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    • The third generation cephalosporin antibiotics can cross the

    2022-07-29

    The third-generation cephalosporin 449 can cross the blood brain barrier (BBB) [94]. In addition, several studies have shown that CEF can also cross the BBB [95,96] through a facilitated transport process [95]. However, due to the fact that CEF has poor bioavailability when taken orally, CEF must be given through the parenteral route for maximum effects. CEF is highly bound to plasma proteins [95,97], and most of CFE is eliminated in urine and biliary excretion [for review see Ref. (98)]. It is known that CEF can increase GLT-1 and xCT expression in the brain; therefore, different studies have investigated different possible mechanisms behind it. For instance, a study found that CEF treatment can facilitate the nuclear P65 translocation and activate the nuclear factor-κB (NF-κB) signaling pathway when tested in primary human fetal astrocytes [99]. Moreover, it was reported that CEF increased the expression of NF-κB and the phosphorylation of Akt in the NAc and PFC in P rats [37]. In addition, CEF was also found to activate the nuclear factor erythroid 2-related factor2 (Nrf2), which was suggested to increase the expression of xCT in the HIP cell line [100]. In this study, we used CEF (200 mg/kg, i.p.) to attenuate HYD reinstatement. Indeed, studies have found that CEF can attenuate reinstatement of morphine [35], heroin [16], methamphetamine [31], cocaine [32] and nicotine [34]. In addition, several studies from our lab revealed that CEF (200 mg/kg, i.p.) attenuated chronic alcohol drinking in P rats [36,37,101,102]. Lower doses of CEF were not considered in this study due to the fact that it was administered every other day during the extinction phase. We have tested CEF at lower dose (50 mg/kg, i.p.) to attenuate cue-induced reinstatement to cocaine-seeking behavior [103]. However, CEF at high dose (200 mg/kg, i.p.) attenuated cue-induced reinstatement to cocaine-seeking behavior and this effect was associated with upregulation of GLT-1 expression in the NAc and PFC. In fact, CEF at lower dose (50 mg/kg, i.p.) did not upregulate the expression of GLT-1, which suggests the non-attenuating effect of this dose in cocaine-seeking behavior. Furthermore, it has been suggested that CEF (200 mg/kg, i.p.) is equivalent to 13 g/day in clinical setting, where the normal dose of CEF is around 2 g/day [104]. Also, it has been proposed that this dose could produce CNS concentration equivalent to the concentration needed to modulate GLT-1 expression (3.5 uM) in vitro [105]. In general, high doses of CEF may cause unspecific adverse effects when used for a long period of time. However, several studies have used CEF to attenuate the reinstatement of other drugs of abuse for more than five consecutive days without reporting serious adverse effects [16,31,32,34,35].
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    Introduction Nowadays, platelets are in the main stream of neurochemical research because they can play a specific role in a range of neurological disorders (Aliprandi et al., 2005, Behari and Shrivastava, 2013, do Nascimento et al., 2006, Rainesalo et al., 2003, Rolf et al., 1993, Yao et al., 2006, Zoia et al., 2004). Platelets are able: (1) to accomplish glutamate uptake by high-affinity Na+-dependent glutamate transporters EAAT 1–3 in the plasma membrane, which use Na+/K+ gradient as a driving force (Begni et al., 2005, Hoogland et al., 2005, Kasatkina and Borisova, 2010, Mangano and Schwarcz, 1981, Rainesalo et al., 2003); (2) to accumulate glutamate in dense secretory granules by special vesicular glutamate transporters VGLUT 1 and 2, which utilize the proton electrochemical gradient generated by the vacuolar H+-ATPase (Tremolizzo et al., 2006); (3) to release granular glutamate by means of exocytosis during activation (Borisova et al., 2011a, Tremolizzo et al., 2006); (4) to express NMDA, AMPA, kainate and mGlu 3,4 receptors, which are involved in the regulation of platelet aggregation/activation (Amisten et al., 2008, Franconi et al., 1998, Sun et al., 2009). Glutamate released from platelets acts in an autocrine manner promoting complete platelet activation, and in a paracrine manner increasing the agonist sensitivity of the recruited platelets (Gawaz, 2001).