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The observation that the feeding effects of dopamine vary with the brain region under study further obscures its role in energy homeostasis. For example, mesolimbic dopamine pathways (comprised of cell bodies in the substantia nigra and ventral tegmental area that project to the nucleus accumbens, striatum and cerebral cortex) seem to contribute to the ‘rewarding’ aspects of consuming palatable foods107. In contrast, dopamine signalling in the hypothalamus via neurons situated in the dorsomedial and arcuate nuclei seems to inhibit food intake. Although reduced dopamine levels in the arcuate nucleus of ob/ob mice103 raise the possibility that decreased hypothalamic dopamine signalling contributes to hyperphagia induced by leptin deficiency, the finding that leptin inhibits dopamine release from rat hypothalamus in vitro104 is inconsistent with this hypothesis. Synapticconcentrationsofneurotransmittersaredeterminednot only by the rate of their release from nerve terminals, but also by their rate of removal from the synaptic cleft. The latter process is dependent on specific transporter proteins that mediate neurotransmitter reuptake,theexpressionofwhichcanbeinfluencedbymetabolicand hormonal factors108. For example, fasting and uncontrolled diabetes reduce synaptic dopamine reuptake (which increases synaptic dopamine levels)109, whereas the reverse is true for noradrenaline108. Because these effects are reversed by insulin infusion directly into the brain, they may be mediated, at least in part, by reduced CNS insulin signalling. Serotonin The serotonin system is comprised of cell bodies in the caudal brainstemincludingthedorsalraphenucleithatprojectwidelythroughout the brain, and is the primary target of several centrally acting drugs developed for obesity treatment (for example, dexfenfluramine and sibutramine). Such drugs increase serotonin-receptor signalling and thereby suppress food intake, whereas antagonists have the opposite effect110. The 5HT2C serotonin-receptor subtype is implicated in this process, as knockout of this receptor increases food intake and body weight111. Maintenance of normal energy homeostasis, therefore, seems to require intact serotonin signalling.