Biomedical subjects

L Stoll

Publications and source records attributed to L Stoll.

10 recordsLinked to original sources

PubMed1991

In vitro down-regulation predicts agonist efficacy at central muscarinic cholinergic receptors.

Agonist induced short-term down-regulation of central muscarinic cholinergic receptors in mechanically dissociated cells of the mouse brain has been shown to predict the efficacy of agonists at muscarinic receptors. Pretreatment of cells with full agonists such as carbachol or oxotremorine M resulted in a loss of available muscarinic cholinergic receptors of about 30% using [3H]N-methylscopolamine [( 3H]NMS) as radioligand, whereas a second group of agonists e.g. RS 86 were only weakly active in this regard producing a significantly smaller loss of cell surface muscarinic cholinergic receptors. The magnitude of down-regulation of muscarinic receptors induced by pretreatment with several cholinergic drugs correlates fairly well with their ability to stimulate the phosphatidylinositol turnover. It seems that the agonist induced down-regulation of muscarinic cholinergic receptors on mechanically dissociated neurons of the mouse brain is a simple screening method to test for centrally acting cholinergic agonists.

Animals↗

PubMed1991

Therapeutic concentrations of lithium and carbamazepine inhibit cGMP accumulation in human lymphocytes. A clinical model for a possible common mechanism of action?

Although a large variety of biochemical effects have been reported for lithium (Li) and carbamazepine (Cbm), the final molecular mechanism underlying their therapeutic efficacy for recurrent affective disorders is still unknown. The data presented here clearly indicate that therapeutic concentrations of both drugs inhibit sodium nitroprusside-induced accumulation of cGMP in human lymphocytes to about the same extent. The effect is not seen for other antidepressants, and shows pronounced interindividual variations in healthy volunteers. A similar effect of lithium and carbamazepine can also be demonstrated for the cGMP accumulation of central neurons using the model of dissociated cells of the mouse brain. The results are discussed in view of a common mechanism of action of both drugs. Furthermore, it is speculated that the individual sensitivity of the cGMP generating system of human lymphocytes to both drugs might be used to predict therapeutic response or nonresponse of the individual patient.

Animals↗

PubMed1991

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↗

PubMed1989

A simple but highly sensitive radioreceptor assay for the determination of scopolamine and biperiden in human plasma.

Simple and sensitive methods are described for the determination of scopolamine and biperiden in human plasma. Each method consists of two steps. After extraction of scopolamine and biperiden with chloroform or n-hexane respectively and evaporation of the organic solvent, both drugs are determined by their ability to inhibit the specific binding of tritiated N-methyl-scopolamine to mouse brain homogenates. The lower limits of detection are plasma levels of about 50 pg/ml scopolamine and about 200 pg/ml biperiden.

Animals↗

PubMed1978