Thesis (Ph.D.)--Michigan State University. Dept. of Physiology, 2008. / Title from PDF t.p. (viewed on Mar. 27, 2009) Includes bibliographical references. Also issued in print.

Thesis (Ph. D.)--Michigan State University. Dept. of Comparative Medicine and Integrative Biology, 2008. / Title from PDF t.p. (viewed July 31, 2009). Includes bibliographical references (p. 165-198). Also issued in print.

Thesis (doctoral)--Malmö, 1983.

Thesis (M.S.)--University of Wisconsin--Madison, 1965. / eContent provider-neutral record in process. Description based on print version record. Bibliography: l. 25-26.

Proefschrift Maastricht. / Auteursnaam op omslag: Jos C.S. Kleinjans. Lit.opg.

No description available.

An excitatory role for norepinephrine (NE) in the regulation of luteinizing hormone (LH) release was first suggested when it was demonstrated that noradrenergic receptor antagonists were able to block ovulation. More recently it has been proposed that NE has both an excitatory role and an inhibitory role in the neuroendocrine regulation of LH release. The excitatory effects may be mediated by alpha-adrenergic receptors and the inhibitory effects may be mediated via beta-adrenergic receptors. These experiments were performed to better understand the role of NE, the receptor type through which NE exerts its effects, and the role of the two major NE pathways in the brain, on LH secretion in the rat. To further understand the role of NE in pulsatile LH release, NE or one of its agonists was infused into the third ventricle of ovariectomlzed rats pretreated with an adrenergic antagonist. In the second set of experiments ascending noradrenergic pathways were electrically stimulated to determine their effect on pulsatile LH release. These experiments demonstrated that the inhibitory effect of NE on pulsatile LH release is blocked when alpha-1- or alpha-2- receptors are blocked but not when beta-receptors are blocked. Electrical stimulation experiments in unprimed ovariectomlzed rats demonstrated that activation of the dorsal noradrenergic tract (DNT) but not the ventral noradrenergic tract (VNT) inhibited pulsatile LH release. Another series of experiments were performed to determine the role NE in the regulation of LH release in the steroid-primed ovariectomlzed rat. These experiments demonstrated that activation of alpha- or beta-adrenergic receptors inhibited the LH surge when adrenergic agonists are infused during the rising phase of the surge. In a similar manner electrical stimulation of either the DNT or VNT inhibited LH release if stimulation occured during the rising phase of the surge. The inhibitory effects of the DNT appear to be via activation of alpha-adrenergic receptors since inhibition was prevented by an alpha-adrenergic antagonist. Under a variety of steroidal conditions and stimulation parameters, activation of the DNT or VNT did not enhance LH release. The lone exception to this was stimulation of the VNT in anaesthetized, steroid-primed ovariectomized rats pretreated with an alpha-adrenergic antagonist. In this case stimulation of the VNT did enhance LH release over non-stimulated and electrically stimulated, saline-treated controls. These results suggest that LH release is enhanced by stimulation of the VNT only when alpha-adrenergic receptors are blocked. In conclusion, it is evident from these studies that activation of alpha-adrenergic receptors either by intraventricular infusion of NE or alpha-agonists, as well as electrical stimulation of noradrenergic tracts inhibits LH secretion. This suggests that the inhibitory effects of NE may be more of a factor in the regulation of LH release than has been previously proposed. In conclusion, NE, in addition to its well established excitatory role, may also have an important inhibitory role in the regulation of LH release. It appears that both inhibitory and excitatory effects of NE on LH release may be mediated by both alpha- and beta-receptors. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

The hypothesis that the noradrenergic projection from the locus coeruleus (LC) to the cerebral cortex and hippocampus is an important neural substrate for learning was evaluated. Maze performance was studied in rats receiving either electrolytic lesions of the LC, or 6-hydroxydopamine (6-0HDA) injections into the region of the dorsal tegmental noradrenergic projection. In contrast to the results of an earlier report (Anlezark, Crow, and Greenway, 1973), LC lesions did not disrupt the acquisition of a running response for food reinforcement in an L-shaped runway, even though hippocampal-cortical noradrenaline (NA) was reduced to 29%. Greater telencephalic NA depletions (to 6 percent of control levels) produced by 6-0HDA also failed to disrupt the acquisition of this behaviour or impair the acquisition of a food reinforced position habit in a T-maze. Neither locomotor activity nor habituation to a novel environment was affected by the 6-0HDA lesions. Rats with such lesions were, however, „ found to be significantly more distractible than controls during the performance of a previously trained response. In another group of rats with identical 6-OHDA injections, the establishment of a lithium chloride-induced conditioned taste aversion was not affected by the lesions. The hypothesis that telencephalic NA is of fundamental importance in learning was not supported. / Medicine, Faculty of / Graduate

The role of noradrenaline (NA) in the behavioural and pharmacological effects of morphine was evaluated in rats. Animals received specific injections of 6-hydroxydopamine (6-OHDA) into the dorsal noradrenergic bundle (DB) resulting in selective depletion of telencephalic NA levels and increased levels of noradrenaline in the spinal cord and cerebellum. Employing changes in the hypoactive phase of morphine-induced locomotor activity as an index of tolerance development, it was observed that injection of 6-OHDA into the dorsal noradrenergic bundle resulted in a slower rate and a lesser degree of tolerance development to morphine. The effect of the DB-6-0HDA lesion on physical dependence was assessed by measuring naltrexone-induced withdrawal in lesioned and control animals who had received chronic morphine treatment. Results indicate that although NA is important in tolerance development, it does not mediate a dominant role in withdrawal, although behavioural evidence suggesting a secondary or modulatory role is presented. The interaction of amphetamine and morphine with the dopamine (DA) system was also assessed by studying the behavioural effects of amphetamine in animals following either acute or chronic morphine treatment. It was observed that amphetamine potentiated the spontaneous locomotor hyperactivity following both acute and chronic morphine treatment. The DB-6-OHDA lesion did not affect the locomotor potentiation of amphetamine in morphine pre-treated animals, and the hypothesis that another transmitter system mediates this effect, specifically DA, is discussed. / Medicine, Faculty of / Graduate

No description available.