Evidence that olfactory sensitivities to calcium and sodium are mediated by different mechanisms in the goldfish Carassius auratus. | - CCMAR -

Journal Article

TítuloEvidence that olfactory sensitivities to calcium and sodium are mediated by different mechanisms in the goldfish Carassius auratus.
Publication TypeJournal Article
AuthorsHubbard, PC, Canario, AVM
Year of Publication2007
JournalNeurosci Lett
Volume414
Questão1
Date Published2007 Feb 27
Pagination90-3
ISSN0304-3940
Palavras-chaveAction Potentials, Animals, Calcium, Dose-Response Relationship, Drug, Electroencephalography, Goldfish, Neurons, Afferent, Olfactory Bulb, Olfactory Mucosa, Olfactory Nerve, Sensory Thresholds, Smell, Sodium
Abstract

The current study investigated whether the olfactory sensitivity to Ca2+ and Na+ is mediated by the same mechanism in the goldfish, a freshwater teleost. The olfactory responses, as assessed by recording the electro-encephalogram (EEG) from the olfactory bulb, to changes in external [Ca2+] and to [Na+] were recorded in the absence and presence of increasing concentrations of the other ion. Low concentrations of Na+ (0-1.0mM) had no significant effects on the olfactory response to changes in [Ca2+] in terms of EC50, Imax or Hill co-efficient (n=8). A relatively high concentration of Na+ (10mM) significantly reduced the Imax and increased the EC50. One hundred millimolars Na+ reduced the olfactory response to Ca2+ to undetectable levels. Conversely, low concentrations of Ca2+ (0.1 and 1.0mM) significantly attenuated the olfactory response to changes in environmental [Na+], reducing the amplitude of response and increasing the threshold of detection (n=7). However, a high concentration of Ca2+ (10mM) failed to attenuate the olfactory response to Na+ completely. Taken together, these results suggest that, at normal environmental concentrations of these ions, Ca2+ and Na+ are detected by distinct and separate cellular mechanisms. However, there seems to be a degree of overlap between the two mechanisms. The exact mechanisms involved, and their biological roles, remain to be established.

DOI10.1016/j.neulet.2006.12.007
Sapientia

http://www.ncbi.nlm.nih.gov/pubmed/17196333?dopt=Abstract

Alternate JournalNeurosci. Lett.
PubMed ID17196333
CCMAR Authors