Can J Physiol Pharmacol. 2008 January/February;86(1-2):46-54. Adenosine reduces the reverse mode of the Na+/Ca2+ exchanger in ferret cardiac fibres. Hleihel W, Lafoux A, Ouaini N, Huchet-Cadiou C. Faculte de Medecine, Universite Saint-Esprit de Kaslik, B.P. 446 Jounieh, Liban, Lebanon. The aim of this study was to investigate the effects of adenosine on reverse mode Na+/Ca2+ exchange. In intact ferret cardiac trabeculae, Na +-free contractures were investigated after treating preparations with ryanodine, a sarcoplasmic reticulum Ca2+-channel inhibitor, and thapsigargin, a sarcoplasmic reticulum Ca2+-pump inhibitor added to suppress the sarcoplasmic reticulum function. The effects of adenosine (50-100 nmol/L), adenosine deaminase (ADA, 0.1-0.5 U/L), the A1 and A2A receptor agonists CCPA (3-100 nmol/L) and CGS 21680 (25-100 nmol/ L), and the A1 and A2A receptor antagonists DPCPX (25 nmol/L) and ZM 241385 (25 nmol/L) were tested on Na+-free contractures. The application of adenosine (50-100 nmol/L) had no significant effect on the characteristics of the Na+-free contractures. However, the results show that treatment with ADA (0.3 U/L), adenosine (>P nmol/L) and CCPA, a specific A1 receptor agonist (3-100 nmol/L), all reduced the Na +-free contracture amplitude. In the presence of ADA, the effects of adenosine and CCPA were also reduced by a specific antagonist of A1 receptors (DPCPX, 25 nmol/L). Furthermore, adenosine, ADA, and CCPA did not affect the properties of the contractile apparatus in Triton- skinned fibres. It is therefore proposed that endogenous adenosine reduced the reverse mode of the Na+/Ca2+ exchanger by acting on A1 receptors present in the sarcolemmal membrane. full article: <https://article.pubs.nrc-cnrc.gc.ca:443/RPAS/RPViewDoc?issn=0008-4212&volume=86&issue=1-2&startPage=46&secure=true> Masui. 2008 Apr;57(4):408-19 Novel assessment of intracellular calcium transient decay in cardiac muscle by curve-fitting with half-logistic function [Article in Japanese] Mizuno J, Arita H, Hanaoka K, Kusakari Y, Kurihara S. Department of Anesthesiology, Teikyo University School of Medicine, Tokyo 173-8605. A decrease in intracellular calcium (Ca2+) concentration in the cardiac muscle is one of the important factors to induce myocardial relaxation. A mono-exponential (m-E) function has been used for assessing myocardial relaxation curve of isometric tension and intracellular calcium transient (CaT) decay, and the m-E time constants for the relaxation curve of isometric tension (F tau E) and CaT decay (Ca tau E) have been recognised as lusitropic indices. However, we found that a half-logistic (h-L) function fits the relaxation curve of isometric tension much more precisely than the conventional m-E function in the ferret right ventricular (RV) papillary muscle. Moreover, we demonstrated that the goodness of the h- L fits for CaT decays was superior to the goodness of the m-E fits in the rabbit RV and murine left ventricular papillary muscles. The changes in the h-L time constants for the relaxation curves of isometric tension (F tau L) and CaT decays (Ca tau L) with the different onsets were significantly smaller than the changes in F tau E and Ca tau E, respectively. The differences in the h-L non-zero asymptotes for the relaxation curves of isometric tension and CaT decays with the different onsets were smaller than the changes in the m-E non-zero asymptotes. The h-L function model characterises the amplitudes and time courses of the relaxation curve of isometric tension and CaT decay more precisely than the m-E function model, and thus F tau L and Ca tau L serve as more novel and reliable lusitropic indices. Simultaneous analysis of myocardial relaxation curve of isometric tension and CaT decay using h-L functions can become a useful method for assessment of myocardial calcium handling. Brain Res. 2008 Mar 10 [Epub ahead of print] Visual-auditory spatial processing in auditory cortical neurons. Bizley JK, King AJ. Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK. Neurons responsive to visual stimulation have now been described in the auditory cortex of various species, but their functions are largely unknown. Here we investigate the auditory and visual spatial sensitivity of neurons recorded in 5 different primary and non-primary auditory cortical areas of the ferret. We quantified the spatial tuning of neurons by measuring the responses to stimuli presented across a range of azimuthal positions and calculating the mutual information (MI) between the neural responses and the location of the stimuli that elicited them. MI estimates of spatial tuning were calculated for unisensory visual, unisensory auditory and for spatially and temporally coincident auditory-visual stimulation. The majority of visually responsive units conveyed significant information about light-source location, whereas, over a corresponding region of space, acoustically responsive units generally transmitted less information about sound-source location. Spatial sensitivity for visual, auditory and bisensory stimulation was highest in the anterior dorsal field, the auditory area previously shown to be innervated by a region of extrastriate visual cortex thought to be concerned primarily with spatial processing, whereas the posterior pseudosylvian field and posterior suprasylvian field, whose principal visual input arises from cortical areas that appear to be part of the 'what' processing stream, conveyed less information about stimulus location. In some neurons, pairing visual and auditory stimuli led to an increase in the spatial information available relative to the most effective unisensory stimulus, whereas, in a smaller subpopulation, combined stimulation decreased the spatial MI. These data suggest that visual inputs to auditory cortex can enhance spatial processing in the presence of multisensory cues and could therefore potentially underlie visual influences on auditory localization. Now, here is another article I am just drooling to get my hands on since it could save ferrets: Vet Clin North Am Exot Anim Pract. 2008 May;11(2):301-314. Toxicology of Ferrets. Dunayer E. American Society for the Prevention of Cruelty to Animals (ASPCA) Animal Poison Control Center (APCC), 1717 S. Philo Road, Suite 36, Urbana, IL 61802, USA; College of Veterinary Medicine, University of Illinois, 2001 S. Lincoln Avenue, Urbana, IL 61802, USA. Because of their curious nature and small size, ferrets are at risk for various toxicoses. At present, there is not a great deal of information on specific toxicants in ferrets. This article initially reviews general consideration in treating poisoning in ferrets, such as obtaining history and decontamination. It then discusses some specific agents that appear to be common causes of poisoning in ferrets based on the experience of the ASPCA Animal Poison Control Center. [Posted in FML 5949]