B. Burgi et al., Ontogeny of diazepam binding inhibitor acyl-CoA binding protein mRNA and peripheral benzodiazepine receptor mRNA expression in the rat, J NEUROENDO, 11(2), 1999, pp. 85-100
The Diazepam Binding Inhibitor/Acyl-CoA Binding Protein (DBI/ACBP) has been
implicated in different functions, as acyl-CoA transporter and as an endog
enous ligand at the GABA, receptor and the peripheral benzodiazepine recept
or (PBR). The latter is thought to be involved in control of steroidogenesi
s, We studied the ontogeny of DBI/ACBP and PER mRNA expression in embryos a
nd offspring of time-pregnant Long Evans rats by in-situ hybridization with
P-33-endlabelled oligonucleotides. Both mRNAs were present in embryo and p
lacenta at gestational day (G)11, the earliest stage studied. DBI/ACBP mRNA
was strongly expressed from embryonic through mid-foetal stages in central
nervous system (maximum in neuroepithelium), cranial and sympathetic gangl
ia, anterior pituitary, adrenal cortex, thyroid, thymus, liver and (late fo
etal) brown adipose tissue, moderately in testis, heart, lung and kidney. I
n brain, a late foetal decrease of DBI/ACBP mRNA was followed by an increas
e at postnatal day 6, Peripheral benzodiazepine receptor mRNA expression st
arted very low and increased to moderate levels in adrenal cortex and medul
la, testis, thyroid, brown adipose tissue, liver, heart, lung, salivary gla
nd at mid- to late-foetal stages. Data suggest a significant role of DBI/AC
BP at early developmental stages. Both proteins may be involved in the cont
rol of foetal steroidogenesis. However, differences in developmental patter
ns indicate that additional functions may be equally important during ontog
eny, such as the involvement in lipid metabolism in the case of DBI/ACBP.