Abstract
The prefrontal cortex integrates a variety of cognition-related inputs, either unidirectional, e.g., from the hippocampal formation, or bidirectional, e.g., with the limbic thalamus. While the former is usually implicated in synaptic plasticity, the latter is better known for regulating ongoing activity. Interactions between these processes via prefrontal neurons are possibly important for linking mnemonic and executive functions. Our work further elucidates such dynamics using in vivo electrophysiology in rats. First, we report that electrical pulses into CA1/subiculum trigger late-onset (>400 ms) firing responses in the medial prefrontal cortex, which are increased after induction of long-term potentiation. Then, we show these responses to be attenuated by optogenetic control of the paraventricular/mediodorsal thalamic area. This suggests that recruitment and plasticity of the hippocampal-prefrontal pathway is partially related to the thalamic-prefrontal loop. When dysfunctional, this interaction may contribute to cognitive deficits, psychotic symptoms, and seizure generalization, which should motivate future studies combining behavioural paradigms and long-range circuit assessment.
Highlights
Excitatory projections from the hippocampal CA1/subiculum area (CA1/sub) and the dorsal midline thalamus have overlapping terminal fields in the rat medial prefrontal cortex, which in turn reciprocates its thalamic afferents[1,2,3]
We observed that long-latency (>400 ms) medial prefrontal cortex (mPFC) firing responses to CA1/sub electrical pulses increase with hippocampal-prefrontal long-term potentiation (LTP)
Subjects received a stimulating electrode in CA1/sub, and recording microwires in mPFC and PV/MD (Fig. 1a,b)
Summary
Excitatory projections from the hippocampal CA1/subiculum area (CA1/sub) and the dorsal midline thalamus have overlapping terminal fields in the rat medial prefrontal cortex (mPFC), which in turn reciprocates its thalamic afferents[1,2,3]. MK-801 into the midline thalamus, but not mPFC, reproduces the systemic effects of this drug on urethane-driven delta oscillations[15], while muscimol or tetrodotoxin into the same thalamic area abbreviates subiculum-generated paroxysms[16,17]. These findings support a common involvement of the thalamic-prefrontal loop and hippocampal-prefrontal plasticity in seizure spread and psychosis-relevant NMDA antagonism, as previously discussed[18]. These response patterns might inform future research with learning paradigms and animal models of psychiatric diseases
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