TY - JOUR
T1 - Age-related functional changes of high-voltage-activated calcium channels in different neuronal subtypes of mouse striatum
AU - Martella, G.
AU - Spadoni, F.
AU - Sciamanna, G.
AU - Tassone, A.
AU - Bernardi, G.
AU - Pisani, A.
AU - Bonsi, P.
PY - 2008/3/18
Y1 - 2008/3/18
N2 - By means of whole-cell patch-clamp recordings, we characterized the developmental profile of high-voltage-activated (HVA) calcium (Ca2+) channel subtypes in distinct neuronal populations of mouse striatum. Acutely dissociated medium spiny neurons (MSNs) and cholinergic interneurons (ChIs) were recorded from mice at five developmental stages: postnatal-days (PD) 14, 23, 40, 150 and 270. During ageing, total HVA Ca2+ current recorded from both MSNs and ChIs was unchanged. However, the pharmacological analysis of the differential contribution of HVA Ca2+ channel subtypes showed a significant rearrangement of each component. In both neuronal subtypes, a large fraction of the total HVA current recorded from PD14 mice was inhibited by the L-type HVA channel blocker nifedipine. This dihydropyridine-sensitive component accounted for nearly 50%, in MSNs, and 35%, in ChIs, of total current at PD14, but its contribution was down-regulated up to 20-25% at 9 months. Likewise, the N-type, ω-conotoxin GVIA-sensitive component decreased from 35% to 40% to about 25% in MSNs and 15% in ChIs. The P-type, ω-agatoxin-sensitive fraction did not show significant changes in both neuronal subtypes, whereas the Q-type, ω-conotoxin MVIIC-sensitive channels did show a significant up-regulation at 9 months. As compared with striatal neurons, we recorded pyramidal neurons dissociated from cortical layers IV-V and found no significant developmental change in the different components of HVA Ca2+ currents. In conclusion, our data demonstrate a functional reconfiguration of HVA Ca2+ channels in striatal but not cortical pyramidal neurons during mouse development. Such changes might have profound implications for physiological and pathophysiological processes of the striatum.
AB - By means of whole-cell patch-clamp recordings, we characterized the developmental profile of high-voltage-activated (HVA) calcium (Ca2+) channel subtypes in distinct neuronal populations of mouse striatum. Acutely dissociated medium spiny neurons (MSNs) and cholinergic interneurons (ChIs) were recorded from mice at five developmental stages: postnatal-days (PD) 14, 23, 40, 150 and 270. During ageing, total HVA Ca2+ current recorded from both MSNs and ChIs was unchanged. However, the pharmacological analysis of the differential contribution of HVA Ca2+ channel subtypes showed a significant rearrangement of each component. In both neuronal subtypes, a large fraction of the total HVA current recorded from PD14 mice was inhibited by the L-type HVA channel blocker nifedipine. This dihydropyridine-sensitive component accounted for nearly 50%, in MSNs, and 35%, in ChIs, of total current at PD14, but its contribution was down-regulated up to 20-25% at 9 months. Likewise, the N-type, ω-conotoxin GVIA-sensitive component decreased from 35% to 40% to about 25% in MSNs and 15% in ChIs. The P-type, ω-agatoxin-sensitive fraction did not show significant changes in both neuronal subtypes, whereas the Q-type, ω-conotoxin MVIIC-sensitive channels did show a significant up-regulation at 9 months. As compared with striatal neurons, we recorded pyramidal neurons dissociated from cortical layers IV-V and found no significant developmental change in the different components of HVA Ca2+ currents. In conclusion, our data demonstrate a functional reconfiguration of HVA Ca2+ channels in striatal but not cortical pyramidal neurons during mouse development. Such changes might have profound implications for physiological and pathophysiological processes of the striatum.
KW - basal ganglia
KW - cholinergic interneuron
KW - cortical pyramidal neuron
KW - development
KW - medium spiny neuron
KW - patch-clamp
UR - http://www.scopus.com/inward/record.url?scp=40849100052&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=40849100052&partnerID=8YFLogxK
U2 - 10.1016/j.neuroscience.2007.12.040
DO - 10.1016/j.neuroscience.2007.12.040
M3 - Article
C2 - 18262727
AN - SCOPUS:40849100052
VL - 152
SP - 469
EP - 476
JO - Neuroscience
JF - Neuroscience
SN - 0306-4522
IS - 2
ER -