1. Intracerebroventricular injection of neuropeptide EI increases serum LH in male and female rats
Maria Ester Celis, Mariela Sánchez-Borzone, Mercedes Lasaga, Andrés M Attademo Peptides . 2004 Nov;25(11):1995-9. doi: 10.1016/j.peptides.2004.06.010.
Melanin concentrating hormone (MCH) precursor-derived neuropeptide EI (NEI) has not yet been extensively studied. The aim of this study was to determine the effect of neuropeptide EI on serum levels of LH in normal male rats and chronically ovariectomized (CHR-OVX) female rats treated with estrogen benzoate (EB) and with a low dose of progesterone. The peptide, administered intracerebroventricularly in male and chronically ovariectomized female rats, increased LH serum levels compared to the controls injected with artificial cerebrospinal fluid. It is important to note that there is some relation between neuropeptide EI-melanin concentrating hormone and alpha-melanocyte stimulating hormone (alpha-MSH) indicating that all three peptides are associated in a complex inter-relationship. Therefore, the question that arises is if neuropeptide EI could also be related with the receptors for melanin concentrating hormone or alpha-melanocyte stimulating hormone.
2. Melanin-concentrating hormone and neuropeptide EI projections from the lateral hypothalamic area and zona incerta to the medial septal nucleus and spinal cord: a study using multiple neuronal tracers
J C Bittencourt, C F Elias Brain Res . 1998 Sep 14;805(1-2):1-19. doi: 10.1016/s0006-8993(98)00598-8.
The projection pathways of neurons containing melanin-concentrating hormone (MCH) and neuropeptide EI (NEI), two peptides colocalized in the lateral hypothalamic area (LHA) of the rat, were mapped using the retrogradely transported fluorescent dyes, true blue (TB) and diamidino yellow (DY). TB and DY were injected into the medial septum/diagonal band complex (MS/DBC) and the thoracic level of the spinal cord (SpCd), respectively. Brains from rats receiving only one or both tracer injections were immunohistochemically stained for MCH in the spinal cord and NEI in the forebrain. In the MS/DBC, NEI-immunoreactive (-ir) fibers are concentrated in the MS and in the vertical and horizontal limbs of the DBC. In the SpCd, MCH-ir fibers are concentrated primarily in lamina X. Of the diencephalic NEI-ir neurons, 37.15% project to the MS/DBC and reside in the rostromedial zona incerta (ZIm), in the LHAt and LHAp, and in the perifornical region. Of the diencephalic MCH-ir neurons, 20.2% project to the SpCd and reside in the LHAt and LHAp. In addition, 2. 2% of the MCH-ir cells and 8.7% of the NEI-ir cells in the hypothalamus were labeled with both retrograde tracers and thus project to both the MS/DBC and SpCd. These dual projection neurons are located mainly in the LHAt and LHAp. Anterograde injections of the tracer Phaseolus vulgaris leucoagglutinin into the LHAt and ZIm corroborated our findings in the retrograde studies. Potential autonomic and behavioral roles of the NEI and MCH systems in the MS/DBC and the SpCd are discussed.
3. Effect of beta-adrenoceptors on the behaviour induced by the neuropeptide glutamic acid isoleucine amide
Mariela E Sánchez-Borzone, Andrés Attademo, Gustavo Baiardi, María Ester Celis Eur J Pharmacol . 2007 Jul 30;568(1-3):186-91. doi: 10.1016/j.ejphar.2007.04.024.
Excessive grooming behaviour is induced by intracerebroventricular injections of the neuropeptide glutamic acid isoleucine amide (neuropeptide-EI), via the activation of A-10 dopaminergic neurons and the noradrenergic system. Our object was to study the latter system involved in these behaviours, using male Wistar rats weighing 250-300 g with i.c.v. implants. The results show that all the adrenoceptor antagonists "per se" do not affect excessive grooming behaviour or motor activity. Intracerebroventricular administration of propranolol, a general beta-adrenoceptor antagonist, before neuropeptide-EI, inhibited the induced excessive grooming behaviour in a dose dependent manner. Metoprolol, a beta(1)-adrenoceptor antagonist, also blocked this behaviour. However, intracerebroventricular injections of phentolamine, an alpha-adrenoceptor antagonist, and ((+/-)-1-[2,3-(Dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol), a beta(2)-adrenoceptor antagonist, had no effect on the behaviour induced by neuropeptide-EI induced behaviour for any of the doses tested. On the other hand, isoproterenol, a general beta-adrenoceptor agonist and dobutamine, a beta(1)-adrenoceptor agonist, both elicited similar behaviours as those induced by neuropeptide-EI. These results support the hypothesis that a relationship exists between neuropeptide-EI and beta-adrenoceptors, more specifically the beta(1)-adrenoceptor, as found with other similar endogenous peptides such as neurotensin, cholecystin, substance P and alpha-melanocyte stimulating hormone. Hence, neuropeptide-EI could probably be exerting a neuromodulating effect on the central nervous system.
