CC BY
359th multidisciplinary international
Conference of Biological Psychiatry
«Stress and Behavior»
Proceedings of the 9th International Multidisciplinary Conference «Stress and behavior» Saint-Petersburg, Russia, 16-19 May 2005 Editor: Allan V. Kalueff, PhD
CONFERENCE ABSTRACTS 2. SLEEP AND BEHAVIOR
CHOLINERGIC RECEPTORS IN THE MEDIAL AND VENTROLATERAL PREOPTIC AREA IN THE REGULATION OF SLEEP-WAKEFULNESS CYCLE IN PIGEONS
T.G. Komarova
Sechenov Institute of Evolutionary Physiology and Biochemistry RAS, St. Petersburg, Russia
The preoptic area of hypothalamus is known to play a key role in the control of different physiological functions, particularly sleep control and thermoregulation. Lesions of the preoptical area produced total suppression of sleep in pigeons, rats and cats [John et al., 1994, Ekimova, Pastukhov, 2005]. Numerous data show that neurons in the ventrolateral preoptic area (VLPO) containing GABA promote sleep by inhibiting neurons of the arousal systems. It is suggested that in the VLPO, GABA-A receptors participate in the maintenance of non-rapid-eye-movement sleep (NREM) [Li et al., 2001]. It may be hypothesized that transmitters used by wake-related arousal networks in mammals, including acetylcholine and noradrenaline, exert an inhibitory action on the VLPO neurons. In the preoptico-anterior hypothalamic area, cholinergic system was found in pigeons [Medina et al., 1994]. The functional meaning of muscarine (M-) and nicotine (N-) cholinergic receptors in the VLPA and MPA is unknown in the regulation of wake-sleep behavior of pigeons. In this study, we identified the role of M- and N- cholinergic receptors of these regions in the regulation of sleep-wakefulness cycle. Experiments were performed on freely moving adult pigeons (Columba livia) housed under controlled conditions (12/12 h light/dark cycle, 23—25 oC, food and water ad libitum). Under nembutal anesthesia, electrodes for recording electroencephalogram, electrooculogram, electromyogram of the pectoral muscle and guide cannulae were chronically implanted. The birds were allowed to recover for 7 days prior to testing. All electrophysiological parameters were continuously recorded, processed and stored using a computer system SASH-8800 (USA). The following drugs were used: arecoline, a M-cholinoreceptor agonist (0.6 mkg/0.2 mkl), amizil, a M-cholinoreceptor antagonist (2 mkg/0.2 mkl), nicotine, a N-cholinoreceptor agonist (0.3 mkg/0.2 mkl) and saline. All microinjections were made 5—10 min before the dark onset. The injection sites were morphologically verified at the end of experiments. The results were analyzed by variance statistics. The microinjections of M-cholinoreceptor agonist into the MPO as well as into the VLPO induced an increase in the total duration of wakefulness and a decrease in NREM and REM sleep in comparison with the control. The mean duration of wakefulness significantly increased without considerable changes in the number of episodes. However, the activation of M-cholinoreceptors in the MPA resulted in a greater increase in wakefulness compared to that elicited in the VLPA. The blockade of M-cholinoreceptors in the VLPA by amysil produced 1-h NREM. Microinjections of nicotinic into the VLPO was responsible for a decrease in NREM sleep duration and an increase in total duration of wakefulness. In contrast, the activation of N-cholinoreceptors in the VLPA increased NREM sleep duration. A comparative analysis of activation of N-cholinoreceptors in the MPA and VLPA indicate the opposite directed participation of N-cholinoreceptors of these regions in the regulation of sleep-wakefulness cycle in pigeons. For example, in the VLPO microinjections of nicotinic led to an increase in NREM, whereas it produced prolonged wakefulness in the MPO. These findings suggest that hypothalamic VLPA and MPA contain different subtypes of N-cholinoreceptor to control sleep-wakefulness cycle. Activation of presynaptic nicotinic receptors located in the GABAergic terminals was known to play a major role in the cholinergic regulation of the inhibitory GABAergic input to supraoptic nucleus neurons in the rat hypothalamic slice
Psychopharmacol. Biol. Narcol. 2005. Vol. 5, N 2. P. 895-896 Psyhopharmacology & biological narcology
ISSN 1606-8181
[Deurveilher, Semba, 2005]. It is reasonable to suggest that activation of nicotinic receptors in VLPO inhibits GABAergic wake-promoting input of the basal forebrain. It disinhibits sleep-positive VLPO neurons. In pigeons, wakefulness promoted by activation of N- and M- cholinergic receptors seems to be associated with their action on noradrenergic transmission. It is known that sleep-promoting VLPO neurons may be dually inhibited by ACh through a muscarinic postsynaptic action and a nicotinic presynaptic action on noradrenergic terminals. Such dual complementary actions allow ACh and nicotine to enhance wakefulness by inhibiting sleep-promoting systems while facilitating other wake-promoting systems [Saint-Mleux et al., 2004]. Our results suggest that in pigeons the wake-sleep control mechanism differ from those observed in rats. The study was supported by the Program of DBS of RAS «Integrative mechanisms of wakefulness-sleep cycle regulation».
Psychopharmacol. Biol. Narcol. 2005. Vol. 5, N 2. P. 895-896 Psyhopharmacology & biological narcology
ISSN 1606-8181
