Original contributionNeurochemical basis of interleukin 2-modified discrimination behaviour
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2012, Pharmacology and TherapeuticsCitation Excerpt :Behaviorally, amphetamine also induces locomotor activity and rearing which was independent from astrocyte proinflammation in the cerebral cortex but was observed at the same time as astrocyte proinflammation in the hippocampus at specific chronic dosing levels (Frey et al., 2006). In addition, roles for immune mediators and receptors linking sensitization with astrocyte proinflammation have been detailed: astrocyte proinflammation in striatum and hippocampus was observed in mice with amphetamine-induced sensitization, and correlated with increased expression of P2Y1 (purinergic) receptor on both astrocytes and neurons (Franke et al., 2003); bFGF expression by astrocytes in the ventral tegmental area and nucleus accumbens in mice correlated with the degree of amphetamine-induced sensitization, and blockade of bFGF astrocyte expression in ventral tegmental area prevented this sensitization (Flores et al., 2000); exogenous systemic IL-6 potentiated amphetamine-induced sensitization (Zalcman et al., 1999); and exogenous systemic IL-2 potentiated amphetamine-induced discrimination, and was blocked by co-administration of naloxone with IL-2 (Ho et al., 1994). Most recently, co-administration of amphetamine with minocycline to humans revealed that glial attenuation blocked the reward, i.e. the “high” and “good” effects experienced following amphetamine (Sofuoglu et al., 2011).
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