Effect of anticonvulsant drugs on peripheral benzodiazepine receptors of human lymphocytes

Peripheral Benzodiazepine Receptor Expression on Leukocytes and Neutrophil Function during Anticonvulsant Monotherapy

“…pBZr expression on monocytes has not been studied previously in epileptic subjects. As for lymphocytes, it has been reported that CBZ or VPA treatment increased pBZr density; however, no change was found during chronic PHT treatment [16,17]. The latter observation is in contrast with our results, and at present we have no explanation for this difference.…”

“…In this regard, it has been reported that the number of pBZrs in circulating lymphocytes might change according to the clinical response to anticonvulsants. In untreated epileptic patients, lymphocyte pBZr density does not differ from that in healthy controls, an observation which argues against the hypothesis that the disease itself may alter this parameter [16,17]. However, preliminary evidence indicates that diazepam-binding inhibitor (an endogenous ligand of pBZrs) levels are enhanced and pBZr density is decreased (possibly as a downregulation phenomenon) in drug-resistant patients compared to controls and drug-sensitive patients [26].…”

“…Overexpression of pBZrs on leukocytes seems unlikely to depend on a direct interaction of anticonvulsant drugs with these receptors since all the patients had increased pBZr density no matter what anticonvulsant drug was taken. Indeed, it has been shown that only CBZ, but not PHT or VPA, binds to pBZrs on human lymphocytes [16]. Modifications of pBZr density may be induced by different factors.…”

“…Epileptic patients maintained on anticonvulsants, such as CBZ, have increased pBZr density on circulating lymphocytes [16,17]. In addition, we have recently provided evi- dence [18] that, in epileptic patients treated with CBZ, pBZrs are overexpressed on neutrophils.…”

Diazepam Binding Inhibitor and Dehydroepiandrosterone Sulphate Plasma Levels in Borderline Personality Disorder Adolescents

“…DBI plasma levels have been assessed before in epileptic patients finding elevated values in adult generalized epilepsy and in drug-resistant both paediatric and adult patients [21]. A DBI alteration in this patient population was analogously hypothesized based on our group's previous report of a differential expression of PBR in PBMC obtained from drug-treated epileptic patients and of a significantly lower receptor density in drug-resistant patients when compared to newly diagnosed patients and to normal age-related controls [24,25]. Interestingly, DBI can modulate the GABAergic tone both by the biosynthesis of neurosteroids (able to directly change the activity of GABA A receptor-associated chloride channels and, more generally, to modulate gene expression), and by its direct action as a GABA A inverse agonist [26].…”