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Task2 K(+) channel expression in the central nervous system is surprisingly restricted to a few brainstem nuclei, including the retrotrapezoid (RTN) region. All Task2-positive RTN neurons were lost in mice bearing a Phox2b mutation that causes the human congenital central hypoventilation syndrome. In plethysmography, Task2(-/-) mice showed disturbed(More)
During the last two decades it has become apparent that vasopressin (VP) and oxytocin (OT), in addition to playing a role as peptide hormones, also act as neurotransmitters. Morphological studies and electrophysiological recordings have shown a close anatomical correlation between the presence of these receptors and the neuronal responsiveness to VP or OT.(More)
The mechanism by which (1S,3R)-ACPD, a metabotropic glutamate receptor agonist, induces burst firing in lateral septal neurons of the rat was investigated in coronal brainstem slices. Membrane currents were characterized in voltage clamp using whole-cell recordings. In the presence of (1S,3R)-ACPD, following depolarizing voltage jumps, repolarization(More)
Immunotoxicotherapy (ITT) is currently used in humans for the treatment of snake venom and cardiac glycoside poisoning. Other toxins have been studied in animals or in vitro to assess their suitability as candidates for detoxification by specific antibodies. Testing conditions are often empirical suggesting that numerous improvements need to be introduced(More)
Anti-colchicine antibodies raised in rabbits are effective at protecting rabbits from acute colchicine intoxication. The positive effect depends on the ratio between the binding site capacity of the specific antibodies and the colchicine dose. Immunized rabbits receiving 6 mg/kg colchicine intravenously (LD100) died within 8 h as rapidly as those of the(More)
Vasopressin can directly excite facial motoneurons in young rats and mice. It acts by generating a persistent inward current, which is Na(+)-dependent, tetrodotoxin-insensitive and voltage-gated. This peptide-evoked current is unaffected by Ca(++) or K(+) channel blockade and is modulated by extracellular divalent cations. In the present work, we determined(More)