Corticosterone microinjected into nucleus pontis oralis increases tonic immobility in rats

• Published in: Hormones and behavior 2011-09, Vol.60 (4), p.448-456
• Main Authors: Sandoval-Herrera, Vicente, Trujillo-Ferrara, José G., Miranda-Páez, Abraham, De La Cruz, Fidel, Zamudio, Sergio R.
• Format: Article
• Language: English
• Subjects: Animal behavior; Animals; Behavior, Animal - drug effects; Behavior, Animal - physiology; Behavioral psychophysiology; Biological and medical sciences; Brain - drug effects; Brain - pathology; Brain - physiology; Corticosterone; Corticosterone - administration & dosage; Corticosterone - pharmacology; Fundamental and applied biological sciences. Psychology; Hormone Antagonists - pharmacology; Hormones; Hormones and behavior; Immobility Response, Tonic - drug effects; Immobility Response, Tonic - physiology; Injections, Intraventricular; Male; Microinjections; Mineralocorticoid Receptor Antagonists; Models, Biological; Motor Activity - drug effects; Motor Activity - physiology; Nucleus pontis oralis; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Rat; Rats; Rats, Wistar; Receptors, Glucocorticoid - antagonists & inhibitors; Rodents; Time Factors; Tonic immobility; Up-Regulation - drug effects
• ISSN: 0018-506X; 1095-6867
• DOI: 10.1016/j.yhbeh.2011.07.013

Tonic immobility (TI) is also known as “immobility response”, “immobility reflex”, “animal hypnosis”, etc. It is an innate antipredatory behavior characterized by an absence of movement, varying degrees of muscular activity, and a relative unresponsiveness to external stimuli. Experimentally, TI is commonly produced by manually forcing an animal into an inverted position and restraining it in that position until the animal becomes immobile. Part of the neural mechanism(s) of TI involves the medullo-pontine reticular formation, with influence from other components of the brain, notably the limbic system. It has been observed that TI is more prolonged in stressed animals, and systemic injection of corticosterone (CORT) also potentiates this behavior. At present, the anatomical brain regions involved in the CORT modulation of TI are unknown. Thus, our study was made to determine if some pontine areas could be targets for the modulation of TI by CORT. A unilateral nucleus pontis oralis (PnO) microinjection of 1μL of CORT (0.05μg/1μL) in rats resulted in clear behavioral responses. The animals had an increased duration of TI caused by clamping the neck (in this induction, besides of body inversion and restraint, there is also clamping the neck), with an enhancement in open-field motor activity, which were prevented by pretreatment injection into PnO with 1μL of the mineralocorticoid-receptor antagonist spironolactone (0.5μg/1μL) or 1μL of the glucocorticoid-receptor antagonist mifepristone (0.5μg/1μL). In contrast, these behavioral changes were not seen when CORT (0.05μg/1μL) was microinjected into medial lemniscus area or paramedian raphe. Our data support the idea that, in stressful situations, glucocorticoids released from adrenals of the prey reach the PnO to produce a hyper arousal state, which in turn can prolong the duration of TI. ► We studied the effects of corticosterone in pons on some motor behaviors. ► Corticosterone intra-PnO increased the duration of tonic immobility in rats. ► Corticosterone intra-PnO increased the open-field motor activity of rats. ► The effects of corticosterone intra-PnO were blocked by MR or GR antagonists. ► Corticosterone released by stress can reach PnO to modulate tonic immobility.