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Defensive responses are neurophysiological processes crucial for survival during threatening situations. Defensive immobility is a common adaptive response, in rodents, elaborated by ventrolateral periaqueductal gray matter (vlPAG) when threat is unavoidable. It is associated with somatosensory and autonomic reactions such as alteration in the sensation of pain and rate of respiration. In this study, defensive immobility was assessed by chemical stimulation of vlPAG with different doses of NMDA (0.1, 0.3, and 0.6 nmol). After elicitation of defensive immobility, antinociceptive and respiratory response tests were also performed. Results revealed that defensive immobility was followed by a decrease in the nociceptive perception. Furthermore, the lowest dose of NMDA induced antinociceptive response without eliciting defensive immobility. During defensive immobility, respiratory responses were also disturbed. Interestingly, respiratory rate was increased and interspersed with prolonged expiratory phase of breathing. These findings suggest that vlPAG integrates three different defensive behavioral responses, contributing to the most effective defensive strategies during threatening situations.

We describe the various side effects occurring in dialysis sessions and indicate measures for their prevention and/or treatment. Next, we analyze dialysis headache in terms of incidence, prevalence, criteria for its inclusion in the classification of the International Headache Society, and factors related to its triggering, ie, bradykinin and nitric oxide (NO), which have increased plasma levels during dialysis. This permits a critical analysis in comparison with NO donor headache in terms of the pathophysiologic mechanisms that mediate the triggering of both conditions. A similarity is particularly detected in terms of the role of NO as the last link in the chain of events that precedes the onset of headache, which is preceded by a latency period of 3 to 4 hours, much longer than the few seconds needed to inactivate NO. A hypothesis is raised to explain this phenomenon, opening new perspectives for the study of the pathophysiology of headaches, including primary headaches.

The action of prednisolone at the neuromuscular junction was studied in mouse isolated phrenic nerve-diaphragm and rat external popliteal/sciatic nerve-tibialis anterior muscle preparations. Prednisolone (0.03 mM and 0.3 mM) did not alter the twitch-tension in phrenic nerve-diaphragm preparations after 120 min, but increased the frequency (170 +/- 4%) and amplitude (200 +/- 13%) of miniature end-plate potentials. Quantal content was not influenced by the glucocorticoid treatment. Prednisolone (400 microg/kg) did not change the twitch-tension in rat external popliteal/sciatic nerve-tibialis anterior muscle preparations. However, this steroid (0.3 mM) prevented the neuromuscular blockade by d-tubocurarine (1.45 microM) in mouse preparations by 70 +/- 10% (P0.05). A similar effect (82 +/- 6% protection, P0.05) occurred in rats treated with prednisolone (400 microg/kg) before d-tubocurarine (225 microg/kg). In phrenic nerve-diaphragm preparations, prednisolone (0.3 mM) increased (13 +/- 4%, p0.05) the twitch-tension in the presence of beta-bungarotoxin (1 microM), and prevented the blockade produced by this toxin (0.15 microM) in its third phase of action. This presynaptic facilitatory effect may contribute to the usefulness of prednisolone in myasthenia gravis.

The application of bradykinin to isolated segments of the epididymal or prostatic portion of the rat vas deferens increased the basal muscular tension mainly of the epididymal portion of the organ. Upon low frequency transmural electrical stimulation, the epididymal and the prostatic end of the organ both reacted to the application of bradykinin with an increase of twitch height. The increase in muscular tension observed in the epididymal portion of the ductus was resistant to tetrodotoxin but obliterated by 1 microM verapamil or nifedipine. The augmentation of the magnitude of the electrically driven muscle twitches was blocked by tetrodotoxin but not affected by 1 microM verapamil or nifedipine. Preincubation of the segments of the ductus with 10 microM indomethacin significantly reduced the increase in basal muscular tension caused by low concentrations of bradykinin but did not affect the electrically driven muscle twitches. Results suggest the existence of bradykinin receptors in the nerve endings of the adrenergic terminals of the organ and in the smooth muscle membrane. Whereas the neurogenic response found in both segments of the organ was of equal magnitude, the musculotropic response was predominantly found in the epididymal half of the organ.