Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow
Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in C...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Negri, Sharon [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2021transfer abstract |
|---|
| Schlagwörter: |
|---|
| Übergeordnetes Werk: |
Enthalten in: Urological Diseases of the Byzantine Emperors (330-1453) - 2011, Amsterdam |
|---|---|
| Übergeordnetes Werk: |
volume:135 ; year:2021 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.biocel.2021.105983 |
|---|
| Katalog-ID: |
ELV054075920 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV054075920 | ||
| 003 | DE-627 | ||
| 005 | 20230626035640.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 210910s2021 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.biocel.2021.105983 |2 doi | |
| 028 | 5 | 2 | |a /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001396.pica |
| 035 | |a (DE-627)ELV054075920 | ||
| 035 | |a (ELSEVIER)S1357-2725(21)00068-6 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | 4 | |a 610 |q VZ |
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.85 |2 bkl | ||
| 100 | 1 | |a Negri, Sharon |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow |
| 264 | 1 | |c 2021transfer abstract | |
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. | ||
| 520 | |a Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. | ||
| 650 | 7 | |a TRPV4 channel |2 Elsevier | |
| 650 | 7 | |a Kir2.1 channels |2 Elsevier | |
| 650 | 7 | |a Cerebral blood flow |2 Elsevier | |
| 650 | 7 | |a GqPCRs |2 Elsevier | |
| 650 | 7 | |a NMDA receptors |2 Elsevier | |
| 650 | 7 | |a Neurovascular coupling |2 Elsevier | |
| 650 | 7 | |a Cerebrovascular endothelial cells |2 Elsevier | |
| 700 | 1 | |a Faris, Pawan |4 oth | |
| 700 | 1 | |a Soda, Teresa |4 oth | |
| 700 | 1 | |a Moccia, Francesco |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |t Urological Diseases of the Byzantine Emperors (330-1453) |d 2011 |g Amsterdam |w (DE-627)ELV010616845 |
| 773 | 1 | 8 | |g volume:135 |g year:2021 |g pages:0 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.biocel.2021.105983 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 936 | b | k | |a 44.85 |j Kardiologie |j Angiologie |q VZ |
| 951 | |a AR | ||
| 952 | |d 135 |j 2021 |h 0 | ||
| author_variant |
s n sn |
|---|---|
| matchkey_str |
negrisharonfarispawansodateresamocciafra:2021----:nohlasgaigthcronuoaclropigheegnrloedteilnadetfeki2canladmtydsatt |
| hierarchy_sort_str |
2021transfer abstract |
| bklnumber |
44.85 |
| publishDate |
2021 |
| allfields |
10.1016/j.biocel.2021.105983 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001396.pica (DE-627)ELV054075920 (ELSEVIER)S1357-2725(21)00068-6 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Negri, Sharon verfasserin aut Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells Elsevier Faris, Pawan oth Soda, Teresa oth Moccia, Francesco oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:135 year:2021 pages:0 https://doi.org/10.1016/j.biocel.2021.105983 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 135 2021 0 |
| spelling |
10.1016/j.biocel.2021.105983 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001396.pica (DE-627)ELV054075920 (ELSEVIER)S1357-2725(21)00068-6 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Negri, Sharon verfasserin aut Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells Elsevier Faris, Pawan oth Soda, Teresa oth Moccia, Francesco oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:135 year:2021 pages:0 https://doi.org/10.1016/j.biocel.2021.105983 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 135 2021 0 |
| allfields_unstemmed |
10.1016/j.biocel.2021.105983 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001396.pica (DE-627)ELV054075920 (ELSEVIER)S1357-2725(21)00068-6 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Negri, Sharon verfasserin aut Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells Elsevier Faris, Pawan oth Soda, Teresa oth Moccia, Francesco oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:135 year:2021 pages:0 https://doi.org/10.1016/j.biocel.2021.105983 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 135 2021 0 |
| allfieldsGer |
10.1016/j.biocel.2021.105983 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001396.pica (DE-627)ELV054075920 (ELSEVIER)S1357-2725(21)00068-6 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Negri, Sharon verfasserin aut Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells Elsevier Faris, Pawan oth Soda, Teresa oth Moccia, Francesco oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:135 year:2021 pages:0 https://doi.org/10.1016/j.biocel.2021.105983 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 135 2021 0 |
| allfieldsSound |
10.1016/j.biocel.2021.105983 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001396.pica (DE-627)ELV054075920 (ELSEVIER)S1357-2725(21)00068-6 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Negri, Sharon verfasserin aut Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells Elsevier Faris, Pawan oth Soda, Teresa oth Moccia, Francesco oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:135 year:2021 pages:0 https://doi.org/10.1016/j.biocel.2021.105983 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 135 2021 0 |
| language |
English |
| source |
Enthalten in Urological Diseases of the Byzantine Emperors (330-1453) Amsterdam volume:135 year:2021 pages:0 |
| sourceStr |
Enthalten in Urological Diseases of the Byzantine Emperors (330-1453) Amsterdam volume:135 year:2021 pages:0 |
| format_phy_str_mv |
Article |
| bklname |
Kardiologie Angiologie |
| institution |
findex.gbv.de |
| topic_facet |
TRPV4 channel Kir2.1 channels Cerebral blood flow GqPCRs NMDA receptors Neurovascular coupling Cerebrovascular endothelial cells |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Urological Diseases of the Byzantine Emperors (330-1453) |
| authorswithroles_txt_mv |
Negri, Sharon @@aut@@ Faris, Pawan @@oth@@ Soda, Teresa @@oth@@ Moccia, Francesco @@oth@@ |
| publishDateDaySort_date |
2021-01-01T00:00:00Z |
| hierarchy_top_id |
ELV010616845 |
| dewey-sort |
3610 |
| id |
ELV054075920 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV054075920</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626035640.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">210910s2021 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.biocel.2021.105983</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001396.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV054075920</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1357-2725(21)00068-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.85</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Negri, Sharon</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021transfer abstract</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TRPV4 channel</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Kir2.1 channels</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Cerebral blood flow</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GqPCRs</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NMDA receptors</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Neurovascular coupling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Cerebrovascular endothelial cells</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Faris, Pawan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Soda, Teresa</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Moccia, Francesco</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="t">Urological Diseases of the Byzantine Emperors (330-1453)</subfield><subfield code="d">2011</subfield><subfield code="g">Amsterdam</subfield><subfield code="w">(DE-627)ELV010616845</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:135</subfield><subfield code="g">year:2021</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.biocel.2021.105983</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.85</subfield><subfield code="j">Kardiologie</subfield><subfield code="j">Angiologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">135</subfield><subfield code="j">2021</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| author |
Negri, Sharon |
| spellingShingle |
Negri, Sharon ddc 610 bkl 44.85 Elsevier TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow |
| authorStr |
Negri, Sharon |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV010616845 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 VZ 44.85 bkl Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells Elsevier |
| topic |
ddc 610 bkl 44.85 Elsevier TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells |
| topic_unstemmed |
ddc 610 bkl 44.85 Elsevier TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells |
| topic_browse |
ddc 610 bkl 44.85 Elsevier TRPV4 channel Elsevier Kir2.1 channels Elsevier Cerebral blood flow Elsevier GqPCRs Elsevier NMDA receptors Elsevier Neurovascular coupling Elsevier Cerebrovascular endothelial cells |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
p f pf t s ts f m fm |
| hierarchy_parent_title |
Urological Diseases of the Byzantine Emperors (330-1453) |
| hierarchy_parent_id |
ELV010616845 |
| dewey-tens |
610 - Medicine & health |
| hierarchy_top_title |
Urological Diseases of the Byzantine Emperors (330-1453) |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV010616845 |
| title |
Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow |
| ctrlnum |
(DE-627)ELV054075920 (ELSEVIER)S1357-2725(21)00068-6 |
| title_full |
Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow |
| author_sort |
Negri, Sharon |
| journal |
Urological Diseases of the Byzantine Emperors (330-1453) |
| journalStr |
Urological Diseases of the Byzantine Emperors (330-1453) |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2021 |
| contenttype_str_mv |
zzz |
| container_start_page |
0 |
| author_browse |
Negri, Sharon |
| container_volume |
135 |
| class |
610 VZ 44.85 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Negri, Sharon |
| doi_str_mv |
10.1016/j.biocel.2021.105983 |
| dewey-full |
610 |
| title_sort |
endothelial signaling at the core of neurovascular coupling: the emerging role of endothelial inward-rectifier k+ (kir2.1) channels and n-methyl-d-aspartate receptors in the regulation of cerebral blood flow |
| title_auth |
Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow |
| abstract |
Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. |
| abstractGer |
Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. |
| abstract_unstemmed |
Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
| title_short |
Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow |
| url |
https://doi.org/10.1016/j.biocel.2021.105983 |
| remote_bool |
true |
| author2 |
Faris, Pawan Soda, Teresa Moccia, Francesco |
| author2Str |
Faris, Pawan Soda, Teresa Moccia, Francesco |
| ppnlink |
ELV010616845 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth |
| doi_str |
10.1016/j.biocel.2021.105983 |
| up_date |
2024-07-06T20:42:20.495Z |
| _version_ |
1803863762398085120 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV054075920</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626035640.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">210910s2021 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.biocel.2021.105983</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001396.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV054075920</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1357-2725(21)00068-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.85</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Negri, Sharon</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Endothelial signaling at the core of neurovascular coupling: The emerging role of endothelial inward-rectifier K+ (Kir2.1) channels and N-methyl-d-aspartate receptors in the regulation of cerebral blood flow</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021transfer abstract</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K+ (Kir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial Kir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TRPV4 channel</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Kir2.1 channels</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Cerebral blood flow</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GqPCRs</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NMDA receptors</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Neurovascular coupling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Cerebrovascular endothelial cells</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Faris, Pawan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Soda, Teresa</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Moccia, Francesco</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="t">Urological Diseases of the Byzantine Emperors (330-1453)</subfield><subfield code="d">2011</subfield><subfield code="g">Amsterdam</subfield><subfield code="w">(DE-627)ELV010616845</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:135</subfield><subfield code="g">year:2021</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.biocel.2021.105983</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.85</subfield><subfield code="j">Kardiologie</subfield><subfield code="j">Angiologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">135</subfield><subfield code="j">2021</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| score |
7.402934 |