Expression of delta opioid receptor mRNA and protein in the rat cerebral cortex and cerebellum is decreased by growth hormone

Abstract

Hormones released from the pituitary have been shown to regulate the expression of different proteins in the central nervous system. We wanted to examine whether peripheral administration of bovine growth hormone (bGH) regulates the expression of delta-opioid receptor (DOR) in the cerebral cortex and cerebellum. Expression of the DOR protein was quantified using Western blot densitometry. DOR mRNA was quantified with a solution hybridization RNase protection assay. Hypophysectomized (Hx) and untreated normal female rats were included in the study. All Hx rats were hormonally treated with cortisol (400 microg/kg/day) and L-thyroxine (10 microg/kg/day) for 19 days. Hypophysectomy resulted in a threefold increase in cerebral cortex and a twofold increase in cerebellum of the DOR protein compared with normal rats. One subgroup of Hx rats received bGH (1 mg/kg body weight) as a daily subcutaneous injection for 19 days. This treatment normalized the levels of DOR protein in the cerebral cortex and cerebellum. Immunohistochemical experiments showed that GH decreased DOR expression especially in layers II-VI in cerebral cortex and in stratum moleculare in cerebellum. Quantification of DOR mRNA by solution hybridization RNase protection assay corresponded to the DOR protein measurements. We conclude that the expression of DORs in cerebral cortex and cerebellum is regulated by GH.

Peripheral administration of bovine GH regulates the expression of cerebrocortical beta-globin, GABAB receptor 1, and the Lissencephaly-1 protein (LIS-1) in adult hypophysectomized rats

“…Whether the lower relative weight gain in experiment 2 should impact anything, it might be that the effect of GH could be somewhat lower relative to hx in the PCR experiments. The present assay did not detect regulation of some previously known GH-regulated transcripts such as the NMDA receptor subunits and PSD-95 [6], the DOR [13], and connexin43 [14]. For these transcripts, the expression levels were too low to allow analysis of expression.…”

“…Serotonin and norepinephrine levels are affected in specific brain regions after GH administration [12]. Furthermore, betaendorphin receptors [13], neuronal glutamate receptors, and the insulin-like growth factor type 1 receptor (IGF-1R), and postsynaptic density protein-95 (PSD-95) [6], and intercellular communication in astrocytes are regulated by GH administration [14,15]. Functionally, GH has been shown to protect the brain against hypoxic-ischemic (HI) injuries in rodents [16,17] but the mechanisms are not fully understood.…”

Comparison of opioid receptor distributions in the rat central nervous system

“…This Chemicon antibody and others raised against the same peptide have been used for immunohistochemical studies of the rat CNS previously (Arvidsson et al, 1995a;Cahill et al, 2001;Milner, 1996, 1997;Dado et al, 1993;Persson et al, 2000;Saland et al, 2005;Varona et al, 2003;Wang et al, 2003). Pre-absorption with the antigen peptide has previously been found to abolish the immunoreactivity of this Chemicon antibody and other N 3-17 anti-δ primary antibodies (Arvidsson et al, 1995a;Cahill et al, 2001;Dado et al, 1993;Persson et al, 2000Persson et al, , 2003.…”

Growth Hormone (GH) and Gonadotropin-Releasing Hormone (GnRH) in the Central Nervous System: A Potential Neurological Combinatory Therapy?

“…Neurotransmission is modulated by GH actions, as GABA B receptors responded to its administration in the cingulate cortex, primary motor cortex and the caudate putamen, and this effect was correlated with an increase in cognitive function [ 47 , 48 ]. There were clear implications of GH in the opioid system function in which it was able to decrease levels of the delta-opioid receptor in layers I–IV of the cerebral cortex [ 87 ]. In brain trauma, GH has demonstrated neurotrophic actions in the cognitive, sensorial, and motor functions [ 57 , 58 , 88 , 89 ].…”