Abstract
Neuronal voltage-gated Ca2+ channels are involved in electrical signalling and in converting these signals into cytoplasmic calcium changes. One important function of voltage-gated Ca2+ channels is generating regenerative dendritic Ca2+ spikes. However, the Ca2+ dependent mechanisms used to create these spikes are only partially understood. To start investigating this mechanism, we set out to kinetically and pharmacologically identify the sub-types of somatic voltage-gated Ca2+ channels in pyramidal neurons from layer 5 of rat somatosensory cortex, using the nucleated configuration of the patch-clamp technique. The activation kinetics of the total Ba2+ current revealed conductance activation only at medium and high voltages suggesting that T-type calcium channels were not present in the patches. Steady-state inactivation protocols in combination with pharmacology revealed the expression of R-type channels. Furthermore, pharmacological experiments identified 5 voltage-gated Ca2+ channel sub-types – L-, N-, R- and P/Q-type. Finally, the activation of the Ca2+ conductances was examined using physiologically derived voltage-clamp protocols including a calcium spike protocol and a mock back-propagating action potential (mBPAP) protocol. These experiments enable us to suggest the possible contribution of the five Ca2+ channel sub-types to Ca2+ current flow during activation under physiological conditions.
Highlights
Pyramidal neurons of layer 5 in the neocortex are the primary output cells of the cortex [1]
To unravel the role of voltage-gated Ca2+ channels in the backpropagating AP and the dendritic Ca2+ spike, we examined the properties of these channels in visually identified Layer 5 (L5) neocortical pyramidal neurons
We first developed the appropriate protocol for characterizing the properties of these channels and examined the activation kinetics of the general Ba2+ current
Summary
Pyramidal neurons of layer 5 in the neocortex are the primary output cells of the cortex [1] They express a wide variety of voltage-gated ion channels, such as Na+, K+ and Ca2+ channels, whose differing distribution and density in the cell membrane determine the unique functioning of each cell [2,3]. Depolarization of the cell membrane causes the channels to conduct Ca2+ into the cytoplasm, raising the intracellular Ca2+ concentration. This increase, in turn, modulates cellular processes such as regulation of Ca2+-dependent channels, mediating neurotransmitter release, possibly influencing generation of action potentials [5], and stimulating intracellular signalling enzymes and gene expression [6,7,8,9,10,11]
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