Supplementary Methods.General surgical procedures. Briefly, animals were anesthetized with an IP dose of Ketamine and Xylazine (Ketaject ® -Phoenix 0.12 ml/100gBW and Anased ® Lloyd 0.07 ml/100gBW) after a light sedation with Halothane (Halothane ® -Halocarbon). During anesthesia, animals were given a SC dose of Ketoprofen (Ketoprofen ® -Dodge 0.5 mg/100g BW), as a post-surgical anti-inflammatory agent.The surgical procedure was standard and included aseptic exposure of the skull surface and the brain surface corresponding to the lesion or injection coordinates. After the lesion, sham or injection procedures, the muscle and overlying skin wounds were closed, fluid therapy was given SC, and rats were allowed to recover in a heated cage and returned to the animal facilities when fully awake.Temporoammonic pathway and total hippocampus electrolytic lesions. Bilateral electrolytic lesions were made with stainless steel 500 µm thick electrodes (FHC ® -Catalog#UESSGESEANNM) as the cathodes and silver wire, inserted in the neck muscles, as anodes. The current delivery electrode was guided to the lesion spots using a Benchmark TM stereotaxic apparatus, in which the animal was positioned according to standard procedures. For TA lesions, a current of 0.4 mA for 5 sec was passed at each spot using a current generator. The current parameters were determined in pilot experiments to optimize the destruction of the TA axons, while sparing the surrounding structures.Sites were chosen in order to optimize the disconnection between the entorhinal cortex and area CA1, based on both anatomical 1,2 and electrophysiological 3-5 findings. The lesion spot coordinates 6 were as follows:Level 6.10 from bregma, 5.6 lateral to the midline and 6.7 and 6.0 mm ventral to the skull surface, 5.5 lateral to the midline and 7.2, 5.6 and 5.0 ventral to the skull surface, 5.3 lateral to the midline and 7.5 and 4.7 ventral to the skull surface, 5.1 lateral to the midline and 7.6 and 4.3 ventral to the skull
The hippocampus and the nearby medial temporal lobe structures are required for the formation, consolidation, and retrieval of episodic memories. Sensory information enters the hippocampus via two inputs from entorhinal cortex (EC): One input (perforant path) makes synapses on the dendrites of dentate granule cells as the first set of synapses in the trisynaptic circuit, the other (temporoammonic; TA) makes synapses on the distal dendrites of CA1 neurons. Here we demonstrate that TA-CA1 synapses undergo both early-and late-phase long-term potentiation (LTP) in rat hippocampal slices. LTP at TA-CA1 synapses requires both NMDA receptor and voltage-gated Ca 2+ channel activity. Furthermore, TA-CA1 LTP is insensitive to the blockade of fast inhibitory transmission (GABA A -mediated) and, interestingly, is dependent on GABA B -dependent slow inhibitory transmission. These findings indicate that the TA-CA1 synapses may rely on a refined modulation of inhibition to exhibit LTP.
Interactions between cortex and hippocampus are believed to play a role in the acquisition and maintenance of memories. Distinct types of coordinated oscillatory activity, namely at theta frequency, are hypothesized to regulate information processing in these structures. We investigated how information processing in cingulate cortex and hippocampus relates to cingulate-hippocampus coordination in a behavioral task where rats choose from four possible trajectories according to a sequence. We found that the accuracy with which cingulate and hippocampal populations encode individual trajectories changes with the pattern of cingulate-hippocampal theta coherence, over the course of a trial. Initial theta coherence at ∼8Hz during trial onsets lowers by ∼1Hz as animals enter decision stages. At these stages, hippocampus precedes cingulate in processing increased amounts of task-relevant information. We hypothesize that lower theta frequency coordinates the integration of hippocampal contextual information by cingulate neuronal populations, to inform choices in a task-phase dependent manner.
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