Találati lista | Tudóstér

001-es BibID:	BIBFORM120025
035-os BibID:	(Scopus)85190380483 (WoS)001200847200001
Első szerző:	Csemer Andrea (molekuláris biológus)
Cím:	Pharmacological Activation of Piezo1 Channels Enhances Astrocyte-Neuron Communication via NMDA Receptors in the Murine Neocortex / Andrea Csemer, Cintia Sokvári, Baneen Maamrah, László Szabó, Kristóf Korpás, Krisztina Pocsai, Balázs Pál
Dátum:	2024
ISSN:	1422-0067
Megjegyzések:	The Piezo1 mechanosensitive ion channel is abundant on several elements of the central nervous system including astrocytes. It has been already demonstrated that activation of these channels is able to elicit calcium waves on astrocytes, which contributes to the release of gliotransmitters. Astrocyte- and N-methyl-D-aspartate (NMDA) receptor-dependent slow inward currents (SICs) are hallmarks of astrocyte?neuron communication. These currents are triggered by glutamate released as gliotransmitter, which in turn activates neuronal NMDA receptors responsible for this inward current having slower kinetics than any synaptic events. In this project, we aimed to investigate whether Piezo1 activation and inhibition is able to alter spontaneous SIC activity of murine neocortical pyramidal neurons. When the Piezo1 opener Yoda1 was applied, the SIC frequency and the charge transfer by these events in a minute time was significantly increased. These changes were prevented by treating the preparations with the NMDA receptor inhibitor D-AP5. Furthermore, Yoda1 did not alter the spontaneous EPSC frequency and amplitude when SICs were absent. The Piezo1 inhibitor Dooku1 effectively reverted the actions of Yoda1 and decreased the rise time of SICs when applied alone. In conclusion, activation of Piezo1 channels is able to alter astrocyte?neuron communication. Via enhancement of SIC activity, astrocytic Piezo1 channels have the capacity to determine neuronal excitability.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk slow inward current NMDA receptor astrocyte Piezo1 Yoda1 Dooku1 neocortex pyramidal cell glutamate
Megjelenés:	International Journal Of Molecular Sciences. - 25 : 7 (2024), p. 3994. -
További szerzők:	Sokvári Cintia (1995-) Maamrah, Baneen (1994-) (molekuláris biológus) Szabó László (1994-) (molekuláris biológus) Korpás Kristóf Levente (1998-) (orvostanhallgató) Pocsai Krisztina (1978-) (élettanász) Pál Balázs (1975-) (élettanász)
Pályázati támogatás:	TKP2020-NKA-04 Egyéb 2020-4.1.1-TKP2020 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM099802
035-os BibID:	(scopus)85122782091 (wos)000757677800001
Első szerző:	Gönczi Mónika (élettanász)
Cím:	Astaxanthin Exerts Anabolic Effects via Pleiotropic Modulation of the Excitable Tissue / Gönczi Mónika, Csemer Andrea, Szabó László, Sztretye Mónika, Fodor János, Pocsai Krisztina, Szenthe Kálmán, Keller-Pintér Anikó, Köhler Zoltán Márton, Nánási Péter, Szentandrássy Norbert, Pál Balázs, Csernoch László
Dátum:	2022
ISSN:	1661-6596 1422-0067
Megjegyzések:	Astaxanthin is a lipid-soluble carotenoid influencing lipid metabolism, body weight, and insulin sensitivity. We provide a systematic analysis of acute and chronic effects of astaxanthin on different organs. Changes by chronic astaxanthin feeding were analyzed on general metabolism, expression of regulatory proteins in the skeletal muscle, as well as changes of excitation and synaptic activity in the hypothalamic arcuate nucleus of mice. Acute responses were also tested on canine cardiac muscle and different neuronal populations of the hypothalamic arcuate nucleus in mice. Dietary astaxanthin significantly increased food intake. It also increased protein levels affecting glucose metabolism and fatty acid biosynthesis in skeletal muscle. Inhibitory inputs innervating neurons of the arcuate nucleus regulating metabolism and food intake were strengthened by both acute and chronic astaxanthin treatment. Astaxanthin moderately shortened cardiac action potentials, depressed their plateau potential, and reduced the maximal rate of depolarization. Based on its complex actions on metabolism and food intake, our data support the previous findings that astaxanthin is suitable for supplementing the diet of patients with disturbances in energy homeostasis.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk astaxanthin metabolism food intake gene expression skeletal muscle cardiac action potential arcuate nucleus excitability inhibitory postsynaptic current
Megjelenés:	International Journal Of Molecular Sciences. - 23 : 2 (2022), p. 917. -
További szerzők:	Csemer Andrea (1994-) (molekuláris biológus) Szabó László (1994-) (molekuláris biológus) Sztretye Mónika (1981-) (élettanász, elektrofiziológus) Fodor János (1973-) (élettanász, biotechnológus) Pocsai Krisztina (1978-) (élettanász) Szenthe Kálmán Keller-Pintér Anikó Köhler Zoltán Márton Nánási Péter Pál (1956-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Pál Balázs (1975-) (élettanász) Csernoch László (1961-) (élettanász)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00040 GINOP GINOP-2.3.3-15-2016-00020 GINOP NKFI FK 134684 Egyéb NKFIH PD-128370 Egyéb OTKA-115397 OTKA NKFIH K 138090 Egyéb EFOP-3.6.3-VEKOP-16-2017-00009 EFOP EFOP-3.6.2-16-2017-00006 EFOP TKP2020-IKA-04 Egyéb 2020-4.1.1-TKP2020 Egyéb TKP-2020-NKA-04 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM130038
Első szerző:	Maamrah, Baneen (molekuláris biológus)
Cím:	Chronic Chemogenetic Activation of Astrocytes in the Murine Mesopontine Region Leads to Disturbances in Circadian Activity and Movement / Maamrah Baneen, Pocsai Krisztina, Hoang Bui Minh, Abdelhadi Ali, Al-Khafaji Mustafa Qais, Csemer Andrea, Sokvári Cintia, Szentesi Péter, Pál Balázs
Dátum:	2025
ISSN:	1661-6596 1422-0067
Megjegyzések:	We have previously shown that neuromodulatory actions on astrocytes can elicit metabotropic glutamate- and N-methyl-D-aspartate receptor-dependent tonic changes in excitability in the mesopontine region. Although in vitro experiments explored robust effects, the in vivo significance of our findings remained unknown. In this project, chronic chemogenetic activation of mesopontine astrocytes and its actions on movement, circadian activity, acoustic startle and spatial memory were tested. The control group of young adult male mice where mesopontine astrocytes expressed only the mCherry fluorescent tag was compared to the group expressing the hM3D(Gq) chemogenetic actuator. Chronic chemogenetic astrocyte activation reduced the amplitude of the acoustic startle reflex and increased the locomotion speed in the resting period. Gait alterations were also demonstrated but no change in the spatial memory was explored. As a potential background of these findings, chronic astrocytic activation decreased the cholinergic neuronal number to 54% and reduced the non-cholinergic neuronal number to 76% of the control. In conclusion, chronic astrocytic activation and the consequential decrease in the neuronal number led to disturbances in movement and circadian activity resembling brainstem-related symptoms of progressive supranuclear palsy, raising the possibility that astrocytic overactivation is involved in the pathogenesis of this disease.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk astrocyte pedunculopontine nucleus mesopontine region chemogenetics acoustic startle activity cycles gait spatial memory
Megjelenés:	International Journal Of Molecular Sciences. - 26 : 10 (2025), p. 1-21. -
További szerzők:	Pocsai Krisztina (1978-) (élettanász) Hoang, Bui Minh Abdelhadi, Ali Al-Khafaji, Mustafa Qais Muhsin Csemer Andrea (1994-) (molekuláris biológus) Sokvári Cintia (1995-) Szentesi Péter (1967-) (élettanász) Pál Balázs (1975-) (élettanász)
Pályázati támogatás:	K146873 OTKA Stipendium Hungaricum PhD program Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: