Changes in beta-adrenergic receptors in the neurohypophysis and intermediate lobe of the rat have been characterized under physiological and stress conditions. Classical immobilization stress (IMO) was also combined with the immersion of rats into water (IMO + COLD stress). Both types of stress were applied for 30, 60 or 150 min. The intensity of stress stimuli were controlled by measuring the level of plasma ACTH. Changes in the level of plasma ACTH indicate that both types of experimental protocol induced reliable and reproducible stress conditions. Binding studies dealing with beta-adrenergic receptors in the intermediate lobe and neurohypophysis were performed in saturation binding studies by using of 125l-iodopindolol. Binding parameters, maximal binding capacity (Bmax) and dissociation constant (Kd) were assessed by nonlinear analysis with computer program Viewfit. In the neurohypophysis, no changes of Kd were found in the stressed animals. However, maximal binding capacity was decreased significantly with the increased exposure to the stress. In the intermediate lobe Kd values were slightly decreased and Bmax values decreased gradually with increasing duration of stress exposure. Our findings suggest that the process of receptor desensitization of beta-adrenergic receptors can also be detected under stress conditions in the neurohypophysis and intermediate lobe of the pituitary gland where it could contribute to the mechanisms involved in stress reactions.
After long-lasting administration of estradiol (4—6 weeks) in the presence or absence of pertussis toxin treatment we followed up the changes in body weight and adenohypophyseal weight in rats subjected to this treatment. The most striking effect was the potentiating effect of pertussis toxin on the estradiol-induced adenohypophyseal growth reaction. Adenylyl cyclase activity in the adenohypophysis was significantly increased in the estradiol- treated group and the addition of pertussis toxin did not further increase this enzyme activity. The lipolytic activity in adipose tissue exhibited a similar response as adenohypophyseal growth. Adrenergic lipolysis stimulated by pertussis toxin was highly significantly increased in tissues of rats treated with pertussis toxin. Our results show that the estrogen-induced adenohypophyseal growth reaction is highly potentiated by the treatment of rats with pertussis toxin and that this effect is in many aspects similar to that observed in adrenergic lipolysis. It thus seems that both processes might be mediated via a pertussis toxin-sensitive G protein which is involved in inhibitory regulation of adenylyl cyclase.
The multitalented neuropeptide galanin was first discovered 30 years ago but initially no biologic activity was found. Further research studies discovered the presence of galanin in the brain and some peripheral tissues, and galanin was identified as a modulator of neurotransmission in the central and peripheral nervous system. Over the last decade there were performed very intensive studies of the neuronal actions and also of nonneuronal actions of galanin. Other galanin family peptides have been described, namely galanin, galanin-like peptide, galanin-message associated peptide and alarin. The effect of these peptides is mediated through three galanin receptors subtypes, GalR1, GalR2
and GalR3 belonging to G protein coupled receptors, and signaling via multiple transduction pathways, including inhibition of cyclic AMP/protein kinase A (GalR1, GalR3) and stimulation of phospholipase C (GalR2). This also explains why one specific molecule of galanin can be responsible for different roles in different tissues. The present review summarizes the information currently available on the relationship between the galaninergic system and known pathological states. The research of novel galanin receptor specific agonists and antagonists is also very promising for its future role in pharmacological treatment. The galaninergic system is important target for current and future biomedical research.