169-173.

Research output: Contribution to journalArticle

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