Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats

Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearanc...
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Autor*in:	Ledo, Ana [verfasserIn] Lourenço, Cátia F. [verfasserIn] Caetano, Miguel [verfasserIn] Barbosa, Rui M. [verfasserIn] Laranjinha, João [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Nitric oxide Aging Fischer 344 rats In vivo Electrochemical detection

Übergeordnetes Werk:	Enthalten in: Cellular and molecular neurobiology - Dordrecht : Springer Science + Business Media B.V, 1981, 35(2014), 1 vom: 02. Okt., Seite 33-44
Übergeordnetes Werk:	volume:35 ; year:2014 ; number:1 ; day:02 ; month:10 ; pages:33-44

Links:	Volltext

DOI / URN:	10.1007/s10571-014-0115-0

Katalog-ID:	SPR011392436

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520			\|a Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging.
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publishDate	2014
allfields	10.1007/s10571-014-0115-0 doi (DE-627)SPR011392436 (SPR)s10571-014-0115-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Ledo, Ana verfasserin aut Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging. Nitric oxide (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Fischer 344 rats (dpeaa)DE-He213 In vivo (dpeaa)DE-He213 Electrochemical detection (dpeaa)DE-He213 Lourenço, Cátia F. verfasserin aut Caetano, Miguel verfasserin aut Barbosa, Rui M. verfasserin aut Laranjinha, João verfasserin aut Enthalten in Cellular and molecular neurobiology Dordrecht : Springer Science + Business Media B.V, 1981 35(2014), 1 vom: 02. Okt., Seite 33-44 (DE-627)306351536 (DE-600)1496697-9 1573-6830 nnns volume:35 year:2014 number:1 day:02 month:10 pages:33-44 https://dx.doi.org/10.1007/s10571-014-0115-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 35 2014 1 02 10 33-44
spelling	10.1007/s10571-014-0115-0 doi (DE-627)SPR011392436 (SPR)s10571-014-0115-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Ledo, Ana verfasserin aut Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging. Nitric oxide (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Fischer 344 rats (dpeaa)DE-He213 In vivo (dpeaa)DE-He213 Electrochemical detection (dpeaa)DE-He213 Lourenço, Cátia F. verfasserin aut Caetano, Miguel verfasserin aut Barbosa, Rui M. verfasserin aut Laranjinha, João verfasserin aut Enthalten in Cellular and molecular neurobiology Dordrecht : Springer Science + Business Media B.V, 1981 35(2014), 1 vom: 02. Okt., Seite 33-44 (DE-627)306351536 (DE-600)1496697-9 1573-6830 nnns volume:35 year:2014 number:1 day:02 month:10 pages:33-44 https://dx.doi.org/10.1007/s10571-014-0115-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 35 2014 1 02 10 33-44
allfields_unstemmed	10.1007/s10571-014-0115-0 doi (DE-627)SPR011392436 (SPR)s10571-014-0115-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Ledo, Ana verfasserin aut Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging. Nitric oxide (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Fischer 344 rats (dpeaa)DE-He213 In vivo (dpeaa)DE-He213 Electrochemical detection (dpeaa)DE-He213 Lourenço, Cátia F. verfasserin aut Caetano, Miguel verfasserin aut Barbosa, Rui M. verfasserin aut Laranjinha, João verfasserin aut Enthalten in Cellular and molecular neurobiology Dordrecht : Springer Science + Business Media B.V, 1981 35(2014), 1 vom: 02. Okt., Seite 33-44 (DE-627)306351536 (DE-600)1496697-9 1573-6830 nnns volume:35 year:2014 number:1 day:02 month:10 pages:33-44 https://dx.doi.org/10.1007/s10571-014-0115-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 35 2014 1 02 10 33-44
allfieldsGer	10.1007/s10571-014-0115-0 doi (DE-627)SPR011392436 (SPR)s10571-014-0115-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Ledo, Ana verfasserin aut Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging. Nitric oxide (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Fischer 344 rats (dpeaa)DE-He213 In vivo (dpeaa)DE-He213 Electrochemical detection (dpeaa)DE-He213 Lourenço, Cátia F. verfasserin aut Caetano, Miguel verfasserin aut Barbosa, Rui M. verfasserin aut Laranjinha, João verfasserin aut Enthalten in Cellular and molecular neurobiology Dordrecht : Springer Science + Business Media B.V, 1981 35(2014), 1 vom: 02. Okt., Seite 33-44 (DE-627)306351536 (DE-600)1496697-9 1573-6830 nnns volume:35 year:2014 number:1 day:02 month:10 pages:33-44 https://dx.doi.org/10.1007/s10571-014-0115-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 35 2014 1 02 10 33-44
allfieldsSound	10.1007/s10571-014-0115-0 doi (DE-627)SPR011392436 (SPR)s10571-014-0115-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Ledo, Ana verfasserin aut Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging. Nitric oxide (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Fischer 344 rats (dpeaa)DE-He213 In vivo (dpeaa)DE-He213 Electrochemical detection (dpeaa)DE-He213 Lourenço, Cátia F. verfasserin aut Caetano, Miguel verfasserin aut Barbosa, Rui M. verfasserin aut Laranjinha, João verfasserin aut Enthalten in Cellular and molecular neurobiology Dordrecht : Springer Science + Business Media B.V, 1981 35(2014), 1 vom: 02. Okt., Seite 33-44 (DE-627)306351536 (DE-600)1496697-9 1573-6830 nnns volume:35 year:2014 number:1 day:02 month:10 pages:33-44 https://dx.doi.org/10.1007/s10571-014-0115-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 35 2014 1 02 10 33-44
language	English
source	Enthalten in Cellular and molecular neurobiology 35(2014), 1 vom: 02. Okt., Seite 33-44 volume:35 year:2014 number:1 day:02 month:10 pages:33-44
sourceStr	Enthalten in Cellular and molecular neurobiology 35(2014), 1 vom: 02. Okt., Seite 33-44 volume:35 year:2014 number:1 day:02 month:10 pages:33-44
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Nitric oxide Aging Fischer 344 rats In vivo Electrochemical detection
dewey-raw	610
isfreeaccess_bool	false
container_title	Cellular and molecular neurobiology
authorswithroles_txt_mv	Ledo, Ana @@aut@@ Lourenço, Cátia F. @@aut@@ Caetano, Miguel @@aut@@ Barbosa, Rui M. @@aut@@ Laranjinha, João @@aut@@
publishDateDaySort_date	2014-10-02T00:00:00Z
hierarchy_top_id	306351536
dewey-sort	3610
id	SPR011392436
language_de	englisch
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author	Ledo, Ana
spellingShingle	Ledo, Ana ddc 610 bkl 44.90 misc Nitric oxide misc Aging misc Fischer 344 rats misc In vivo misc Electrochemical detection Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats
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topic_title	610 ASE 44.90 bkl Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats Nitric oxide (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Fischer 344 rats (dpeaa)DE-He213 In vivo (dpeaa)DE-He213 Electrochemical detection (dpeaa)DE-He213
topic	ddc 610 bkl 44.90 misc Nitric oxide misc Aging misc Fischer 344 rats misc In vivo misc Electrochemical detection
topic_unstemmed	ddc 610 bkl 44.90 misc Nitric oxide misc Aging misc Fischer 344 rats misc In vivo misc Electrochemical detection
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title	Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats
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title_full	Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats
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journal	Cellular and molecular neurobiology
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author_browse	Ledo, Ana Lourenço, Cátia F. Caetano, Miguel Barbosa, Rui M. Laranjinha, João
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title_sort	age-associated changes of nitric oxide concentration dynamics in the central nervous system of fisher 344 rats
title_auth	Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats
abstract	Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging.
abstractGer	Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging.
abstract_unstemmed	Abstract The increase in life expectancy is accompanied by an increased risk of developing neurodegenerative disorders and age is the most relevant risk factor for the appearance of cognitive decline. While decreased neuronal count has been proposed to be a major contributing factor to the appearance of age-associated cognitive decline, it appears to be insufficient to fully account for the decay in mental function in aged individuals. Nitric oxide (•NO) is a ubiquitous signaling molecule in the mammalian central nervous system. Closely linked to the activation of glutamatergic transmission in several structures of the brain, neuron-derived •NO can act as a neuromodulator in synaptic plasticity but has also been linked to neuronal toxicity and degenerative processes. Many studies have proposed that changes in the glutamate-•NO signaling pathway may be implicated in age-dependent cognitive decline and that the exact effect of such changes may be region specific. Due to its peculiar physical–chemical properties, namely hydrophobicity, small size, and rapid diffusion properties, the rate and pattern of •NO concentration changes are critical determinants for the understanding of its bioactivity in the brain. Here we show a detailed study of how •NO concentration dynamics change in the different regions of the brain of Fisher 344 rats (F344) during aging. Using microelectrodes inserted into the living brain of anesthetized F344 rats, we show here that glutamate-induced •NO concentration dynamics decrease in the hippocampus, striatum, and cerebral cortex as animals age. performance in behavior testing of short-term and spatial memory, suggesting that the impairment in the glutamate:nNOS pathway represents a functional critical event in cognitive decline during aging.
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title_short	Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats
url	https://dx.doi.org/10.1007/s10571-014-0115-0
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author2	Lourenço, Cátia F. Caetano, Miguel Barbosa, Rui M. Laranjinha, João
author2Str	Lourenço, Cátia F. Caetano, Miguel Barbosa, Rui M. Laranjinha, João
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doi_str	10.1007/s10571-014-0115-0
up_date	2024-07-03T22:22:54.199Z
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Age-Associated Changes of Nitric Oxide Concentration Dynamics in the Central Nervous System of Fisher 344 Rats

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