ReviewChronic food restriction: Enhancing effects on drug reward and striatal cell signaling
Section snippets
Effects of chronic FR on measures of drug reward and reward seeking
Early results of this laboratory indicated that chronic FR lowers the electrical brain stimulation reward threshold, in perifornical hypothalamic sites, in a manner that covaries with body weight, suggesting that negative energy balance, and perhaps adipose depletion in particular, triggers neuroadaptations in brain reward circuitry [35]. Subsequent studies implicated endogenous opioid mechanisms [36] and the endocrine adiposity hormones, leptin [37] and insulin [38] in this effect. To
D-1 DA receptor binding, signal transduction, and neuropeptide gene expression
In agreement with the results of a previous autoradiographic study [56], radiologand binding assays, using the D-1 DA receptor antagonist [3H]SCH-23390, indicated no difference between FR and AL subjects with regard to the density or ligand affinity of binding sites in CPu or NAc [65]. Further, unlike behavioral sensitization induced by chronic psychostimulant treatment and stress [e.g., [66], [67], stimulation of adenylyl cyclase activity by SKF-82958 in CPu and NAc was not increased by FR [64]
NMDA receptor involvement in signaling responses to D-1 DA receptor stimulation and relation to mechanisms involved in synaptic plasticity
In striatal medium spiny neurons, the D-1 DA and NMDA glutamate receptors are coexpressed [74], [75] and are functionally associated in controlling excitatory synaptic currents [76], [77], signal transduction [78], gene expression [79], and instrumental [80] and Pavlovian [81] learning. Most importantly, NMDA receptor stimulation activates the ERK cascade [for review, see Ref. [82]], and stimulation of the D-1 DA receptor leads to phosphorylation of the NMDA receptor NR1 subunit [83], thereby
Possible changes in DA synthesis and utilization
There is reason to consider whether the upregulated striatal cell signaling in response to D-1 DA receptor stimulation in FR rats represents a compensatory response to decreased physiological DA release. The decreased basal levels of preprodynorphin and preprotachykinin mRNA observed in NAc of FR relative to AL rats, could be reflective of a persistently lower level of D-1 DA receptor stimulation in these subjects (Fig. 9) [73]. Further, there is the microdialysis result indicating that under
Potential endocrine contributions
A consistently observed characteristic of the enhancing effect of FR on drug reward sensitivity is that it reverses over a period of days/weeks in parallel with body weight recovery when ad libitum access to food is reinstated (e.g., Fig. 2) [42], [47]. This raises the possibility of a role for one of the endocrine adiposity hormones – leptin or insulin – which circulate in plasma and cerebrospinal fluid (CSF) in proportion to body adipose mass [114], [115], penetrate the blood–brain-barrier
Summary and conclusions
In summary, chronic FR increases central sensitivity to drugs of abuse, as evidenced in various assays of drug reward magnitude, locomotor activation, and immediate-early and neuropeptide gene expression in subcortical DA terminal fields. Upregulation of striatal cell signaling upon D-1 DA receptor stimulation represents one set of neuroadaptations associated with FR that may play a role in these effects. The NMDA receptor-dependent activation of CaMK II, ERK 1/2, and CREB have been implicated
Acknowledgements
The author would like to thank Drs. Soledad Cabeza de Vaca, Sandra Haberny, and Yemiliya Berman for the major contributions to the research of the laboratory summarized in this review. Essential support was provided by NIDA/NIH (DA03956 and K02 DA00292).
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