Abstract
The influences of noradrenaline on the modulation of learning and memory functions, as well as synaptic plasticity, e.g., long‐term potentiation (LTP), via β‐adrenoceptors are well documented, whereas the role of α1‐adrenoceptors has not been studied extensively. Therefore, the effects of α1‐agonists (ST 587 and methoxamine) on the induction of LTP were examined in the CA1 area of the hippocampus in vitro. Submaximal LTP in extracellular excitatory postsynaptic potentials (EPSP) was induced with theta burst stimulation using 4 bursts. The effects of a β‐agonist, isoproterenol, on synaptic potentiation were studied as a comparison in this preparation. At a concentration of 1 μM, ST 587 slightly increased the magnitude of potentiation in EPSPs (measured 30 min after stimulation) compared to a control pathway potentiated 30 min before drug infusion, whereas a lower concentration (0.3 μM) was not effective. Methoxamine did not induce any increase in the amount of submaximal LTP at concentrations of 0.3, 1.0, or 3.0 μM. Isoproterenol (1.5 μM) increased the amount of LTP when measured 30 min after stimulation, and also transiently increased synaptic transmission, measured both in the slope and amplitude of the field EPSP in the prepotentiated control pathway. Thus, the present results indicate that (1) α1‐adrenoceptors have only a minor role in hippocampal synaptic plasticity in the CA1 area, but (2) the synaptic plasticity in the CA1 area of the hippocampus assessed by induction and early maintenance of LTP in vitro can be modulated through β‐adrenoceptors. J. Neurosci. Res. 51:309–315, 1998.