1. The aim of this study was investigation of neuronal mechanisms underlying inputs from the fastigial nucleus (FN) to the lateral hypothalamic area (LHA). 2. In male anesthetized rats, 295 extracellular and 82 intracellular recordings of LHA responses to electrical stimulation of the FN, which elicited stimulus-locked pressor responses, were examined. 3. Contralateral FN stimulation evoked three types of responses in 48% of spontaneously firing LHA neurons: inhibition with 11 ± 6 (SD) ms latency followed by excitation (30%), excitation with 15 ± 12.5 ms latency (14%), and excitation followed by inhibition with 6 ± 4 ms latency (4%). 4 Contralateral FN stimulation after transection of the inferior cerebellar peduncle (ICP), which resulted in a substantial fall of the fastigial pressor response, also evoked the three types of responses. These responses were unaffected by transection of the ICP. 5. Neuronal activity was recorded intracellularly from 82 LHA neurons, of which 36 (44%) responded to FN stimulation. Of the 36 neurons, 24 showed inhibitory postsynaptic potentials (IPSPs) with a mean latency of 7.5 ± 2 ms. Of the 24 neurons, 16 were checked for change in IPSP latency with stimulus intensity, and 11 were considered to be monosynaptically connected since their latencies were constant when FN stimulation intensity was changed. The remaining 12 exhibited excitatory postsynaptic potentials (EPSPs) with a longer latency of 10.5 ± 3 ms, which indicated polysynaptic conduction. The reversal potentials of the IPSP and EPSP were estimated to be about -77 mV and -13 mV, respectively. 6. Most glucose-sensitive neurons (78%), which were identified by their inhibition in response to electrophoretically applied glucose, were inhibited by FN stimulation, whereas only 7% of the glucose-insensitive neurons responded to such stimulation. 7. From the results, it was concluded that LHA neurons receive inhibitory monosynaptic and excitatory polysynaptic inputs from the FN via the superior cerebellar peduncle. These connections may contribute to the hypothalamic modulation of feeding behavior.
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