Topic
Toad
About: Toad is a research topic. Over the lifetime, 1624 publications have been published within this topic receiving 28732 citations.
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Journal Article•
TL;DR: Observations that the outflux of potassium in metabolizing, desheathed, sciatic nerves of the toad, Bufo marinus, undergoes only a transitory decline upon application of 0.1% cocaine are accounted for qualitatively by the postulate that only the outermost layer of the membrane is affected by the local anesthetic.
Abstract: The outflux of potassium in metabolizing, desheathed, sciatic nerves of the toad, Bufo marinus, undergoes only a transitory decline upon application of 0.1% cocaine. However, when the outflux has been increased previously by a combination of anoxia and iodoacetate poisoning, cocaine produces a sustained depression of this outflux. These observations seem accounted for qualitatively by the postulate that only the outermost layer of the membrane is affected by the local anesthetic, the permeability to both potassium and sodium being reduced in this restricted region.
6 citations
6 citations
TL;DR: It is demonstrated that human rIL-2 is not by itself mitogenic in the toad, but it can act as a co-stimulator of antigen-induced mitogenesis, and an absence of an endogenous ligand, coupled with a reduced capacity to express IL-2 receptors, may be responsible for impaired T cell clonal expansion in metamorphosing Xenopus.
6 citations
Journal Article•
TL;DR: It is suggested that ethanol empedes the flow of water across the toad bladder by facilitating a physicochemical interaction between the membrane "pore" and the water molecules.
Abstract: Ethanol (9%) decreases the potential difference across the toad bladder when present at the mucosal surface, the short-circuit current was unchanged. The electrical resistance decreased indicating a change in ion movements across the bladder. Unidirectional 22Na and 36Cl flux measurements showed an increase in the movement of Cl, but no change in Na. The vasopressin-induced increase in Na transport (natriferic response) was also unaffected by the presence of ethanol. It is suggested that ethanol may be altering the apical tight junctions and affecting an anion selective pathway. The hydro-osmotic response of the toad bladder to vasopressin was decreased by 70% in the presence of 3% ethanol. The hydro-osmotic action of cyclic adenosine monophosphate was also inhibited by ethanol, indicating an action subsequent to the endogenous formation of this nucleotide. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. The vasopressin-induced increase in diffusional water flow was similarly reduced. Osmotic water movements across glutaraldehyde and N-ethylmaleimide-"fixed" vasopressin-stimulated bladders were also decreased in the presence of ethanol. However, 3% ethanol had no effect on osmotic water transfer across artificial collodion membranes. Ethanol, therefore, probably interacts with the bladder membrane. The Ktrans (permeability coefficient) of ethanol and water is increased by vasopressin. suggesting that their movement is through similar pathways. It is suggested that ethanol empedes the flow of water across the toad bladder by facilitating a physicochemical interaction between the membrane "pore" and the water molecules.
6 citations