Submitted on September 28, 2007
Accepted on November 14, 2007
Activation of postsynaptic GABAB receptors modulates the bursting pattern and synaptic activity of olfactory bulb juxtaglomerular neurons
Nikolay Karpuk1 and Abdallah Hayar1*
1 Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
* To whom correspondence should be addressed. E-mail: abdallah{at}hayar.net.
Olfactory bulb glomeruli are formed by a network of 3 major types of neurons collectively called juxtaglomerular (JG) cells, which include external tufted (ET), periglomerular (PG) and short axon (SA) cells. There is solid evidence that GABA released from olfactory bulb PG neurons presynaptically inhibits glutamate release from olfactory nerve terminals via activation of GABAB receptors (GABAB-Rs). However, it is still unclear whether ET cells have GABAB-Rs. We have investigated whether ET cells have functional postsynaptic GABAB-Rs using extracellular and whole-cell recordings in olfactory bulb slices. In the presence of fast synaptic blockers (CNQX, APV and gabazine), the GABAB-R agonist, baclofen, either inhibited completely the bursting, or reduced the bursting frequency and increased the burst duration and the number of spikes/burst in ET cells. In the presence of fast synaptic blockers and TTX, baclofen induced an outward current in ET cells suggesting a direct postsynaptic effect. Baclofen reduced the frequency and amplitude of spontaneous EPSCs in PG and SA cells. In the presence of sodium and potassium channel blockers, baclofen reduced the frequency of miniature EPSCs, which were inhibited by the calcium channel blocker, cadmium. All baclofen effects were reversed by application of the GABAB-R antagonist, CGP55845. We suggest that activation of GABAB-Rs directly inhibits ET cell bursting, and decreases excitatory dendrodendritic transmission from ET to PG and SA cells. Thus, the postsynaptic GABAB-Rs on ET cells may play an important role in shaping the activation pattern of the glomeruli during olfactory coding.
