and control agent, lithium chloride (100 mg/kg, i.p ., reduced sucrose intake 24 h after association with sucrose; however, only lithium chloride reduced sucrose intake 72 h later.
In an obese rat model lacking the CCK-1 receptors (Oletf), treatment with D2R antagonist raclopride, but not D1R antagonist SCH23390, showed increased potency to reduce sucrose real intake, indicating that D2R are involved in heightened increased consumption of sucrose observed in these obese rats.
Supportively, in the preclinical experiments, we showed that pharmacological suppression of the GHS-R1A reduced high sucrose consumption as well as operant self-administration of sucrose in rats.
Thus, in comparison with the no sucrose exposure group, the mice exposed to unlimited sucrose in early life show mildly reduced sucrose preference resulting in little change in overall consumption.
25– 27 This increased consumption of highly palatable foods appears to be due to increased liking, as morphine microinjections into this area increased the number of positive affective reactions, 28 and microinjection of a selective mu-opioid antagonist reduced sucrose drinking.
Prolonged social isolation of adult rats reduced sucrose drinking [ 18].
Unlimited access to sucrose early in life reduced sucrose-seeking when work was required to obtain it.
CUMS also reduced open-field activity, sucrose consumption, as well as increased immobility duration in FST and TST.
AM-251 (3 mg/kg) also reduced adolescent but not adult sucrose consumption.
The results showed that CVS reduced open-field activity and sucrose consumption significantly, but increased immobility time in forced swimming test.
