Changes in muscarinic cholinergic, PCP, GABAA, D1, and 5-HT2A receptor binding, but not in benzodiazepine receptor binding in the brains of aged rats

Nabeshima, Toshitaka; Yamada, Kiyofumi; Hayashi, Tetsuo; Hasegawa, Takaaki; Ishihara, Seiichi; Kameyama, Tsutomu; Morimasa, Tadaomi; Kaneyuki, Takao; Shohmori, Toshikiyo

doi:10.1016/0024-3205(94)00320-3

Cited by 42 publications

(13 citation statements)

References 32 publications

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“…Since no neuronal cell loss in aged rodent neostriatum could be detected by McNeill and Koek (1990) and Zoli et al (1993) and the levels of extracellular adenosine remain unaffected in this area during ageing (Pazzagli et al, 1995), the lower density of A1 receptors seen here could indicate a specific reduction, as a result of the ageing process. Interestingly, several investigators have detected decreased density of D1 and D2 dopamine receptors, as well as dopamine uptake sites in the aged striatum (Morelli et al, 1990;Giorgi et al, 1992;Nabeshima et al, 1994;Araki et al, 1997). As the adenosinergic system interacts with the dopaminergic system in an A1/D1 and A2a/D2 receptor-receptor interaction in the basal ganglia Popoli et al, 1998), the diminuation of A1 adenosine receptors in this brain area could probably reflect a compensatory mechanism in order to re-establish the balance between the adenosinergic and the dopaminergic system during ageing.…”

Section: A1 Receptor Quantitative Autoradiographymentioning

confidence: 94%

“…These results are in accordance with the work of Cunha et al (1995), which showed an age-related decrease in the quantity of A1 adenosine receptors. The decreases observed in the A1 receptor density seem to be a part of a general ageing process affecting many neurotransmitter systems and their receptors, since the density of the receptors of cholinergic (Nabeshima et al, 1994; but also see Araki et al, 1996), dopaminergic (Morelli et al, 1990;Giorgi et al, 1992;Nabeshima et al, 1994;Araki et al, 1997), glutamatergic (Magnusson and Cotman. 1993;Nabeshima et al, 1994;Magnusson, 1995;Wardas et al, 1997) and GABAergic (Matsokis and Valkana, 1983;Nabeshima et al, 1994;Araki et al, 1996;Dalezios and Matsokis, 1998) systems decreases substantially in the aged rat and mouse brain (for review see also Gianquinto, 1988;Cotman and Peterson, 1989).…”

Section: A1 Receptor Quantitative Autoradiographymentioning

confidence: 95%

“…1993;Nabeshima et al, 1994;Magnusson, 1995;Wardas et al, 1997), and GABA (Matsokis and Valkana, 1983;Nabeshima et al, 1994;Araki et al, 1996;Dalezios and Matsokis, 1998) in the ageing brain. Adenosine, a major neuromodulator of synaptic activity (Kostopoulos, 1988;Fredholm, 1995), has been shown to regulate the release of many neurotransmitters such as acetylcholine, dopamine, and glutamate in synapses of the CNS (Corradetti et al, 1984a;Barrie and Nichols, 1993;Jin et al, 1993;Broad and Fredholm, 1996).…”

mentioning

confidence: 95%

“…In order to obtain a better understanding of the ageing process in the nervous system, many researchers have investigated the involvement of certain neurotransmitter systems such as those of acetylcholine (Nabeshima et al, 1994;Araki et al, 1996), dopamine (Morelli et al, 1990;Giorgi et al, 1992;Nabeshima et al, 1994;Araki et al, 1997), glutamate (Magnusson and Cotman. 1993;Nabeshima et al, 1994;Magnusson, 1995;Wardas et al, 1997), and GABA (Matsokis and Valkana, 1983;Nabeshima et al, 1994;Araki et al, 1996;Dalezios and Matsokis, 1998) in the ageing brain.…”

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confidence: 99%

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Age-dependent changes in adenosine A1 receptor and uptake site binding in the mouse brain: An autoradiographic study

2000

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Ageing is a multifactorial, inevitable event of life span, which affects neurotransmission in the CNS. Since adenosine is a major neuromodulator of the synaptic activity, it was of interest to investigate the possible modification of the adenosinergic system in the brain during ageing. Using "in vitro" quantitative autoradiography and the radioactive ligands [(3)H]Cyclohexyladenosine and [(3)H]Nitrobenzylthioinosine, we have studied the distribution of A1 adenosine receptors and adenosine uptake sites in the aged mice (26 months) compared to the young ones (3 months). Our results showed a widespread reduction in A1 receptor binding in the aged animals, which was brain area-specific, occurring in areas where adenosine plays a significant neuromodulatory role such as the hippocampus, cortex, basal ganglia, and thalamus. Interestingly, the significant reduction in NBI-sensitive adenosine uptake sites was restricted to few areas of the aged brain, mainly in thalamic nuclei. Since the alterations in the density of A1 receptors and adenosine uptake sites showed no regional correlation and since no significant changes in either neuronal or glial cell number are observed, at least in hippocampus and cortex in this mouse strain during ageing, our findings could be explained by a selective age-dependent reduction of these adenosinergic components rather than by a general neuronal cell degeneration. As adenosine depresses electrical activity in hippocampus, a downregulation of adenosinergic function could probably be related to enhanced excitability seen in hippocampal neurons of the CA1 subregion and dentate gyrus of aged animals.

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Section: A1 Receptor Quantitative Autoradiographymentioning

confidence: 94%

Section: A1 Receptor Quantitative Autoradiographymentioning

confidence: 95%

mentioning

confidence: 95%

mentioning

confidence: 99%

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Age-dependent changes in adenosine A1 receptor and uptake site binding in the mouse brain: An autoradiographic study

2000

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“…Biochemical, electrophysiological, and behavioral studies have suggested that neurotransmitters and their receptors are a possible site of cellular dysfunction in aging, contributing to behavioral and functional disturbances (Bartus et al, 1982;Nabeshima et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

No changes in cerebrospinal fluid levels of nitrite, nitrate and cyclic GMP with aging

Yamada

Nishiwaki

Hattori

et al. 1997

J. Neural Transmission

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Nitric oxide (NO) is a free radical gas that plays a role in various signal transduction processes. NO has been proposed to have a function in the mechanism of synaptic plasticity, including long-term potentiation and memory formation in vivo. Because a failure in synaptic plasticity is considered to be involved in aging-associated brain dysfunction, NO production in the brain may be altered by aging. In the present study, we measured the levels of NO metabolites, nitrite and nitrate, and cyclic GMP in the cerebrospinal fluid (CSF) of human subjects without neurological or psychiatric disorders. There were no age-related changes in the CSF levels of either nitrite, nitrate or cyclic GMP. These results suggest that NO production in the brain may be maintained during the aging process.

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Changes in NMDA receptor/ nitric oxide signaling pathway in the brain with aging

Yamada

Nabeshima

1998

Microsc. Res. Tech.

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Changes in muscarinic cholinergic, PCP, GABAA, D1, and 5-HT2A receptor binding, but not in benzodiazepine receptor binding in the brains of aged rats

Cited by 42 publications

References 32 publications

Age-dependent changes in adenosine A1 receptor and uptake site binding in the mouse brain: An autoradiographic study

Age-dependent changes in adenosine A1 receptor and uptake site binding in the mouse brain: An autoradiographic study

No changes in cerebrospinal fluid levels of nitrite, nitrate and cyclic GMP with aging

Changes in NMDA receptor/ nitric oxide signaling pathway in the brain with aging

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