Related Experiment Video
Updated: Apr 22, 2026
Recording Temperature-induced Neuronal Activity through Monitoring Calcium Changes in the Olfactory Bulb of Xenopus laevis
Published on: June 3, 2016
Presynaptic T-type Ca2+ channels modulate dendrodendritic mitral-mitral and mitral-periglomerular connections in
Adam Fekete1, Jamie Johnston2, Kerry R Delaney3
1Department of Biology, University of Victoria, Victoria, British Columbia, V8W 2Y2, Canada, Program in Neurosciences and Mental Health, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada, and.
Abstract:
Mitral cells express low-voltage activated Cav3.3 channels on their distal apical tuft dendrites (McKay et al., 2006; Johnston and Delaney, 2010). They also discharge Na(+)-dependent dendritic action potentials and release glutamate from these dendrites. Around resting membrane potentials, between -65 and -50 mV, Cav3.x channels are a primary determinant of cytoplasmic [Ca(2+)]. In this study using C57 mice, we present evidence that subthreshold Cav3.x-mediated Ca(2+) influx modulates action potential evoked transmitter release and directly drives asynchronous release from distal tuft dendrites. Presynaptic hyperpolarization and selective block of Cav3.x channels with Z941 (Tringham et al., 2012) reduce mitral-to-mitral EPSP amplitude, increase the coefficient of variation of EPSPs, and increase paired-pulse ratios, consistent with a reduced probability of transmitter release. Both hyperpolarization and Cav3.x channel blockade reduce steady-state cytoplasmic [Ca(2+)] in the tuft dendrite without reducing action potential evoked Ca(2+) influx, suggesting that background [Ca(2+)] modulates evoked release. We demonstrate that Cav3.x-mediated Ca(2+) influx from even one mitral cell at membrane potentials between -65 and -50 mV is sufficient to produce feedback inhibition from periglomerular neurons. Deinactivation of Cav3.x channels by hyperpolarization increases T-type Ca(2+) influx upon repolarization and increases feedback inhibition to produce subthreshold modulation of the mitral-periglomerular reciprocal circuit.
Insights
Low-voltage activated calcium channels (Cav3.x) in mitral cells regulate neurotransmitter release. Blocking these channels reduces release probability and modulates feedback inhibition in the olfactory system.
Area of Science:
- Neuroscience
- Cellular Physiology
- Olfactory System Research
Background:
- Mitral cells possess low-voltage activated Cav3.3 channels on distal apical tuft dendrites.
- These channels are crucial for cytoplasmic calcium concentration around resting membrane potentials (-65 to -50 mV).
- Mitral cells generate Na(+)-dependent dendritic action potentials and glutamate release from dendrites.
Purpose of the Study:
- To investigate the role of subthreshold Cav3.x calcium influx in mitral cells.
- To determine how Cav3.x channels modulate action potential-evoked and asynchronous transmitter release.
- To examine the impact of Cav3.x activity on feedback inhibition mediated by periglomerular neurons.
Main Methods:
- Utilized C57 mice for experimental studies.
- Employed presynaptic hyperpolarization and selective Cav3.x channel blockade using Z941.
- Measured mitral-to-mitral excitatory postsynaptic potential (EPSP) amplitude, coefficient of variation, and paired-pulse ratios.
- Assessed steady-state cytoplasmic calcium levels in tuft dendrites.
Main Results:
- Presynaptic hyperpolarization and Z941 reduced EPSP amplitude, increased EPSP variation, and increased paired-pulse ratios, indicating reduced transmitter release probability.
- Both interventions decreased steady-state cytoplasmic calcium without affecting action potential-evoked calcium influx.
- Cav3.x-mediated calcium influx from a single mitral cell induced feedback inhibition from periglomerular neurons.
- Hyperpolarization-induced deinactivation of Cav3.x channels increased T-type calcium influx upon repolarization, enhancing feedback inhibition.
Conclusions:
- Subthreshold Cav3.x calcium influx in mitral cell dendrites modulates evoked transmitter release.
- Background Cav3.x calcium levels influence evoked release and contribute to feedback inhibition.
- Cav3.x channels play a significant role in the subthreshold modulation of the mitral-periglomerular reciprocal circuit.
More Related Videos
10:16Perforated Patch-clamp Recording of Mouse Olfactory Sensory Neurons in Intact Neuroepithelium: Functional Analysis of Neurons Expressing an Identified Odorant Receptor
Published on: July 13, 2015
09:54Morphological and Functional Evaluation of Ribbon Synapses at Specific Frequency Regions of the Mouse Cochlea
Published on: May 10, 2019
Related Concept Videos
01:25Olfaction
The olfactory receptors are embedded in the cilia of the...
01:20Physiology of Smell and Olfactory Pathway
The olfactory...
01:03Olfactory Receptors: Location and Structure