TY - JOUR
T1 - Central opioid receptor subtype antagonists differentially reduce intake of saccharin and maltose dextrin solutions in rats
AU - Beczkowska, Iwona W.
AU - Koch, James E.
AU - Elizabeth Bostock, M.
AU - Leibowitz, Sarah F.
AU - Bodnar, Richard J.
PY - 1993/8/6
Y1 - 1993/8/6
N2 - Opioid modulation of ingestion includes general opioid antagonism of deprivation-induced water intake and intake of sucrose and saccharin solutions. Previous studies using selective subtype antagonists indicated that opioid effects upon deprivation-induced water intake occured through the mu2 receptor and that opioid effects upon sucrose intake occured kappa and mu2 receptors. The present study compared the effects of intracerebroventricular administration of opioid receptor subtype antagonists upon intakes of saccharin solution and a maltose dextrin (MD) solution to determine which receptor subtypes were involved in modulation of ingestion of different preferred tastants. Significant reductions in saccharin intake (1 h) occured following naltrexone (20-50 μg: 66%) and naltrindole (delta, 20 μg: 75%), whereas [d-Ala2, Leu5, Cys6]-enkephalin (DALCE, delta1, 40 μg: 45%) had transient (5 min) effects. Neither beta-funaltrexamine (B-FNA, mu), naloxanazine (mu1, nor nor-binaltorphamine (Nor-BNI, kappa) significantly altered saccharin intake. Significant reductions in MD intake (1 h) occured following naltrexone (5-50 μg: 69%) and B-FNA (1-20 μg: 38%). MD intake was not reduced by naltrindole, DALCE, naloxanazine and Nor-BNI. Peak antagonist effects were delayed (20-25 min) to reflect interference with the maintenance, rather than the initiation of saccharin or MD intake. Comparisons of opioid antagonist effects across intake situations revealed that naltrexone had consistently low ID40 values for saccharin (29 nmol), MD (25 nmol), sucrose (6 nmol) and deprivation (38 nmol) intake. Despite its significant effects relative to naloxanazine, B-FNA had significantly higher ID40 values for saccharin (800 nmol), MD (763 nmol) and sucrose (508 nmol) relative to deprivation (99 nmol) intake, suggesting that mu2 receptors may be mediating maintenance of intake rather than taste effects. Nor-BNI had low40 values intake of sucrose (4 nmol), but not for saccharin (168 nmol), MD (153 nmol) and deprivation (176 nmol), suggesting that kappa receptors may mediate ingestion of sweet-tasting stimuli. That delta (naltrindole: ID40 = 60 nmol), but not delta1, (DALCE: ID40 = 288 nmol) antagonist consistently reduce saccharin intake suggests a role for the delta2 receptor subtype in the modulation of hedonic orosensory signals.
AB - Opioid modulation of ingestion includes general opioid antagonism of deprivation-induced water intake and intake of sucrose and saccharin solutions. Previous studies using selective subtype antagonists indicated that opioid effects upon deprivation-induced water intake occured through the mu2 receptor and that opioid effects upon sucrose intake occured kappa and mu2 receptors. The present study compared the effects of intracerebroventricular administration of opioid receptor subtype antagonists upon intakes of saccharin solution and a maltose dextrin (MD) solution to determine which receptor subtypes were involved in modulation of ingestion of different preferred tastants. Significant reductions in saccharin intake (1 h) occured following naltrexone (20-50 μg: 66%) and naltrindole (delta, 20 μg: 75%), whereas [d-Ala2, Leu5, Cys6]-enkephalin (DALCE, delta1, 40 μg: 45%) had transient (5 min) effects. Neither beta-funaltrexamine (B-FNA, mu), naloxanazine (mu1, nor nor-binaltorphamine (Nor-BNI, kappa) significantly altered saccharin intake. Significant reductions in MD intake (1 h) occured following naltrexone (5-50 μg: 69%) and B-FNA (1-20 μg: 38%). MD intake was not reduced by naltrindole, DALCE, naloxanazine and Nor-BNI. Peak antagonist effects were delayed (20-25 min) to reflect interference with the maintenance, rather than the initiation of saccharin or MD intake. Comparisons of opioid antagonist effects across intake situations revealed that naltrexone had consistently low ID40 values for saccharin (29 nmol), MD (25 nmol), sucrose (6 nmol) and deprivation (38 nmol) intake. Despite its significant effects relative to naloxanazine, B-FNA had significantly higher ID40 values for saccharin (800 nmol), MD (763 nmol) and sucrose (508 nmol) relative to deprivation (99 nmol) intake, suggesting that mu2 receptors may be mediating maintenance of intake rather than taste effects. Nor-BNI had low40 values intake of sucrose (4 nmol), but not for saccharin (168 nmol), MD (153 nmol) and deprivation (176 nmol), suggesting that kappa receptors may mediate ingestion of sweet-tasting stimuli. That delta (naltrindole: ID40 = 60 nmol), but not delta1, (DALCE: ID40 = 288 nmol) antagonist consistently reduce saccharin intake suggests a role for the delta2 receptor subtype in the modulation of hedonic orosensory signals.
KW - Delta receptor
KW - Kappa receptor
KW - Maltose dextrin
KW - Mu receptor
KW - Opioid antagonists
KW - Palatability
KW - Saccharin
KW - Sucrose
UR - http://www.scopus.com/inward/record.url?scp=0027197663&partnerID=8YFLogxK
U2 - 10.1016/0006-8993(93)91274-V
DO - 10.1016/0006-8993(93)91274-V
M3 - Article
C2 - 8397050
AN - SCOPUS:0027197663
SN - 0006-8993
VL - 618
SP - 261
EP - 270
JO - Brain Research
JF - Brain Research
IS - 2
ER -