Long-term potentiation of CA1 field potentials was induced by weak tetanic orthodromic stimulation of the Schaffer collateral/commissural fibers in isolated hippocampal slices perfused with a medium containing arginine vasopressin fragment AVP(4-9)in micromolar concentrations. It is hypothesized that AVP(4-9)affects induction of long-term potentiation at the intracellular level.

β-Amyloid peptide 1-42 in a concentration of 200 nM impairs induction of long-term posttetanic potentiation of population spike in CA1 pyramidal neurons in rat hippocampal slices. Application of donepezil, a drug used for the treatment of Alzheimer disease, in a concentration of 1 μM eliminates the suppressive effect of β-amyloid peptide 1-42 on long-term posttenanic potentiation in the hippocampus.

Tacrine, when applied by the concentration clamp technique to isolated Purkinje cells from rat cerebellum, dose-dependently reduced the amplitude of GABA-activated chloride currents recorded by the patch clamp technique. Half-maximal inhibition (IC50) of currents activated by 2 pM GABA was observed at a tacrine concentration of 107 ~aM. Tacrine produced a right shift of the dose-response curves for GABA-induced currents without affecting their peak amplitudes. It is suggested that suppression of GABA-induced currents caused by tacrine can not be attributed to its interaction with the benzodiazepine site of the GABA A receptor.