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1

Identyfikacja anatomiczna i funkcjonalna neuronow obwodowych w badaniach neurofizjologicznych

100%
Szulczyk P.
Postępy Higieny i Medycyny Doświadczalnej
|
2000
|
tom 54
|
nr 3
351-361
2

The effect of acute rise intracranial pressure on the sympathetic cardiac, vertebral and phrenic nerve acyitities

100%
Szulczyk P.
Acta Physiologica Polonica
|
1976
|
tom 27
|
nr 1
3

Functional organization of the sympathetic nervous system

100%
Szulczyk P.
Acta Physiologica Polonica
|
1981
|
tom 32
|
nr 2
4

Properties and latencies of potentials evoked in postganglionic sympathetic nerves by electrical stimulation of aortic, sinus and hypoglossal nerves in cats

100%
Szulczyk P.
Acta Neurobiologiae Experimentalis
|
1978
|
tom 38
|
nr 5
5

The local effect of pH changes in the cerebrospinal fluid on the ventrolateral areas of medulla oblongata and on spinal cord surface on the activity of cardiac and vertebral sympathetic nerves

63%
Szulczyk P., Trzebski A.
Acta Physiologica Polonica
|
1976
|
tom 27
|
nr 1
6

Effects of carotid chemoreceptor and baroreceptor stimulation upon the sympathetic preganglionic and postganglionic cardiac nerve and single fiber activity in cats

63%
Szulczyk P., Trzebski A.
Acta Neurobiologiae Experimentalis
|
1977
|
tom 37
|
nr 1
7

Properties of Na+ currents in muscle and skin vasoconstrictor sympathetic neurones in rats

63%
Rola R., Szulczyk P.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
8

Niektóre aspekty regulacji aktywności bioelektrycznej włókien współczulnych zaopatrujących układ krążenia krwi

63%
Szulczyk P., Trzebski A.
Acta Physiologica Polonica
|
1978
|
tom 29
|
nr Supl.17[5]
9

Spinal and supraspinal transmission time of the baro- and chemoreceptor reflex

63%
Janig W., Szulczyk P.
Acta Physiologica Polonica
|
1979
|
tom 30
|
nr 1
10

Effect of muscarinic receptors activation on membrane potential in medial prefrontal cortex (mPFC) pyramidal neurons

63%
Kurowski P. M., Szulczyk P.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 3
The aim of this study was to clarify the mechanisms involved in regulation of membrane potential in mPFC pyramidal neurons by muscarinic receptors. Recordings of membrane potential were performed with the gramicidin perforated-patch method on mPFC pyramidal neurons in slices obtained from 20-day-old rats. It was determined that muscarinic receptor stimulation by carbachol (100 µM) evoked membrane potential depolarization (10.0±1.3 mV), which was completely eliminated by the M1 receptor antagonist pirenzepine (2 µM), by removing Na+ ions from the extracellular solution, in the presence of a TTX-resistant Na+ channel blocker amitriptyline (100 µM) and significantly reduced by the inhibitor of G-protein βγ-subunits gallein (20 µM). We conclude that muscarinic M1 receptor-dependent depolarisation in mPFC pyramidal neurons is evoked by activation of TTX-resistance Na+ currents by G-protein βγ-subunits. Supported by grants no: NN401584638 and NN301572940
11

Alpha2-adrenergic mediation of membrane potential changes in medial prefrontal cortex (mPFC) pyramidal neurons in young rats

63%
Grzelka K., Szulczyk P.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUD AND AIMS: Impairment of the signal transduction from adrenergic receptors to cellular effectors in prefrontal cortex (PFC) neurons occurs in many neuropsychiatric disorders (acute stress disorder, ADHD). Application of clonidine (α2-adrenergic receptor agonist) evokes hyperpolarisation of the resting membrane potential in mPFC pyramidal neurons. The aim of the study was to define the cellular effectors and the exact signal transduction pathway from the receptor to the effector, which still remains unclear. METHODS: The membrane potential was recorded in layer V mPFC pyramidal neurons in slices isolated from 3-week-old rats. Recordings were performed in perforated-patch configuration at a temperature of 34°C. Adrenergic antagonists, inhibitors of cellular effectors and intracellular signalling were applied to the bath medium before, during and after clonidine application (100 µM). Their effects on clonidine-dependent membrane potential changes were analysed. RESULTS: The α2-receptor antagonists yohimbine (60 µM, n=15) and atipamezole (20 µM, n=6) did not completely block clonidinedependent hyperpolarisation. The effect of clonidine was attenuated by the blocker of hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels (ZD7288, 50 µM, n=10) and by the selective Na+ / K+ -ATPase inhibitor (ouabain, 100 µM, n=7). The hyperpolarisation was affected neither by the adenylyl cyclase inhibitor (SQ22536, 100 µM, n=6), protein kinase A inhibitor (H-89, 40 µM, n=6), phospholipase C inhibitor (U73122, 10 µM, n=7) nor the protein kinase C inhibitor (chelerythrine, 5 µM, n=5), but it was attenuated by the G-protein βγ-subunit inhibitor (gallein, 20 µM, n=12). CONCLUSIONS: α2-Adrenergic receptor activation evokes hyperpolarisation due to HCN channel inhibition and modification of the Na+ /K+ -ATPase function. The transduction pathway occurs in a membrane-delimited fashion and involves the Gβγ subunit released from the G-protein. Supported by grants no: NN401584638 and NN301572940.
12

Influence of clondine on cardiac vagal component of baroreceptor reflex in normotensive and spontaneously hypertensive rats

63%
Szulczyk P., Januszewicz P.
Acta Physiologica Polonica
|
1977
|
tom 28
|
nr 3
13

Control of membrane potential in medial prefrontal cortex (mPFC) pyramidal neurons by alpha2-adrenergic receptors in young rats

63%
Grzelka K., Szulczyk P.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 3
The aim was to clarify the effect of α2-adrenergic receptor activation on membrane potential, determine the cellular effector and the signal transduction pathway responsible for membrane potential changes. Recordings were made in slices in layer V mPFC pyramidal neurons in perforated-patch configuration at 33.8°C. Clonidine evoked a dose-dependent membrane hyperpolarisation. It was affected neither by the adenylyl cyclase inhibitor, protein kinase A inhibitor, phospholipase C inhibitor nor the protein kinase C inhibitor, but it was attenuated by the G-protein βγ-subunit inhibitor. The blocker of hyperpolarisation-activated cyclic nucleotidegated (HCN) channels abolished the hyperpolarisation and the α2-receptor antagonists reduced it. We conclude that α2-adrenergic receptor activation evokes hyperpolarisation in mPFC pyramidal neurons due to HCN channel inhibition in a membrane-delimited fashion by the Gβγ subunit released from the G-protein. Supported by NN401584638, NN301572940.
14

Participation of the supramedullary structures in escape mechanism of the sympathetic baroreceptor reflex

63%
Szulczyk P., Trzebski A.
Acta Physiologica Polonica
|
1979
|
tom 30
|
nr 1
15

The effect of stimulation of carotid sinus chemoreceptors on the activity of the sympathetic cardiac nerve and vertebral nerve

63%
Szulczyk P., Trzebski A.
Acta Physiologica Polonica
|
1975
|
tom 26
|
nr 5
16

Noradrenaline modulates the membrane potential in medial prefrontal cortex pyramidal neurons via β1-adrenergic receptors and HCN channels

51%
Grzelka K., Gawlak M., Szulczyk P.
Acta Neurobiologiae Experimentalis
|
2018
|
tom 78
|
nr Suppl.1
The noradrenergic system is essential in medial pre‑ frontal cortex (mPFC) physiology: noradrenaline (NA) acting via adrenergic receptors (α1, α2 and β) plays a sig‑ nificant role in the regulation of cognitive brain functions and affective processes. Impaired modulation of the mPFC by NA has been implicated in many neuropsychiatric dis‑ eases, e.g. posttraumatic stress disorder, attention deficit hyperactivity disorder, and depression. While the pres‑ ence of all adrenergic receptor subtypes has been report‑ ed in the mPFC, little is known regarding the mechanisms by which NA modulates mPFC neurons. The aim of this study was to investigate which adrenergic receptor sub‑ type controls the resting membrane potential and hold‑ ing currents in mPFC neurons. Secondly, we wanted to de‑ fine the cellular effector(s) and signaling pathway(s) in‑ volved in the action of NA. To answer these questions, we recorded the membrane potential and holding current us‑ ing patch‑clamp techniques. Gramicidin perforated‑patch and classical whole‑cell recordings were obtained from layer V mPFC pyramidal neurons in slices isolated from young rats. Distribution of the adrenergic receptor sub‑ types in mPFC was visualized with fluorescent immuno‑ histochemistry. NA evoked depolarization and inward cur‑ rent in the tested cells. Stimulation of α1‑ and α2‑receptors failed to evoke similar effects. Meanwhile, the nonselective β‑receptor agonist, as well as the selective β1‑receptor ag‑ onist, mimicked the effect of NA on holding current. The NA‑dependent inward current was considerably reduced by the selective β1‑receptor antagonist. The effect of NA was also attenuated, though to a smaller degree, by the se‑ lective β3‑receptor antagonist. At the same time, applica‑ tion of two different selective β3‑agonists evoked inward currentsin the tested neurons. Expression of β1‑ and β3‑re‑ ceptors in mPFC was confirmed with confocal microscopy. The β1‑related inward current was greatly decreased in the presence of Cs+ ions and ZD7288, a selective blocker of HCN (hyperpolarization‑activated cyclic nucleotide–gated) channels. It was not affected by selective blockers of dif‑ ferent signaling pathways known to be responsible for me‑ diating the effects from G‑protein‑coupled receptors (e.g. adenylyl cyclase‑PKA and phospholipase C‑PKC). However, it was significantly diminished by blockers of the βγ sub‑ unit‑dependent transduction system. We conclude that NA modulates the membrane potential and holding current of mPFC pyramidal neurons preferentially via β1‑receptors. The effects occur due to HCN channel activation and are probably mediated in a membrane delimited fashion by a βγ subunit released from the G‑protein. Stimulation of β3‑receptors may be partially responsible for the NA‑relat‑ ed effects. Supported by National Science Centre, Poland, grant 2014/15/N/NZ4/04760 and FW5/PM2/16.
17

Modulation of Caplus channel current by µ opioid receptors in prefrontal cortex pyramidal neurons in rats

51%
Rola R., Jarkiewicz M., Szulczyk P.
Acta Neurobiologiae Experimentalis
|
2008
|
tom 68
|
nr 1
Our work assesses the effects of µ opioid receptor activation on high-threshold Ca2+/Ba2+ currents in freshly dispersed pyramidal neurons of the medial prefrontal cortex in rats. Application of the specific µ receptor agonist (D-Ala2, N-Me-Phe4, Gly5-ol)-enkephalin (DAMGO) at 1 µM decreased Ca2+ current amplitudes from 0.72 to 0.49 nA. The effect was abolished by naloxone and ω-Conotoxin GVIA. Inhibition was not abolished by strong depolarisation of the cell membrane. In addition, a macroscopic Ba2+ current recorded in cell-attached configuration was inhibited when DAMGO was applied outside the patch pipette. An adenylyl cyclase inhibitor (SQ 22536) and a protein kinase A inhibitor (H-89) decreased Ca2+ current amplitude. Moreover, the inhibitory effect of µ opioid receptors on Ca2+ currents required the activation of protein kinase A. We conclude that activation of µ opioid receptors in medial prefrontal cortex pyramidal neurons inhibits N type Ca2+ channel currents, and that protein kinase A is involved in this transduction pathway.
18

Kinetic properties of leak channel currents in medial prefrontal cortex (mPFC) pyramidal neurons in rats

51%
Ksiazek A., Witkowski G., Szulczyk P.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
The prefrontal cortex is involved in cognitive function. It has been suggested that dysfunction of mPFC occurs in widespread neuropsychiatric disorders. The purpose of this study was to classify K+ channel currents along their kinetic properties in mPFC pyramidal neurons. Channel current recordings were performed from dispersed pyramidal neurons in cell-attached configuration in symmetrical K+ solutions. The kinetic properties of 100 channel currents were analysed. A total of 27% resembled leak, TREKlike channel currents. Their mean amplitude was 6.9 pA, dwell time was 1.31 ms, and NPo was 0.009 at -50 mV. Their outward and inward conductances were 160 and 150 pS, respectively. The channel currents were strongly mechanosensitive. A total of 27% resembled TASK-like channel currents. Their mean amplitude was 2.0 pA, dwell time was 0.58 ms and NPo 0.11 at -50 mV. Inward and outward conductances were 48 and 71 pS, respectively. A total of 34% were BK-like channel currents. Their amplitude was 5.8 pA, dwell time was 1.1 ms, and NPo was 0.03 at +25 mV. Their outward conductance was 177 pS. In cell-attached configuration, the BK channel currents were only outward. The application of Ca2+ ions from the intracellular side in inside-out configuration strongly activated these channels. A total of 5% channel currents were not classified. Surprisingly, we did not find voltage dependent K+ channel currents. We concluded that the leak-type channel currents could be important players in setting the level of membrane potential in mPFC pyramidal neurons.
19

Neuron czuciowy bolowy

51%
Szulczyk P., Rola R., Szulczyk B., Witkowski G.
Postępy Higieny i Medycyny Doświadczalnej
|
2002
|
tom 56
|
nr 3
361-375
20
Content available remote

Effect of cyclic adenosine monophosphate on the G protein-dependent inward rectifier Kplus-like channel current in medial prefrontal cortex pyramidal neurons

51%
Witkowski G., Rola R., Szulczyk P.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 5
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