CC BY
61STH 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
5. PSYCHONEUROIMMUNOLOGY
ENHANCED STRESS-REACTIVITY IN RATS INDUCED BY IL-1BETA TREATMENT IN EARLY POSTNATAL ONTOGENESIS
O.E. Zubareva, V.M. Klimenko Institute for Experimental Medicine, RAMS,
Saint-Petersburg, Russia
In the last decade, there have been substantial efforts to characterize the effects of illness and inflammation on behavior, and understand how the immune system signals the central nervous system to induce the behavioral changes. These changes include mobility, feeding, exploration, social interaction, sexual behavior, cognitive function, and sleep. Key role in neuro-immune interactions has proinflammatory cytokine interleukin-lbeta (IL- lbeta). Delayed consequences of IL-lbeta enhancement in blood in early childhood on forming and development of reactivity and resistance are poorly investigated.
Methods. Wistar rat pups were injected i.p. with IL-lbeta at pyrogenic (1 mkg/kg) and subpyrogenic (100 ng/kg) doses during the 1st, 2nd and 3rd week of life (1st, 2nd and 3rd group, respectively). Control animals received saline. The behavior of rats was evaluated twice at the age of 35—40 days (adolescents) and later at 3 months (adults) in the open field, elevated plus-maze and intruder-resident tests before and after stress (electrical footshock). The content of biogenic amines in hypothalamus, hippocampus and neocortex was measured by HPLC.
Results and discussion. An increased locomotor activity (more behavioral patterns in the open field), abnormally low level of anxiety and affected exploration were observed in adolescents treated with IL-1 beta (maximal changes seen in animals treated during 1-st and 3-d weeks). Behavioral testing of adult rats revealed slight differences between the control and experimental groups. These changes were accompanied by enhanced brain dopamine level, especially in the rats of 35 days age, treated by IL-1beta during the 3rd week of life. Communicability in «intruder-resident» test after stressing action decreased in rats treated by saline during the 1-st week, by IL-1beta in subpyrogenic dose during the 1-st week, and by IL-1beta at pyrogenic dose during the
2-nd week. Decreased locomotor activity (number of acts) in the open field test induced by stress was revealed in all groups beside of rat received saline during the 1 week of life. The decrease was maximal in animals treated by pyrogenic doses of cytokine during the 1-st week, by pyrogenic and subpyrogenic doses of IL-1beta during the 2-nd week, by saline and cytokine in both doses during the 3-d week. Exploration was affected in all experimental groups (duration of hole-pocking). Reduced exploration was robust in rats treated by pyrogenic doses of IL-1beta during 1-st and 2-nd weeks and by subpyrogenic doses of IL-1beta during 2-nd and
3-d weeks. Overall, changes of behavior after the stress were more expressed in animals treated by IL-1beta in early postnatal ontogenesis, compared with control. The difference in stress-reactivity depended on a treatment time: pyrogenic dose of IL-1beta produced more expressed stress-induced changes if done during the 1-st week, subpyrogenic dose — during the 3-d week. During the 2-nd week, both doses produced considerable enhancement of behavioral response to stress. The latter fact has a special significance because animals under normal (stress-free) conditions display minimal behavioral disturbances.
Psychopharmacol. Biol. Narcol. 2005. Vol. 5, N 2. P. 917—918
Psyhopharmacology & biological narcology
ISSN 1606—8i8i
Conclusion. Treatment by IL-1b in early postnatal ontogenesis enhanced stress-reactivity in rats. This effect of IL-ibeta is accompanied with increase of brain dopamine level in hypothalamus. The high susceptibility of nervous system to IL-ibeta in early postnatal ontogenesis can be due to immaturity of mechanisms inhibiting IL-ibeta action in the brain.
Psychopharmacol. Biol. Narcol. 2005. Vol. 5, N 2. P. 9i7-9i8
Psyhopharmacology & biological narcology
ISSN i606—8i8i
