Specific changes in levels of autoantibodies to glutamate and opiate receptors induced by morphine administration in rats

Autoantibodies against opioid or glutamate receptors are associated with changes in morphine reward and physical dependence in mice

“…Presently, we did not observe a morphine-induced elevation of aAbs titers in the vehicle control groups. This represents an apparent discrepancy with previous work (Granstrem et al 2006), where subchronic administration of morphine (5 mg/kg for 14 days) led to a significant elevation of both GluR1 and MDOR aAbs levels. Obviously, results from these two studies cannot be compared due to different animal species (rats vs mice), treatment regimen (fixed vs escalating morphine dosages), distance between last morphine administration and sacrifice (1 day vs 1 week).…”

“…In other words, the fact that the autoimmune reactions somewhat converge may further confirm that these two neuroreceptor pathways are closely interrelated. A similar profile, reporting reciprocal production of both GluR1 and MDOR aAbs with either immunization, was recently observed in rats after subchronic morphine administration (Granstrem et al 2006). Presently, we did not observe a morphine-induced elevation of aAbs titers in the vehicle control groups.…”

“…With respect to drug abuse, elevated levels of anti-idiotypic antibody against opiate receptors have been demonstrated in chronic opiate addicts (Roy et al 1988). In our recent study (Granstrem et al 2006), repeated administration of morphine induced a drastic elevation of aAbs to μ-δ opioid receptors (MDOR) and AMPA (but not NMDA) glutamate subunits in rats. In contrast, neither a psychostimulant drug such as amphetamine, nor a commonly abused substance such as nicotine, had any effects on these aAbs levels following a similar regimen of administration.…”

Transgenerational modification of hippocampus TNF-α and S100B levels in the offspring of rats chronically exposed to morphine during adolescence

“…The mechanisms of this transgenerational effect could be considered in future studies. S100B autoantibody is increased in the brain of rats following chronic morphine exposure, and this was associated with changes in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and μ-opioid receptor autoantibodies (52). The increase in S100B antibodies may represent an augmented level of S100B protein and its entrance into the plasma, which is caused by chronic exposure of astrocytes and neural cells to opioids.…”

GluR2-3Y Inhibits the Acquisition and Reinstatement of Morphine-Induced Conditioned Place Preference in Rats

“…Chronic morphine treatment changes the composition and properties of AMPARs, and the expression and distribution of AMPAR subunits. For example, repeated morphine administration elevates the level of GluR1 [4], increases synaptic GluR1 labeling in the ventral tegmental area (VTA) [5], increases the expression of AMPARs lacking GluR2 in hippocampal synaptic fractions, and affects long-term depression (LTD) in hippocampal neurons [6]. Combined with other studies reporting that the proportion of membrane GluR2 decreases after chronic morphine treatment [7], repeated morphine administration may induce the endocytosis of AMPARs containing GluR2, while AMPARs lacking GluR2 insert into the membrane.…”