The lateral hypothalamus and anterior hypothalamic nucleus differentially contribute to rats' defensive responses in the elevated plus-maze and shock-probe burying tests.

Lesions or pharmacological inhibition of the lateral septum reduce rats' open-arm avoidance in the elevated plus-maze and their burying behavior in the shock-probe test. The current study examined whether hypothalamic areas that receive direct input from the lateral septum also influence open-arm avoidance and defensive burying. Bilateral infusions of the GABA-A receptor agonist muscimol (20 ng) into the lateral hypothalamus selectively increased rats' open-arm avoidance without affecting shock-probe burying. In contrast, infusions of muscimol into the anterior hypothalamic nucleus suppressed burying without affecting rats' open-arm avoidance. These dissociations suggest that the lateral hypothalamus contributes to the exploration of potentially threatening environments, whereas the anterior hypothalamus influences defensive responses to proximal discrete threat stimuli.

Filament size influences temperature changes and brain damage following middle cerebral artery occlusion in rats.

Postischemic spontaneous hyperthermia as a complication of occlusion of the middle cerebral artery with an intraluminal filament has been observed by some authors, but many other reports do not discuss this factor. The possible reasons why some of the authors have not seen severe hyperthermia in their experiments include differences in surgical technique, the strain of animals, the type of the anesthesia, and the occluder filament. The aim of this study was to examine the changes in the core temperature of rats using different types of filaments. The middle cerebral artery was occluded for 2 h with three different types of filaments. The changes in the temperature were continuously monitored during occlusion and for the next 4 h. Groups with uncontrolled hyperthermia and with controlled normal core temperature were used. In addition, the necrotic and penumbral areas were measured 4 and 48 h after the ischemia in both groups. Spontaneous postischemic hyperthermia was detected using all types of filaments. A close correlation was found between the size of the occluder filament and the time-course and degree of hyperthermia. Moreover, the size of the filament correlated well with the size of the infarct at both 4 and 48 h after the occlusion. We suggest that filament size is a major contributor to the degree of hyperthermia and the development of brain damage in the middle cerebral artery occlusion model. Our results call attention to the need to standardize the methods used to screen for therapeutic agents for stroke.

Anterior hypothalamic lesions inhibit antigen-induced airway eosinophilia in rats.

OBJECTIVE: Although previous studies have found that electrolytic lesions of the anterior hypothalamic area (AHA) resulted in the suppression of anaphylaxis, their effect on late allergic responses has scarcely been investigated. To clarify the role of the AHA on possible late asthmatic responses, including their neuroendocrinological mechanisms, we examined the effect of electrolytic AHA lesions on antigen-induced eosinophilic infiltration into the airway tract and measured the plasma corticosterone and catecholamine levels in sensitized rats, i.e. a model of bronchial asthma. METHODS: The rats were randomly divided into 3 groups, including: (1) an unoperated control group; (2) a sham AHA-lesioned group and (3) an AHA-lesioned group. Then, we investigated antigen-induced eosinophilic infiltration into right bronchoalveolar lavage fluid (BALF) and the lamina propria mucosae of the left main bronchus. RESULTS: The AHA-lesioned group showed the significantly lowest number of eosinophils in both the BALF (p < 0.01) and the main bronchus (p < 0.05). The plasma adrenaline levels in the AHA-lesioned group were significantly higher than those in the other groups (p < 0.05). No differences were found in the plasma corticosterone or noradrenaline levels among the 3 groups. CONCLUSION: This study provides evidence that AHA lesions inhibit not only anaphylaxis, but also late asthmatic response related to airway eosinophilic infiltration, possibly via an alteration of the sympathetic nervous function.

Adult respiratory distress syndrome (ARDS): the pathophysiologic role of catecholamine-kinin interactions.

The pathophysiology of the adult respiratory distress syndrome (ARDS) seems to be based on a cybernetic imbalance of the central nervous system (CNS), with activation of secondary peripheral effectors (PE). Lung vascular hyperpermeability is a crucial feature of PE actions in ARDS. Kinins (Bk), as PE, are important vascular hyperpermeability-inducing factors, with potential participation in ARDS induction. To test this hypothesis, we produced experimental ARDS in male Wistar rats using the anterior hypothalamic nuclei lesion model. Adrenalectomy, adrenal demedullation and denervation, alpha-adrenergic blockade, and catecholamine (CA) depletion reduced ARDS severity whereas beta-adrenergic blocking and CA uptake I inhibition resulted in a potentiated aspect. The Bk depletion or inhibition of the generation of these peptides resulted in attenuation of the pathologic features of ARDS. Bk half-life prolongation produced intense potentiation of the respiratory syndrome. This work suggests that Bk and CA systems are interactive and interdependent in their pathogenic actions on lungs in ARDS, involving, probably, a reciprocally-activating mechanism.