Alterations in brain and pituitary β-endorphin content in genetically epilepsy-prone rats

Carr, J.A; Carpenter, A.M; D'Souza, M.M; Elmore, A.R; Lovering, A.T; Reigel, C.E

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Volume 31, Issue 2 , Pages 113-122, July 1998

Alterations in brain and pituitary β-endorphin content in genetically epilepsy-prone rats

J.A Carr
- Department of Biological Sciences, Texas Tech University, Box 4-3131, Lubbock, TX 79409-3131, USA
- Corresponding author. Tel.: +1 806 7422724; fax: +1 806 7422963; e-mail: gtjac@ttacs.ttu.edu
A.M Carpenter
- Department of Biological Sciences, Texas Tech University, Box 4-3131, Lubbock, TX 79409-3131, USA
M.M D'Souza
- Department of Biological Sciences, Texas Tech University, Box 4-3131, Lubbock, TX 79409-3131, USA
A.R Elmore
- Department of Biological Sciences, Texas Tech University, Box 4-3131, Lubbock, TX 79409-3131, USA
A.T Lovering
- Department of Biological Sciences, Texas Tech University, Box 4-3131, Lubbock, TX 79409-3131, USA
C.E Reigel
- Department of Pharmacology, Texas Tech University, Health Sciences Center, Lubbock, TX 79430, USA

Received 15 December 1997; received in revised form 24 February 1998; accepted 24 March 1998.

Abstract

We measured β-endorphin concentrations in the anterior and neurointermediate lobes of the pituitary gland and in microdissected brain regions of moderate-seizure genetically epilepsy-prone rats (GEPR-3), severe-seizure GEPR-9s and Sprague–Dawley non-epileptic control rats. Plasma concentrations of β-endorphin and α-melanocyte-stimulating hormone (α-MSH) were also measured as indicators of pituitary POMC-peptide secretion. Concentrations of β-endorphin in the anterior lobe of GEPR-3s were 53% higher compared to controls and 57% higher compared to GEPR-9s. There were no differences in neurointermediate lobe β-endorphin concentrations between control and either GEPR strain. Plasma β-endorphin concentrations were significantly lower in GEPR-9s than controls. Plasma levels of α-MSH did not differ between control and GEPRs. In the hypothalamus of GEPR-9s β-endorphin concentrations in the arcuate nucleus were significantly greater than in GEPR-3s. Concentrations of β-endorphin in the central amygdala of GEPR-9s were two- to threefold greater than in control or GEPR-3s. β-Endorphin concentrations in the central gray of GEPR-3s were 58% lower than control or GEPR-9s. These data suggest that anterior lobe β-endorphin secretion is reduced in GEPR-9s. Furthermore, brain endorphinergic pathways appear to be differentially altered in GEPR-3s and GEPR-9s. Alterations in pituitary β-endorphin secretion and brain endorphinergic systems may contribute to seizure susceptibility in GEPRs and to differences in seizure severity between GEPR-3s and GEPR-9s.