Developmental changes in the expression of low-voltage-activated Ca2+ channels in rat visual cortical neurones.

1. The functional properties of low-voltage-activated (LVA) Ca2+ channels were studied in pyramidal neurones from different rat visual cortical layers in order to investigate changes in their properties during early postnatal development. Ca2+ currents were recorded in brain slices using the whole-cell patch-clamp technique in rats from three age groups: 2, 3 and 12 days old (postnatal day (P) 2, P3 and P12). 2. It was demonstrated that LVA Ca2+ currents are present in neurones from superficial (I-II) and deep (V-VI) visual cortex layers of P2 and P3 rats. No LVA Ca2+ currents were observed in neurones from the middle (III-IV) layers of these rats. The LVA Ca2+ currents observed in P2 and P3 neurones from both superficial and deep layers could be completely blocked by nifedipine (100 microM) and were insensitive to Ni2+ (25 microM). 3. The density of LVA Ca2+ currents decreased rapidly during the early stages of postnatal development, while the density of high-voltage-activated (HVA) Ca2+ currents progressively increased up to the twelfth postnatal day. No LVA Ca2+ currents were found in P12 neurones from any of the layers. Only HVA Ca2+ currents with high sensitivity to F- applied through the patch pipette were observed. 4. The kinetics of LVA Ca2+ currents could be well approximated by the m2h Hodgkin-Huxley equation with an inactivation time constant of 24 +/- 6 ms. The steady-state inactivation curve fitted by a Boltzmann function had the following parameters: membrane potential at half-inactivation, -86.9 mV; steepness coefficient,3.4 mV. 5. It is concluded that, in visual cortical neurones, LVA Ca2+ channels are expressed only in the neurones of deep and superficial layers over a short period during the earliest postnatal stages. These channels are nifedipine sensitive and similar in functional properties to those in the laterodorsal (LD) thalamic nucleus. However, the cortical neurones do not express another ('slow') type of LVA Ca2+ channel, which is permanently present in LD thalamic neurones after the second postnatal week, indicating that the developmental time course of cortical and thalamic cells is different.

Two types of low-voltage-activated Ca2+ channels in neurones of rat laterodorsal thalamic nucleus.

1. The pharmacological and kinetic properties of two types of low-voltage-activated (LVA) Ca2+ currents were studied in thalamocortical neurones of the laterodorsal (LD) thalamic nucleus during early postnatal development. The whole-cell patch-clamp technique was used on brain slices from rats of three age groups: 12, 14 and 17 days old (postnatal day (P) 12, P14 and P17). 2. In P12 neurones, the population of LVA Ca2+ channels was homogeneous. LVA Ca2+ current elicited by depolarizing voltage steps from a holding potential more negative than -70 mV was sensitive to nifedipine (Kd = 2.6 microM). This current reached a maximum at about -55 mV and had a fast monoexponential decay with a time constant, tau h,f, of 32.3 +/- 4.0 ms. 3. The population of LVA Ca2+ channels in P14 and P17 neurones was found to be heterogeneous. A subpopulation of nifedipine-insensitive LVA Ca2+ channels was observed. The current-voltage curve of the Ca2+ current had a characteristic hump with two peaks at about -65 and -55 mV. As well as the fast component (designated IT,f), the decay of the LVA current also included a slow component (designated IT,s), with inactivation time constants (tau h,s) of 54.2 +/- 4.5 and 68.6 +/- 3.17 ms for P14 and P17 neurones, respectively. 4. The kinetics of both components could be well approximated by the m2h Hodgkin-Huxley equation. No significant difference in activation kinetics was observed. The activation time constants for the fast (tau m,f) and slow (tau m,s) components were 6.3 +/- 1.0 and 7.3 +/- 1.5 ms, respectively. 5. La3+ at a concentration of 1 microM effectively blocked the IT,f component but Ni2+ (25 microM) completely eliminated the IT,s component. 6. Steady-state inactivation curves of both components could be best fitted by a Boltzmann function with membrane potential values at half-maximal inactivation of -85.5 and -98.1 mV for the fast and slow components, respectively. 7. It was concluded that two different subtypes of LVA Ca2+ channel are present in LD neurones. Only the fast type is well expressed at the earliest postnatal stage (P12). The slow type could be found at the end of the second week (P14). The amplitude of the slow current increased progressively up to P17, obviously coinciding with dendritic expansion as judged by progressive increase of the membrane capacitance of the corresponding neurones. This property appears to differentiate neurones of the associative nuclei from neurones of other thalamic nuclei.

[Effect of a catalytic subunit of cAMP-dependent protein kinase on acetylcholine-induced chloride currents in mollusk neurons]. / Vliianie kataliticheskoi sub"edinitsy tsAMP-zavisimoi proteinkinazy na atsetilkholinindutsiruemye khlornye tochki v neironakh molliuska.

It is shown that the amplitude of ACh-induced chloride currents decreases with introduction of cAMP in dialyzed neurons of Helix pomatia, the rate of desensitization of the acetylcholine receptors (AChR) being insignificantly changed. Introduction of an active catalytic subunit (c.s.) of cAMP-dependent protein kinase (cAMP-PK) mimics this effect. It is supposed that the influence of cAMP on the functional properties of the AChR is mediated by the activation of cAMP-PK and further phosphorylation of the AChR by the catalytic subunits of this protein kinase.