Modulation of hypothalamic arcuate nucleus on gastric motility in rats

AIM: To investigate whether the arcuate nucleus (ARC) could modulate gastric motility, and if so, what are the mechanisms or pathways. METHODS: Wistar rats, anaesthetized with urethan, parameters of stimulation and electrolytic lesion sites were determined according to the Paxinos and Watson "ATLAS of rat brain in steriotaxic coordinate". Intragastric pressure (IGP) and gastric motility were measured by Reybould's method. RESULTS: Electrical stimulation of ARC could obviously decrease the IGP by 42.2% ± 5.4%, n = 15, P<0.01, and the phasic gastric contractions disappeared. The analysis showed that the locus coeruleus (LC) and dorsal raphe (DR) nuclei may be involved in central, but without the involvement of βendorphinergic neurons rich in the ARC, while in periphery, the peripheral neural pathways are both vagus and sympathetic nerves. The fibers in vagus may be non cholinergic. Humoral factors may also be involved. At the receptor level, Tonic action of adrenergic nerve in the stomach is mainly inhibitory; β-receptors, which may be present on the stomach wall and mediate inhibition; and α-receptors, which come into play through vagus, mediate inhibition, but those present on the smooth muscle mediate sympathetic excitation. Microinjection of TRH into ARC could significantly increase the IGP by 183.02% (0.53 kPa ± 0.08 kPa vs 1.5 kPa ± 0.6 kPa, n = 10, P<0.001), the rate and amplitude of phasic gastric contraction were also increased (3 cpm vs 6 cpm - 8 cpm). The peripheral pathway of such excitatory effects were transmitted with cholinergic vagus nerve mediated by M-receptor. CONCLUSION: ARC could modulate gastric motility biphasically, inhibitory and excitatory, depending on the nature of stimuli.