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Biomedical subjects

C M Gelbmann

Publications and source records attributed to C M Gelbmann.

3 recordsLinked to original sources

Central cholinergic functioning and aging.

Normal aging in experimental animals and humans has been demonstrated to affect various aspects of central cholinergic functions. Although deficits at the levels of the number of cholinergic neurons, the acetylcholine synthesis, and the number of muscarinic cholinergic receptors are probably less relevant, deficits at the levels of acetylcholine release, muscarinic cholinergic receptor plasticity, as well as muscarinic cholinergic receptor function are fairly pronounced and seem to justify the assumption that the functioning of the central cholinergic system is impaired by aging. However, whether these cholinergic deficits of normal aging are the sole neurochemical basis to explain age-associated memory impairment or whether other transmitter systems also play a role is still a matter of controversy.

Aging

Specific decrease of high-affinity agonist states of alpha 2-adrenoceptors in the aging mouse brain.

Using the specific binding of the full alpha 2-adrenergic agonist 3H-UK-14,304 the contribution of high-affinity agonist states to the total number of alpha 2-adrenoceptors as labeled by the specific binding of the antagonist 3H-yohimbine has been investigated in the brain of young and aged mice. In contrast to findings with human platelet membranes, in young mice all central alpha 2-adrenoceptors are present in a high-affinity agonist conformation. While the total number of alpha 2-adrenoceptors was not changed in the brain of aged animals, a specific decline of the high-affinity agonist sites by about 30% was observed. It is suggested that the specific decrease of high-affinity agonist sites of central alpha 2-adrenoceptors might represent one of the mechanisms leading to a general impairment of central noradrenergic neurotransmission with aging.

Adrenergic alpha-Agonists

Chronic treatment with phosphatidylserine restores muscarinic cholinergic receptor deficits in the aged mouse brain.

Chronic treatment (21 days) with phosphatidylserine (BC-PS) partially restored the reduced density of muscarinic cholinergic receptors in several regions of the aged (18 months) mouse brain. The effect was similar whether 3H-QNB or 3H-NMS was used as radioligand. The affinity of both radioligands was not altered by BC-PS treatment. Similar treatment of young (3 months) animals was without any effect on muscarinic cholinergic receptor density in all brain regions investigated. The effect was dose-dependent with elevations of receptor density between 15 and 28% for daily IP doses between 10 and 40 mg/kg, respectively. Similar treatment of aged mice with phosphatidylcholine (40 mg/kg) was without any effect. The data give further evidence that chronic treatment of aged animals with BC-PS reverses a variety of aged-related deficits of brain function.

Aging