Related Experiment Videos
Glomerular synaptic responses to olfactory nerve input in rat olfactory bulb slices
V Aroniadou-Anderjaska1, M Ennis, M T Shipley
1Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore 21201, U.S.A.
Neuroscience
|July 1, 1997
Summary
Olfactory nerve stimulation in rats activates early kainate/AMPA receptor responses and later N-methyl-D-aspartate receptor responses in mitral/tufted cells. GABAergic inhibition modulates these olfactory bulb responses, impacting synaptic integration and plasticity.
Area of Science:
- Neuroscience
- Olfactory System Research
- Synaptic Plasticity
Background:
- The olfactory bulb is the primary processing center for smell.
- Understanding synaptic mechanisms in the olfactory bulb is crucial for deciphering olfactory processing.
- Previous studies have identified different receptor types involved in olfactory neurotransmission.
Purpose of the Study:
- To characterize the receptor mechanisms underlying olfactory nerve-evoked field potentials in the rat olfactory bulb.
- To investigate the roles of AMPA and NMDA receptors in synaptic transmission within the olfactory bulb glomeruli.
- To elucidate the influence of GABAergic inhibition on olfactory bulb neuronal activity.
Main Methods:
- Extracellular field potential recordings in olfactory bulb slices from young rats.
- Pharmacological manipulation using AMPA receptor antagonist CNQX and NMDA receptor antagonist DL-2-amino-5-phosphonovalerate.
- Knife cuts to isolate olfactory bulb layers and laminar analysis of field potentials.
- Intracellular recordings in mitral cells to correlate field potentials with neuronal firing.
- Application of GABA(A) receptor antagonist bicuculline methiodide and glycine receptor antagonist strychnine.
Main Results:
- Olfactory nerve stimulation evoked two components: an early AMPA receptor-mediated (N1) and a late NMDA receptor-mediated (N2) response.
- Both N1 and N2 potentials were generated within the glomeruli and reversed polarity in the external plexiform and mitral cell layers.
- N1 correlated with brief mitral cell spiking, while N2 was associated with prolonged mitral cell firing.
- GABA(A) receptor blockade selectively enhanced N2, indicating inhibitory modulation of the NMDA receptor-mediated response.
- Strychnine showed effects similar to bicuculline only at high concentrations affecting GABA(A) receptors.
Conclusions:
- Olfactory nerve activation elicits distinct AMPA and NMDA receptor-mediated synaptic responses in mitral/tufted cells.
- NMDA receptor activation triggers prolonged mitral cell discharge, suggesting a role in sustained olfactory processing.
- GABA(A) receptor-mediated inhibition preferentially suppresses the NMDA receptor component.
- Prolonged NMDA receptor activity in the olfactory system may be vital for synaptic integration and plasticity.
- These findings provide insights into the complex neurochemical basis of olfactory information processing.