PARAGIGANTOCELLULARIS STIMULATION INDUCES BETA-ADRENERGIC HIPPOCAMPAL POTENTIATION

The nucleus paragigantocellularis (PGi) is the major excitatory glutamatergic input to the locus coeruleus (LC). Glutamate activation of the LC has previously been shown to produce beta-adrenergic-dependent potentiation of the perforant path- (PP) evoked population spike in the dentate gyrus (DG). The present study asks if electrical stimulation of the PGi, by activating the LC endogenously, can produce a parallel beta-receptor-dependent potentiation of the PP-evoked population spike. An optimal interstimulus interval (ISI) was determined for PGi-PP stimulation in urethane-anesthetized rats and propranolol was used to assess the role of noradrenergic beta-receptors. PGi stimulation potentiated the PP-evoked population spike at an optimal ISI of 30 ms. The population synaptic response slope and spike latency were not affected. Propranolol blocked the PGi-induced potentiation, as would be expected for beta-receptor-dependent modulation. The parallels between PGi- and LC-induced induced effects on the PP-evoked population spike suggest PGi stimulation offers an alternate method of LC activation for studies of LC's role in behavior.