S. Watanabe et al., DIFFERENTIAL ROLES OF 2 TYPES OF VOLTAGE-GATED CA2+ CHANNELS IN THE DENDRITES OF RAT CEREBELLAR PURKINJE NEURONS, Brain research, 791(1-2), 1998, pp. 43-55
The distribution and function of voltage-gated Ca2+ channels in Purkin
je neurons in rat cerebellar slices were studied using simultaneous Ca
2+ imaging and whole-cell patch clamp recording techniques. Voltage-ga
ted Ca2+ channels were activated by applying depolarizing voltage step
s through the pipette attached at the soma in a voltage-clamp mode in
the presence of tetrodotoxin. Poor space clamp due to extensive arbori
zation of the dendrites allowed the dendrites to fire Ca2+ spikes. Ca2
+ imaging with Fura-2 injected through the pipette, showed a steady [C
a2+](i) increase at the soma and transient, spike-linked [Ca2+](i) jum
ps in the dendrites. omega-Agatoxin-IVA (200 nM) abolished the depolar
ization-induced Ca2+ spikes, the spike-linked [Ca2+](i) increase in th
e dendrites, and the steady [Ca2+](i) increase at the soma. omega-Cono
toxin-GVIA (5 mu M) and nifedipine (3 mu M) had no significant effect
on the depolarization-induced responses. In the presence of 4-aminopyr
idine(2 mM) and omega-Agatoxin-IVA, transient [Ca2+](i) increases rema
ined in the dendrites. Low concentrations of Ni2+(100 mu M) reversibly
suppressed this [Ca2+](i) increase. The voltage for half-maximal acti
vation and inactivation of this component were lower than -50 mV and -
31 mV, respectively. in normal conditions, low concentration of Ni2+ s
lowed the onset of the Ca2+ spike without changing the time course of
the spikes or the amplitude of the accompanying [Ca2+](i) increase. Th
ese results show that omega-Agatoxin-IVA-sensitive Ca2+ channels are d
istributed both in the soma and the dendrites, and are responsible for
dendritic Ca2+ spikes, whereas low-voltage activated, Ni2+-sensitive
Ca2+ channels are distributed in the whole dendrites including both th
ick and fine branches, and provide boosting current for spike generati
on. (C) 1998 Elsevier Science B.V.