| Abstract No.: | C-B3034 |
| Country: | Canada |
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| Title: | LOW-VOLTAGE ACTIVATED CA CHANNELS IN MITRAL CELLS OF THE MAIN OLFACTORY BULB
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| Authors/Affiliations: | 1 Jamie Johnston*; 1 Kerry Delaney;
1 University of Victoria, BC, Canada
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| Content: | Objectives: To determine the location and function of low-voltage activated (LVA) Ca2+ channels in mitral cells.
Materials and Methods: Immunohistochemistry and combined 2-photon laser scanning microscopy with current/voltage-clamp have been used in this study on horizontal slices of olfactory bulbs taken from P16-26 mice.
Results: Immunohistochemistry performed on B6.Cg-Tg (Thy1-YFP)16Jrs mice, which in the olfactory bulb express YFP selectively in mitral cells, shows strong expression of Cav3.3 channels in the primary dendrite and fine branches of the tuft.
We find that around 50% of mitral cells possess a Ca2+ current which activates on stepping to –50mV from a pre-pulse of –90mV. This current has a strong voltage dependence of inactivation. From the resting membrane potential, hyperpolarizing steps to –80mV resulted in a decrease in resting [Ca2+] with an overshoot on return to rest, consistent with removal of inactivation of a Ca2+ channel. The LVA Ca2+ current and the decrease in resting [Ca2+] were completely blocked with 500uM Ni2+ whereas 50uM Ni2+ had no effect. The hyperpolarizing decrease in [Ca2+] was absent or much smaller in the secondary dendrites. Consistent with this observation the resting [Ca2+] (determined by the ratio of Fluo-4/Alexa 594) was also found to be lower in secondary dendrites compared to primary dendrites.
To mimic in vivo membrane oscillations caused by breathing we gave sine wave current injections. Oscillations below action potential threshold still resulted in [Ca2+] increases, which was blocked by 500uM Ni2+.
To determine whether neuromodulation explained the absence of LVA Ca2+ channels in some mitral cells, we bath applied mGLUR agonists. This resulted in more open channels and a higher [Ca2+] at resting membrane potentials. However the mGLUR-activated Ca2+ channels did not display strong voltage-dependent inactivation.
Conclusion: A population of mitral cells express LVA Ca2+ channels. These channels contribute to resting [Ca2+] and mediate action potential independent Ca2+ entry during sub-threshold oscillations.
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