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001-es BibID:	BIBFORM120025
035-os BibID:	(cikkazonosító)3994
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
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001-es BibID:	BIBFORM113771
035-os BibID:	(cikkazonosító)e13939 (WOS)001035767500001 (Scopus)85165549817
Első szerző:	Csemer Andrea (molekuláris biológus)
Cím:	Astrocyte- and NMDA receptor-dependent slow inward currents differently contribute to synaptic plasticity in an age-dependent manner in mouse and human neocortex / Csemer Andrea, Kovács Adrienn, Maamrah Baneen, Pocsai Krisztina, Korpás Kristóf, Klekner Álmos, Szücs Péter, Nánási Péter P., Pál Balázs
Dátum:	2023
ISSN:	1474-9718 1474-9726
Megjegyzések:	Slow inward currents (SICs) are known as excitatory events of neurons elicited by astrocytic glutamate via activation of extrasynaptic NMDA receptors. By using slice electrophysiology, we tried to provide evidence that SICs can elicit synaptic plasticity. Age dependence of SICs and their impact on synaptic plasticity was also investigated in both on murine and human cortical slices. It was found that SICs can induce a moderate synaptic plasticity, with features similar to spike timing-dependent plasticity. Overall SIC activity showed a clear decline with aging in humans and completely disappeared above a cutoff age. In conclusion, while SICs contribute to a form of astrocyte-dependent synaptic plasticity both in mice and humans, this plasticity is differentially affected by aging. Thus, SICs are likely to play an important role in age-dependent physiological and pathological alterations of synaptic plasticity.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk NMDA receptor aging astrocyte human brain neocortex pyramidal cell slow inward current synaptic plasticity
Megjelenés:	Aging Cell. - 22 : 9 (2023), p. e13939. -
További szerzők:	Kovács Adrienn (1989-) (molekuláris biológus) Maamrah, Baneen (1994-) (molekuláris biológus) Pocsai Krisztina (1978-) (élettanász) Korpás Kristóf Levente (1998-) (orvostanhallgató) Klekner Álmos (1970-) (idegsebész) Szűcs Péter (1974-) (kutatóorvos) Nánási Péter Pál (1956-) (élettanász) Pál Balázs (1975-) (élettanász)
Pályázati támogatás:	138090 OTKA 2020-4.1.1-TKP2020 Egyéb 2017-1.2.1-NKP-2017-00002 Egyéb KTIA_NAP_13-2-2014-0005 Egyéb KTIA_13_NAP-A-I/10 Egyéb Stipendium Hungaricum PhD program Egyéb NKFIH-K138090 Egyéb
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001-es BibID:	BIBFORM109964
035-os BibID:	(scopus)85148082398 (wos)000935540500006
Első szerző:	Maamrah, Baneen (molekuláris biológus)
Cím:	KCNQ4 potassium channel subunit deletion leads to exaggerated acoustic startle reflex in mice / Maamrah Baneen, Pocsai Krisztina, Bayasgalan Tsogbadrakh, Csemer Andrea, Pál Balázs
Dátum:	2023
ISSN:	0959-4965
Megjegyzések:	The potassium voltage-gated channel subfamily Q member 4 (KCNQ4) subunit forms channels responsible for M-current, a muscarine-sensitive potassium current regulating neuronal excitability. In contrast to other KCNQ subunits, its expression is restricted to the cochlear outer hair cells, the auditory brainstem and other brainstem nuclei in a great overlap with structures involved in startle reflex. We aimed to show whether startle reflexis affected by the loss of KCNQ4 subunit and whether these alterations are similar to the ones caused by brainstem hyperexcitability. Young adult KCNQ4 knockout mice and wild-type littermates, as well as mice expressing hM3D chemogenetic actuator in the pontine caudal nucleus and neurons innervating it were used for testing acoustic startle. The acoustic startle reflex was significantly increased in knockout mice compared with wild-type littermates. When mice expressing human M3 muscarinic (hM3D) in nuclei related to startle reflex were tested, a similar increase of the first acoustic startle amplitude and a strong habituation of the further responses was demonstrated. We found that the acoustic startle reflex is exaggerated and minimal habituation occurs in KCNQ4 knockout animals. These changes are distinct from the effects of the hyperexcitability of nuclei involved in startle. One can conclude that the exaggerated startle reflex found with the KCNQ4 subunit deletion is the consequence of both the cochlear damage and the changes in neuronal excitability of startle networks.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Neuroreport. - 34 : 4 (2023), p. 232-237. -
További szerzők:	Pocsai Krisztina (1978-) (élettanász) Bayasgalan, Tsogbadrakh (1983-) (Általános orvos) Csemer Andrea (1994-) (molekuláris biológus) 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
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