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1

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

100%
Szulczyk B.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
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.
2

Therapeutic concentrations of valproic acid inhibit fast TTX-sensitive voltage-gated sodium channels in prefrontal cortex pyramidal neurons

100%
Szulczyk B.
Acta Neurobiologiae Experimentalis
|
2018
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tom 78
|
nr Suppl.1
Valproic acid is a widely used antiepileptic and mood‑stabilizing drug. Its mechanism of action has not been fully elucidated. The aim of this study was to test the effect of different therapeutic concen‑ trations of valproic acid on fast TTX‑sensitive volt‑ age‑gated sodium channels. These channels play a very important role in neuronal physiology and in epileptic activity. Voltage‑gated sodium currents were recorded using the voltage‑clamp technique. Dispersed prefrontal cortical pyramidal neurons were tested. At a –90 mV holding potential, valpro‑ ic acid (200 μM) slightly inhibited the maximal am‑ plitude of sodium channels. The effect of the drug on the maximal amplitude of sodium currents was much more pronounced when a –50 mV depolarized holding potential was applied. At this holding po‑ tential, three doses were tested: 200 µM, 2 µM and 0,02 µM. Valproic acid did not influence activation but shifted the inactivation curve of fast voltage‑gat‑ ed sodium channels towards hyperpolarization. This means that the sodium channels were inhibited by valproate over the range of membrane potentials. Recovery from inactivation was the same in the con‑ trol and in the presence of valproic acid. Use‑de‑ pendent blockade was tested at 10 Hz and 50 Hz. In every condition, valproic acid did not influence the use‑dependent blockade. The main finding of this study is that therapeutic concentrations of valproic acid inhibit fast voltage‑gated TTX‑sensitive sodium currents when they are evoked from a depolarized holding potential. Thus, fast voltage‑gated sodium channels contribute to the pharmacological effect of valproate.
3

Somatic and dendritic perforated-patch recordings reveal b-adrenergic receptor-induced depolarization in medial prefrontal cortex pyramidal neurons

100%
Szulczyk B.
Acta Neurobiologiae Experimentalis
|
2016
|
tom 76
|
nr 2
The aim of this perforated-patch study was to test the effect of isoproterenol on the membrane potential in mPFC (medial prefrontal cortex) pyramidal neurons. Isoproterenol depolarized the membrane potential recorded from the soma. This effect was absent in the presence of metoprolol, suggesting the involvement of β1-adrenergic receptors. The adenylate cyclase activator forskolin also depolarized the membrane potential. Moreover, the effect of isoproterenol was abolished by the adenylate cyclase inhibitor SQ 22536. This suggested that adenylate cyclase was involved in mediating the effect of the β-adrenergic receptor agonist. The isoproterenol-induced depolarization persisted after inhibition of protein kinase A with H-89. The effect of β-adrenergic receptor activation on the membrane potential was dependent on Ih channels because it was abolished in the presence of the Ih channel inhibitor ZD 7288. Dendritic recordings were also performed. In the dendritic segments between 100 μm and 150 μm from the soma and between 200 μm and 250 μm from the soma, isoproterenol also depolarized the membrane potential. The magnitude of the β-adrenergic receptor-stimulated depolarization was the same in the soma and in both dendritic localizations. The depolarization exerted by isoproterenol may influence PFC cognitive functions.
4

Beta-receptor agonist increases voltage-gated Naplus currents in medial prefrontal cortex pyramidal neurons

100%
Szulczyk B.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 3
Voltage-gated Na+ currents were recorded in cell-attached configuration from mPFC pyramidal neurons in slices obtained from 3-weeks-old rats. Isoproterenol (2 µM) did not influence maximal amplitude of Na+ currents (43.7±8.6 pA in control and 41.6±8.1 pA in the presence of the drug, P>0.05, n=9). The β-receptor agonist however increased submaximal Na+ currents (145±6.0% after β-receptor stimulation vs. 100% in control, P<0.001, n=10). This effect was abolished by β-receptor antagonist propranolol (30–60 µM). Isoproterenol (2 µM) depolarized the membrane potential recorded in perforated-patch configuration (−71.7±3.5 mV in control and −69.5±3.9 mV in the presence of the drug P<0.05, n=3). This depolarization was absent when cesium ions (3 mM) were added to the bath. It is concluded that isoproterenol increses submaximal voltage-gated Na+ currents in mPFC pyramidal neurons.
5

Effects of D1 receptor agonist on voltage-gated sodium currents in mPFC pyramidal neurons in rats of different ages

63%
Szulczyk B., Grzelka K.
Acta Neurobiologiae Experimentalis
|
2012
|
tom 72
|
nr 2
We recorded voltage-gated Na+ currents from mPFC pyramidal neurons in slices. The recordings were made in cell-attached configuration (macropatches) in young (3-weeks-old) and adult (9-weeks-old) rats. Fast synaptic transmission was blocked. The maximal Na+ currents amplitude varied in different recordings because of different number of channels in different patches. The mean amplitude of Na+ currents was 16.7 ± 1.4 (n=45) in young rats and 8.4 ± 1.2 pA (n=45) in adult rats (P<0.001). Sodium currents of big amplitude were selected to test the effects of a D1 receptor agonist (SKF 38393 10 µM). In young rats the maximal sodium current amplitude was 28.9 ± 3.7 pA in control and 29.7 ± 3.8 pA in the presence of SKF 38393 (P>0.05, n=7). Moreover in young rats the potential of half-maximal activation (V0.5) was not significantly different in control and with SKF 38393 in the bath (−11.5 ± 1.9 mV and −14.7 ± 1.2 mV respectively, n=7, P>0.05).In adult rats the maximal sodium current amplitude was 33.5 ± 10 pA and 32.5 ± 8.9 pA in control and in the presence of SKF 38393 respectively (P>0.05, n=5). Also in adult rats the potential of halfmaximal activation was −11.9 ± 1.6 mV in control and −14.2 ± 1.8 mV with SKF 38393 in the bath (n=5, P<0.05). We suggest that D1 receptor agonist does not influence maximal Na+ currents and exerts small effects on their kinetic properties in rats of different ages. Supported by grant no. NCN/MNiSzW- N N401 030037.
6

Neuron czuciowy bolowy

51%
Szulczyk P., Rola R., Szulczyk B., Witkowski G.
Postępy Higieny i Medycyny Doświadczalnej
|
2002
|
tom 56
|
nr 3
361-375
7

Effect of dopamine receptor stimulation on voltage-dependent fast-inactivating Na plus currents in medial prefrontal cortex (mPFC) pyramidal neurons in adult rats

51%
Szulczyk B., Ksiazek A., Ladno W., Szulczyk P.
Acta Neurobiologiae Experimentalis
|
2012
|
tom 72
|
nr 4
Impaired working memory is a common feature of neuropsychiatry disorders. It is dependent on control of the medial prefrontal cortex (mPFC) neurons by dopamine. The purpose of this study was to test the effects of a D1/5-type dopamine receptor agonist (SKF 38393, 10 ^M) on the membrane potential and on voltage-dependent fast-inactivating Na+ currents in mPFC pyramidal neurons obtained from adult (9-week-old) rats. Treatment of the pyramidal neurons with SKF 38393 did not affect the membrane potential recorded with the perforated-patch method. When recordings were performed in cell- attached configuration, the application of SKF 38393 did not change the Na+ current amplitude and shifted the current- voltage relationship of the Na+ currents towards hyperpolarisation, thus resulting in an increase of the current amplitudes in response to suprathreshold depolarisations. Pretreatment of the cells with a D1/5 receptor antagonist (SCH 23390, 10 ^M) abolished the effect of the D1/5-type receptors on Na+ currents. The effect of the D1/5 agonist was replicated by treating the cells with a membrane-permeable analogue, cAMP (8-bromo-cAMP, 100 ^M), and the effect was blocked by treating the cells with a protein kinase A inhibitor, (H-89, 2 ^M). In recordings performed from mechanically and enzymatically dispersed pyramidal neurons in the whole-cell configuration, when the cell interior was dialysed with pipette solution, application of the D1/5 agonist decreased the Na+ current amplitude without changing the current-voltage relationship. We conclude that in the mPFC pyramidal neurons in slices with an intact intracellular environment (recordings in the cell-attached configuration), the activation of D1/5 dopamine receptors increases the fast-inactivating Na+ current availability in response to suprathreshold depolarisations. The maximum Na+ current amplitude was not changed. A cAMP/protein kinase A pathway was responsible for the signal transduction from the D1/5 dopamine receptors to the Na+ channels.
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