Ventricular microinjection studies found that whereas mu (
beta-funaltrexamine, B-FNA), mu1 (
naloxonazine) and kappa (nor-binaltorphamine,
Nor-BNI)
opioid receptor antagonists, but not delta antagonists, reduce deprivation-induced intake, kappa and mu, but not mu1 or delta antagonists reduce both
2-deoxy-D-glucose (2DG)
hyperphagia and
sucrose intake. Since
opioid agonists stimulate spontaneous food intake in the accumbens, the present study examined whether administration of either
naltrexone, B-FNA or
Nor-BNI in the accumbens altered intake under deprivation (24 h), glucoprivic (2DG: 500 mg/kg, i.p.) or palatable
sucrose (10%) conditions.
Naloxonazine's effects in the accumbens were also evaluated for deprivation-induced intake. Deprivation-induced intake was significantly decreased over 4 h by
naltrexone (5-20 micrograms, 44%), B-FNA (1-4 micrograms, 55%) and
Nor-BNI (4 micrograms, 31%) but not
naloxonazine (10 micrograms) in the accumbens. 2DG
hyperphagia was significantly decreased by
naltrexone (10-20 microgram, 79%), B-FNA (1-4 micrograms, 100%) and
NOR-BNI (104 micrograms, 75%) in the accumbens.
Sucrose intake was significantly decreased by
naltrexone (50 micrograms, 27%) and B-FNA (1-4 micrograms, 37%), but not
NOR-BNI in the accumbens. These data suggest that
mu receptors, and particularly the mu2 binding site in the accumbens are responsible for the
opioid modulation of these forms of intake in this nucleus, and that this control may be acting upon the amount of intake per se.