D1 receptor agonist increases the availability of voltage-gated sodium currents in mPFC pyramidal neurons from adult rats

• Autorzy: Szulczyk B.
• Języki publikacji: EN

Abstrakty

EN

This abstract presents the effects of D1 receptor stimulation on action potentials and voltage-gated sodium currents in medial prefrontal cortex pyramidal neurons. Perforated-patch and cellattached recordings (macropatches) from neurons in slices were obtained from adult rats (9 weeks old). Fas synaptic transmission was blocked. Surprisingly, a D1 agonist (SKF 38393, 10 μM) did not significantly change the membrane potential of mPFC pyramidal neurons in perforated-patches. Also, the D1 receptor agonist influenced neither excitability nor single action potential properties of mPFC pyramidal neurons in perforated patches. The maximal amplitude of sodium currents was not influenced by the D1 receptor agonist (17.5 ± 1.9 pA in control and 17.9 ± 1.6 pA in the presence of SKF 38393, n=7, p>0.05). The potential of half-maximal activation (V0.5) was more negative after D1 receptor stimulation (-8.2 ± 2.5 mV in control and -17.8 ± 1.5 mV in the presence of SKF 38393, n=7, p<0.05). Moreover, given depolarization step activated bigger fraction of available current after D1 receptor stimulation (0.98 ± 0.03) than in control (0.62 ± 0.07, -5 mV depolarization step, n=7, p<0.05). The effects were absent with D1 receptor antagonist (SCH 23390) in the bath. In the presence of the antagonist the potential of half maximal activation was -11.6 ± 1.7 mV in control and -9.6 ± 2.6 mV in the presence of SKF 38393 (n=3, p>0.05). Moreover the D1 receptor agonist did not exert its effects on sodium channels activation curve in the presence of kinase A and kinase C antagonists. This suggests that these two kinases are involved in the signal transduction pathway from the D1 receptor. The up-regulation of sodium channels may enhance persistent activity in mPFC pyramidal neurons from adult rats. Supported by MniSzW, grant No N N401 03 0037.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2011
• Tom: 71
• Numer: S
• Opis fizyczny: p.50

Twórcy

autor

Szulczyk B.

• Department of Physiology and Pathophysiology, Medical University of Warsaw, Warsaw, Poland

Uwagi

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