Cholinergic neurotransmission in the hippocampus of aged rats: influence of L-alpha-glycerylphosphorylcholine treatment.

The influence of aging and of L-alpha-glycerylphosphorylcholine (GFC) treatment on the acetylcholine synthesizing and degradating enzymes choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) and on cholinergic muscarinic M-1 and M-2 receptors were assessed in the hippocampus using immunocytochemical, histochemical and radioligand binding techniques, respectively. The investigation was performed on male Wistar rats of 2 months (young), 12 months (adult), and 27 months (old). Oral GFC was given at the dose of 100 mg/Kg/day from the 21st to the 27th month of age.

Muscarinic cholinergic receptors in the hippocampus of the aged rat: effects of long-term hydergine administration.

The effects of senescence and of long-term hydergine treatment on the density and the pattern of muscarinic cholinergic receptors in rat hippocampus were studied using combined radioreceptor binding and autoradiography with [3H]-quinuclidinyl-benzilate ([3H]-QNB) as a ligand. [3H]-QNB accumulated in the hippocampus of 3 month old rats, primarily in the stratum oriens of the CA1 and CA2 fields, followed in descending order by the molecular layer of granule cells of the dentate gyrus and the CA3 field. The density and pattern of [3H]-QNB binding sites in the hippocampus of 16 month old rats were the same.

Effects of long-term Hydergine administration on lipofuscin accumulation in senescent rat brain.

The effects of ageing and of 6 months of Hydergine treatment on lipofuscin deposition within the cytoplasma of pyramidal neurons of rat prefrontal cortex, hippocampus (fields CA1 and CA3) and of Purkinje neurons were assessed microfluorimetrically. No lipofuscin autofluorescence was detected in the nerve cell populations of 3-month-old rats, but lipopigment had accumulated in nerve cell bodies of 16-month-old animals and increased significantly thereafter in rats of 22 months of age. In 22-month-old rats, Hydergine administration (0.

Inhibition of voluntary ethanol intake in rats by a combination of dihydroergotoxine and thioridazine.

Dihydroergotoxine (DHET) decreased voluntary ethanol intake in rats selected for their stable ethanol preference (mean daily ethanol intake 8 g/kg). DHET inhibition was markedly potentiated by thioridazine. The potentiation is explained with a synergistic inhibitory effect on dopaminergic transmission: that is, DHET acting on dopamine (DA) autoreceptors and thioridazine preferentially inhibiting postsynaptic DA receptors.