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1

Rebound depolarization (RD) in medial prefrontal cortex (mPFC) pyramidal neurons

100%
Kurowski P. N., Szulczyk P. J.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
INTRODUCTION: Rebound depolarization (RD) is an evoked membrane depolarization following the hyperpolarization of a neuron that converts an arriving inhibitory signal into cell excitation, which is subsequently transmitted to other neurons. RD is involved in the rhythmic discharges and oscillations of cortical neurons. AIM(S): The aim of this study was to clarify the intrinsic mechanism responsible for RD in medial prefrontal cortex (mPFC) pyramidal neurons. METHOD(S): Experiments were performed on layer V mPFC pyramidal neurons in slices obtained from 60-day-old rats. Recordings of membrane potential were performed in whole‑cell current‑clamp configuration in the absence of Ca2+ ions and in the presence of tetrodotoxin (TTX), glutamatergic and GABAergic blockers in extracellular solution. RESULTS: The resting membrane potential in tested neurons was −67.3±0.95 mV (n=154). RD exhibited the following properties: evoked after prior cell hyperpolarization below −80 mV, a threshold of −63.8±1.3 mV, an amplitude of 33.2±1.7 mV above the resting membrane potential, a duration of 552.7±43.1 ms, and dependence on inward TTX-resistant Na+ current. RD was abolished when pyramidal neurons were treated with Nav1.9 antibodies. RD was only evoked in the absence of Ca2+ in the extracellular solution or in the presence of Ca2+ together with a BK-type Ca2+-dependent K+ channel current blocker (paxilline, 10 µM) in the extracellular solution. CONCLUSIONS: The obtained results suggest that hyperpolarization-dependent RD in layer V mPFC pyramidal neurons is evoked by the de-inactivation and subsequent activation of a voltage-dependent, low-threshold and TTX-resistant, inward Nav1.9-like Na+ current. In the presence of Ca2+ ions in the extracellular solution, RD was suppressed due to the activation of BK channel currents. FINANCIAL SUPPORT: The study was supported by National Science Centre (Poland) grant no: 2015/17/N/ NZ4/02889.
2

Direct action of noradrenaline on the medial prefrontal cortex (mPFC) pyramidal neurons in young rats

100%
Grzelka K., Szulczyk P. J.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Noradrenaline (NA) and adrenergic receptors (α1, α2 and β) are crucial in regulating medial prefrontal cortex (mPFC) functions. Impaired modulation of the mPFC by NA has been implicated in many neuropsychiatric diseases, e.g. posttraumatic stress disorder, attention deficit hyperactivity disorder, depression. However, the mechanisms by which NA modulates mPFC neurons are not well understood. AIM(S): The aim of this study was to investigate which adrenergic receptor subtype controls the resting membrane potential and holding currents in mPFC neurons and what are the cellular mechanisms underpinning the effects of NA. METHOD(S): The resting membrane potential and holding currents were recorded in layer V mPFC pyramidal neurons. Gramicidin perforated-patch and classical whole-cell recordings were obtained from neurons in brain slices of young rats. Tested compounds were applied to the bath and/or to the solution in the recording pipette. RESULTS: NA evoked depolarization of the membrane potential and the inward holding current. Stimulation of α1‑ and α2‑receptors failed to evoke similar effects. Meanwhile, the nonselective β‑receptor agonist as well as the selective β1‑receptor agonist mimicked the effect of NA on holding currents. The NA-dependent inward current was considerably reduced by the selective β1‑receptor antagonist. The β1‑related inward current was significantly decreased in the presence of Cs+ ions and the selective blocker of HCN channels – ZD7288. It was not affected by selective blockers of different signaling pathways known to be responsible for mediating the effects from β‑receptors (e.g. adenylyl cyclase-PKA, PLC-PKC, protein tyrosine kinases). CONCLUSIONS: We conclude that NA changes the membrane potential/holding currents of the mPFC pyramidal neurons acting via β1‑receptors. The effects occur due to HCN channel activation and are not mediated by the classical signaling pathways. FINANCIAL SUPPORT: Supported by National Science Centre, Poland, grant 2014/15/N/NZ4/04760 and FW5/ PM2/16.
3

Properties of calcium currents in cardiac postganglionic sympathetic neurones

81%
Kukwa W., Macioch T., Szulczyk P. J.
Acta Neurobiologiae Experimentalis
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1999
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tom 59
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nr 3
4

Distribution of compound potentials recorded from the surface of isolated stellate ganglia following stimulation of postganglionic branches, in rats and cats

80%
Kukula K., Szulczyk P. J., Urbanowicz A.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
|
nr 2
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