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]