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The aim of this study was to elucidate the role of the neuropil located in the LHA in the acquisition of the association between a taste (conditioned stimulus = saccharin) and a visceral distress (unconditioned stimulus = lithium chloride) leading to long delayed learning of a conditioned taste aversion (CTA). In 82 male rats guide-cannulae were directed bilaterally into the basolateral LHA where bilateral microinjections were made after the conditioned stimulus and before the unconditioned stimulus. We found that: (1) tetrodotoxin, a non-specific blocker of neuronal activity disrupted the acquisition of the CTA; (2) SCH 23390, a specific D1 receptor blocker also disrupted learning of the CTA, while sulpiride, a D2 receptor blocker, did not; (3) neither the specific blockade of D1 nor of D2 receptors could prevent the visceral distress-induced decrease in water intake, showing that the visceral distress was actually experienced; and (4) the sham taste aversion learning (i.e. without visceral distress) revealed that neither the D1 nor the D2 receptors blockade induced by themselves either a taste preference or a taste aversion towards saccharin, indicating that the impaired acquisition of the CTA was not due to a superimposed taste preference that could have been induced by the intra-LHA D1 receptors blockade. It is concluded that the neuropil in the LHA is necessary in the process of the acquisition of long delayed learning and that it uses a D1 receptor specific mechanism.

Energy metabolism and food intake affect each other. Many studies demonstrated that the lateral hypothalamus (LH) participates in the control of both feeding behavior and energy metabolism. We assessed the effect of a bipolar near threshold feeding eliciting electrical stimulation of the LH first on the feeding response and then on the background metabolism (metabolism free from the part due to locomotion) and respitory quotient (RQ), on Wistar male rats, during either the light or the dark phase of the nycthemeron. LH stimulation resulted in a delayed and rather long increase in background metabolism that was more dramatic during the light phase. This metabolic response paralleled the delayed feeding response (more than 10 min) we obtained during behavioral tests. The increase in energy production was sustained by release of energy substrates from the endogenous stores, and this showed a circadian dependence. Mainly carbohydrates (rise in RQ) were used during the light phase stimulation whereas lipids (decrease in RQ) were released in the dark phase.