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The nucleus reuniens thalami (RE) originates dense projections to CA1, forming asymmetrical synapses on spines (50%) and dendrites (50%). The hypothesis that RE input modulates transmission in CA1 through excitation of both pyramidal cells and interneurons was tested using electrophysiological methods in the anesthetized rat. The RE-CA1 afferents were selectively stimulated at their origin; evoked field potentials and unit activity were recorded in CA1. RE-evoked depth profiles showed a prominent negative deflection in the stratum lacunosummoleculare and a positive one in the stratum radiatum. The lacunosum-moleculare sink-radiatum source configuration is compatible with RE-elicited depolarization of apical dendrites of pyramidal cells. Despite a consistent and robust paired pulse facilitation of RE-evoked field potentials, population spikes in the stratum pyramidale were not detected at any tested condition. This indicates the inability of RE-CA1 input to discharge pyramidal cells. However, stimulation of RE-elicited spiking of extracellularly recorded units in strata oriens/alveus and distal radiatum, indicative of the activation of local interneurons. Thus, RE seems to modulate transmission in CA1 through a (subthreshold) depolarization of pyramidal cells and a suprathreshold excitation of putative inhibitory oriens /alveus and radiatum interneurons.RE-evoked monosynaptic or disynaptic field potentials were associated with stimulation of rostral or caudal RE, respectively. Anatomically, a projection from caudal to rostral RE was demonstrated that can account for the disynaptic RE-CA1 input. Because caudal RE receives input from the hippocampus via the subiculum, we propose the existence of a closed REhippocampal circuit that allows RE to modulate the activity in CA1, depending on hippocampal output. Key words: rat; electrophysiology; neuroanatomical tracing; hippocampus; midline thalamus; limbic system; learning and memoryThe involvement of thalamic midline nuclei in early stages of Alzheimer's disease Braak, 1991, 1992) and in diencephalic amnesia (Rousseau, 1994) has recently drawn attention to the connectivity between the nucleus reuniens (RE) and structures of the medial temporal lobe (Herkenham, 1978;Wouterlood et al., 1990;Dolleman-Van der Weel and Witter, 1996). In this study we focused on the RE projection to hippocampal field CA1, a crucial structure for learning and memory processes (Squire, 1992).A few investigators have studied the contribution of RE to hippocampal f unctioning. Vanderwolf et al. (1985) examined whether the medial thalamic nuclei, including RE, were involved in generating hippocampal atropine-resistant theta rhythm. Their extensive radiofrequency lesions, however, resulted in little or no effect on this type of rhythmical activity. Hirayasu and Wada (1992a,b) injected NMDA in the thalamic midline of the rat. When NMDA was administered to RE, it caused tonic and/or clonic generalized convulsions associated with temporal limbic EEG seizure discharge. They proposed that RE partic...

The pathways from the hippocampal formation to the nucleus accumbens and the prefrontal cortex are likely to play a role in several aspects of learning and memory. In the present study we addressed the question of how plastic changes in these structures may occur simultaneously. This question can be studied in an appropriate way in the hippocampal/fornix-fimbria to prefrontal cortex/nucleus accumbens system, since electrical stimulation of the fornix-fimbria fibre bundle evokes characteristic field potentials in the two target areas simultaneously. First, we examined the termination field in the nucleus accumbens (medial shell and core region with an extension into the ventro-medial caudate-putamen) and the prefrontal cortex (deeper layers of the ventral prelimbic and ventral infralimbic areas) by recording single unit activity evoked by stimulation of fornix-fimbria fibres in halothane anaesthetized rats. Second, we studied short-term plasticity, namely paired pulse facilitation, in these two areas upon stimulation of the fornix-fimbria fibres. In the nucleus accumbens, paired pulse facilitation was encountered for double pulse intervals between 25 and 500 ms, peaking around 100 ms. In the medial prefrontal cortex it was confined to intervals between 25 and 200 ms, with a peak around 75 ms. Third, we investigated whether LTP could be elicited simultaneously in the two target structures by a single tetanic stimulation (50 Hz, 2 s) of the fornix-fimbria fibres. LTP that was sustained for more than 90 min in the medial prefrontal cortex, reached levels of 130% of control values. In the nucleus accumbens, however, only a transient form of potentiation was found which lasted no more than 60 min. These data show that synaptic weights can be changed in several target structures of the hippocampal formation, simultaneously, in a distributed way.