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At least 883 records · Page 49Linked to original sources
PubMed1994

Effect of sodium pyridinethione on the uptake and distribution of nickel in rats, ferrets and guinea-pigs.

Oral administration of sodium pyridinethione together with Ni2+ (using 63Ni2+ as a tracer) to rats, ferrets and guinea-pigs produced highly increased tissue levels of the metal in several tissues in comparison with animals given the Ni2+ alone. Ni2+ forms a lipophilic complex with pyridinethione and it can be assumed that a facilitated passage of the Ni2+ across the cellular membranes of various tissues is important for the observed effects. Pigmented tissues (e.g. the eye melanin), the pancreatic islets, the nervous system and striated muscles showed high levels of Ni2+ in animals given sodium pyridinethione. However, in some instances marked species differences were observed. Thus, microautoradiography indicated an uptake of Ni2+ both in the beta- and alpha-cells in the pancreatic islets in the rat, whereas in the guinea-pig only some cells (probably the alpha-cells) accumulated high levels of Ni2+. In the ferret sodium pyridinethione induced a high uptake of Ni2+ in the heart muscle, which was not seen in the other species. The Ni2+ is probably taken up in the various tissues complexed to pyridinethione. Within the tissues the complex may dissociate and the Ni2+ may bind to some endogenous tissue components. The affinity of the Ni2+ for the endogenous ligands in relation to the affinity for the pyridinethione may be of importance for the effects on the disposition of the Ni2+. The species variations may be related to differences in the structural conformations of the endogenous Ni(2+)-binding ligands.

Animals↗
PubMed2004

Spatial distribution of inhibitory synaptic connections during development of ferret primary visual cortex.

Intracortical inhibition in the primary visual cortex plays an important role in creating properties like orientation and direction selectivity. However, the development of the spatial pattern of inhibitory connections is largely unexplored. This was investigated in the present study. Tangential slices of layers 2/3 of ferret striate cortex were prepared for whole-cell patch clamp recordings, and presynaptic inhibitory inputs to pyramidal neurons were scanned by local photolysis of Nmoc-caged glutamate. Inhibitory synaptic currents (IPSCs) were first detected around postnatal day (P) 17. They originated locally around the recorded cells. Both the number and the total areas supplying the inhibitory inputs increased thereafter and peaked at the time around and shortly after eye opening (P29-37). A refinement period then followed in which the areas providing the majority of inhibitory inputs shrank from 600 microm around the recorded neurons to 200-300 microm in more mature animals (>/=P38). The amplitude of IPSCs increased progressively with increasing age. Long-range inhibitory inputs (>600 microm) were present around eye opening and they often developed into a clustered patchy pattern in more mature animals (>/=P38). In summary, our results show a refinement and clustering in the spatial pattern of inhibitory connections during postnatal development of ferret visual cortex.

Aging↗
PubMed2002

Radial mass transfer of cross-bridges in a tetanized ferret heart muscle.

An X-ray diffraction experiment on ferret heart muscle was made to examine the relationship between tension and mass transfer from the thick to the thin filament associated with the interaction of cross-bridges with actin. A ferret papillary muscle was electrically stimulated for 8 s in the presence of 5 microM ryanodine to give a tetanus. At different extracellular Ca2+ concentrations (2-20 mM), a linear relationship was found between the tension and the mass transfer. It was concluded that a change in tension caused by altering the extracellular Ca2+ concentration is due to a change in the number of myosin heads bound to actin. This is in contrast to the results obtained on skinned preparations, which showed a markedly nonlinear relationship between the number of heads in the vicinity of the thin filaments and force. It was found that the tension per myosin head is similar in twitch and tetanus of cardiac muscle. Also, a similar fraction of myosin heads is recruited in tetanus of cardiac and skeletal muscles.

Aequorin↗
PubMed1999

Organization of the disynaptic pathway from the anteroventral cochlear nucleus to the lateral superior olivary nucleus in the ferret.

The medial nucleus of the trapezoid body (MNTB) is one of three major nuclei of the superior olivary complex and provides an important inhibitory input from the contralateral ear to the lateral superior olivary nucleus (LSO) in the initial binaural pathway for coding interaural intensity differences. The major input to the MNTB from the contralateral anteroventral cochlear nucleus (AVCN) involves giant, calyx-like endings that have a one-to-one relationship with cells in the MNTB as confirmed in the ferret in this study. The main objective of the present study was to define the subsequent organization of projections from cells receiving these calyx-like endings. Several anatomical tracers (Phaseolus vulgaris leucoagglutinin, dextran-biotin, and biocytin) were used that are transported both anterogradely and retrogradely within neuronal projections in order to define the organization of MNTB connections with the LSO in the adult ferret. Analysis focused on determining the topography in both the transverse and longitudinal planes of the projections. Focal tracer injections in the LSO resulted in retrograde labeling of a long, narrow column of cells in the MNTB. The orientation and location of labeled cells was dependent on the medial-lateral position of the injection site. In the rostral-caudal dimension of MNTB, there was no such topographic relation between the injection site and the position of labeled cells. Labeled cells in the MNTB were distributed more or less evenly in a longitudinal column regardless of whether the injection site was restricted to the rostral, middle or caudal part of the LSO. In keeping with this pattern, tracer injections in the MNTB resulted in bands of labeled axons that distributed endings throughout the rostral-caudal axis of the LSO. These bands or sheets varied in medial-lateral position relative to the location of the injection site, but lacked any such rostral-caudal gradient. Thus, overall the MNTB-LSO projections have a convergent-divergent pattern of organization. While MNTB cells receive singular calyx-like endings from the AVCN, LSO cells receive projections from a long column of cells in the MNTB. Implications for processing interaural intensity differences are discussed.

Animals↗
PubMed1991

Enzymatic conversion of beta-carotene into beta-apo-carotenals and retinoids by human, monkey, ferret, and rat tissues.

Whether the conversion of beta-carotene into retinoids involves an enzymatic excentric cleavage mechanism was examined in vitro with homogenates prepared from human, monkey, ferret, and rat tissue. Using high-performance liquid chromatography, significant amounts of beta-apo-12'-, -10'-, and -8'-carotenals, retinal, and retinoic acid were found after incubation of intestinal homogenates of the four different species with beta-carotene in the presence of NAD+ and dithiothreitol. No beta-apo-carotenals or retinoids were detected in control incubations done without tissue homogenates. The production of beta-apo-carotenals was linear for 30 min and up to tissue protein concentrations of 1.5 mg/ml. The rate of formation of beta-apo-carotenals from 2 microM beta-carotene was about 7- to 14-fold higher than the rate of retinoid formation in intestinal homogenates, and the rate of beta-apo-carotenal production was fivefold greater in primate intestine vs rat or ferret intestine (P less than 0.05). The amounts of beta-apo-carotenals and retinoids formed were markedly reduced when NAD+ was replaced by NADH, or when dithiothreitol and cofactors were deleted from the incubation mixture. Both beta-apo-carotenal and retinoid production from beta-carotene were inhibited completely by adding disulfiram, an inhibitor of sulfhydryl-containing enzymes. Incubation of beta-carotene with liver, kidney, lung, and fat homogenates from each species also resulted in the appearance of beta-apo-carotenals and retinoids. The identification of three unknown compounds which might be excentric cleavage products is ongoing. These data support the existence of an excentric cleavage mechanism for beta-carotene conversion.

Animals↗
PubMed1993

Intestinal perfusion of beta-carotene in the ferret raises retinoic acid level in portal blood.

To determine whether beta-carotene (beta-C) can serve as a source of intestinally-derived retinoic acid (RA), either 15,15'-[14C]beta-C or unlabeled beta-C was perfused through 30 cm jejunal segments of ferrets in vivo. Portal vein blood was sampled periodically via an indwelling catheter. RA was identified in portal blood by comparing retention times in HPLC, by UV absorption, and by derivatization (methylation) and subsequent GC-MS analysis. The RA concentration in the portal blood increased 3-fold with perfusion of beta-C (P < 0.05), and remained at 18 nmol/L during the perfusion of beta-C. The single peak of RA in HPLC was shown to consist of four separate peaks by GC-MS, which may be cis-trans isomers of RA. The concentration of RA in portal blood returned to the initial level (5 nmol/L) after a 2 h period of intestinal perfusion with 5% dextrose. Retinyl ester concentration in portal blood did not change before or after the perfusion, whereas retinol decreased significantly during the perfusion of beta-C. This study clearly indicates that a considerable quantity and number of polar metabolites, including RA, are formed from beta-C in the ferret intestine which are transported via the portal vein to the liver.

Animals↗
PubMed1982

Late onset of hearing in the ferret.

Onset of hearing in the ferret was judged by simple behavioral, physiological and anatomical indices. The ear canals do not open until the end of the first postnatal month. This coincides with the appearance of a startle response to loud hand claps and the recording of acoustically activated neurons in the midbrain. The late onset of hearing in the ferret (around 32 days postnatal) contrasts with the cat (6 days) and the mouse (12 days).

Aging↗
PubMed1987

Source of cholinergic input to ferret visual cortex.

The source of cholinergic input to ferret visual cortex was investigated with a combination of retrograde transport of horseradish peroxidase and choline acetyltransferase immunohistochemistry. Cholinergic projections to ferret visual cortex arise from basal forebrain cells in the septum, diagonal and nucleus basalis magnocellularis; the largest contribution comes from cells in the caudal part of the nucleus basalis magnocellularis. There is no discernible source in the brainstem.

Afferent Pathways↗
PubMed1991

Neonatal testosterone masculinizes sexual behavior without affecting the morphology of the dorsal preoptic/anterior hypothalamic area of female ferrets.

We examined whether testosterone (T) administered to female ferrets neonatally--a treatment known to enhance masculine coital capacity--induces formation of the sexually dimorphic male nucleus in the dorsal preoptic/anterior hypothalamic area (MN-POA/AH), and/or sensitizes dorsal POA/AH neurons to the stimulatory effect of later androgen treatment on somal dimensions. In males, the MN-POA/AH was present in all subjects, and exposure to androgen following castration at postnatal day 56 (P56) increased both MN-POA/AH volume as well as mean somal areas of MN-POA/AH neurons relative to oil-treated controls. Females given androgen from P5 to P20 and for one month beginning after ovariectomy on P56 failed to develop the MN-POA/AH, but displayed high levels of masculine sexual behavior. Somal areas of dorsal POA/AH neurons in females that received either T or a control neonatally did not increase following androgen treatment at P56. Thus, the correlation that exists between somal enlargement of dorsal POA/AH neurons and masculine sexual behavior in androgen-treated males is not found in behaviorally masculinized females. Masculine coital ability does not appear related to aspects of dorsal POA/AH morphology, supporting data from a previous study in which lesions of the MN-POA/AH caused negligible deficits in masculine sexual behavior of adult male ferrets.

Animals↗
PubMed1995

Estrogen receptor immunoreactivity in ferret brain is regulated by estradiol in a region-specific manner.

The effects of estrogen on estrogen receptor (ER) immunoreactivity in the male ferret brain were examined. Estrogen treatment reduced the mean number of ER-immunopositive (ER+) cells/unit area in periventricular preoptic area but increased the mean number of ER+ cells/unit area in the medial division of the ventromedial hypothalamic nucleus, while having no effect on the number of ER+ cells/unit area in the lateral VMH and arcuate nucleus. Thus, estrogen regulates brain ER immunoreactivity in male ferrets and the direction and magnitude of this regulation are brain region-specific.

Animals↗
PubMed1992

Effects of endothelin on intracellular Ca2+ and contractility in single ventricular myocytes from the ferret and human.

We investigated the role of endothelin-1 on peak intracellular Ca2+ ([Ca2+]i) and peak shortening of ventricular myocytes (loaded with indo-1/AM) from failing human hearts. 10 nM of ET-1 significantly increased the cell peak shortening (84 +/- 29%, P less than 0.05) without significantly increasing the peak [Ca2+]i (15 +/- 7%, P greater than 0.05). Further studies on ferret cardiac myocytes indicated that in addition to producing dose-dependent (0.1-10 nM) significant increases in peak shortening (max 55 +/- 6% P less than 0.01) and non-significant increases in peak [Ca2+]i (max 35 +/- 19%, P greater than 0.05), endothelin-1 significantly shifted the peak [Ca2+]i-peak shortening curve upward. The results suggest that endothelin-1 acts directly on human and ferret cardiac myocytes to produce a positive inotropic effect that may predominantly be due to an enhanced myofilament Ca2+ responsiveness.

Adult↗
PubMed1992

Pharmacology of the 5-hydroxytryptamine-induced depolarization of the ferret vagus nerve in vitro.

Grease-gap recordings revealed that 5-hydroxytryptamine (5-HT) depolarized the ferret vagus nerve (pEC50 = 4.9). This response was mimicked by 2-methyl-5-HT and 1-phenylbiguanide, but not by 5-carboxamidotryptamine. Paroxetine (1 microM) or ketamine (10 microM) did not potentiate the response. Ketanserin (1 microM) did not reduce the depolarization, but four 5-HT3 receptor antagonists did. It is concluded that 5-HT depolarizes the ferret vagus nerve via 5-HT3 receptors, but these receptors may differ pharmacologically from those in other species.

Animals↗
PubMed1993

The tachykinin NK1 receptor antagonist CP-99,994 attenuates cisplatin induced emesis in the ferret.

The tachykinin NK1 receptor antagonist CP-99,994 ((+)-(2S,3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine) (0.3-3 mg/kg i.v.), but not its inactive enantiomer CP-100,263, attenuated the retching and vomiting induced by cisplatin (10 mg/kg i.v.) in the ferret. CP-99,994, 3 mg/kg i.v., prevented vomiting in all ferrets tested. Since substance P is the preferred ligand at the NK1 receptor subtype these data support a role for the release of this peptide during the emetic response induced by cytotoxic chemotherapeutic agents.

Analysis of Variance↗
PubMed1993

Anti-emetic profile of a non-peptide neurokinin NK1 receptor antagonist, CP-99,994, in ferrets.

In the ferret, 5-HT3 receptor antagonists are effective in controlling emesis produced by cytotoxic agents or radiation. To investigate the possibility that substance P has a role, as well as 5-HT, in the emetic reflex pathway, we have examined the anti-emetic effects of a NK1 receptor antagonist (racemic CP-99,994) in the ferret. Racemic CP-99,994 was effective against a range of emetogens, comprising cytotoxic drugs, radiation, morphine, ipecacuanha and copper sulphate.

Animals↗
PubMed1993

Mechanisms of cisplatin- and m-chlorophenylbiguanide-induced emesis in ferrets.

We investigated the involvement of peripheral and central serotonin (5-HT)3 receptors in cisplatin- and 5-HT3 receptor agonist-induced emesis in ferrets. Cisplatin (10 mg/kg i.v.)-induced emesis was inhibited by intravenous YM060 (0.003-0.1 microgram/kg). A highly selective and potent 5-HT3 receptor agonist, m-chlorophenylbiguanide (1-10 mg/kg i.p.), dose dependently elicited emesis an effect which was inhibited by YM060 (0.003-0.3 microgram/kg i.v.). Vagotomy markedly reduced this emesis, and the combination of abdominal vagotomy and greater splanchnicectomy abolished emesis. Lesion of greater splanchnic nerves alone did not markedly inhibit emesis. Intracerebroventricularly (4th ventricle) administered YM060 inhibited cisplatin- and m-chlorophenylbiguanide-induced emesis only at higher doses (0.01-0.1 and 0.01-0.03 microgram, respectively). Intracerebroventricularly (4th ventricle) administered m-chlorophenylbiguanide (30-100 micrograms) produced only a weak retching response. These results indicate that stimulation of abdominal vagal afferent nerves via peripheral 5-HT3 receptors is important for triggering cisplatin- and m-chlorophenylbiguanide-induced emesis in ferrets.

Animals↗
PubMed1994

Endothelin-1 does not alter Ca2+ responsiveness in saponin-skinned ferret papillary muscles.

Endothelin is a potent vasoconstrictor and a positive inotropic agent in myocardium. Endothelin has been reported to increase myocardial contractility with little or no increase in intracellular Ca2+, thus apparently enhancing myofilament responsiveness to Ca2+. We investigated the effects of endothelin on tension development and Ca2+ responsiveness in both intact and saponin-skinned ferret right ventricular papillary muscles. Isolated ferret papillary muscles were stimulated for 2 h in the presence or absence of endothelin (100 nM). The muscles were then chemically skinned with saponin and exposed to relaxing and contracting solutions containing varying amounts of Ca2+, and the developed force of contraction was measured. The [Ca2+] required for half-maximal activation (pCa50) was determined by fitting force versus Ca2+ data to the Hill equation. In isometrically contracting muscles, endothelin (100 nM) caused a mean percent increase in developed tension of 34.7% +/- 11.3% (mean +/- S.E.). In muscles that were exposed to endothelin for 2 h and then skinned, neither the pCa50 nor the maximal Ca(2+)-activated force (Fmax) were significantly different from control skinned papillary muscles. After skinning, when endothelin (100 nM) was added to the Ca2+ buffers, both pCa50 and Fmax were significantly decreased. When papillary muscles were pretreated with phorbol 12-myristate 13-acetate (PMA) and then skinned, there was a significant increase in the pCa50. These results indicate that endothelin acts directly on the myofilaments to impair force development by directly decreasing the Ca2+ responsiveness of myofilaments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effects of bradykinin receptor agonists, and captopril and thiorphan in ferret isolated trachea: evidence for bradykinin generation in vitro.

Bradykinin B2 receptor agonists, but not a B1 receptor agonist, were potent spasmogens of ferret isolated trachea. Bradykinin-induced contractions were unaffected by several pharmacological agents, indicating a direct effect on airway smooth muscle B2 receptors. Captopril plus thiorphan caused contractions in approximately 70% of preparations that were abolished by B2 receptor antagonists, but not by B1 receptor antagonist. Thus, ferret tracheal tissues appear capable of releasing and degrading kinins in vitro. Inhibition of peptide degradation with captopril and thiorphan may allow the endogenous kinins to accumulate in concentrations sufficient to elicit tracheal contraction via activation of B2 receptors.

Animals↗
PubMed1985

Role of extrinsic and intrinsic nerves in the relationship between intestinal motility and transmural potential difference in the anesthetized ferret.

In the anesthetized ferret jejunum, the role of extrinsic and intrinsic nerves in the relationship between intestinal motor activity and transmural potential difference (PD) was studied. In the vagally intact ferret and after sympathetic blockade, spontaneous bursts of jejunal motor activity were associated with fluctuations in transmural PD. Both responses were abolished by vagotomy, atropine, and tetrodotoxin. Prolonged electrical stimulation of the cervical vagus nerve induced a cyclical motility pattern. Furthermore, there was an initial rise in transmural PD which then plateaued, and superimposed on this were fluctuations in transmural PD. Atropine abolished the phasic pattern of motor activity and the fluctuations in transmural PD, although the tonic increase in transmural PD was not blocked. The results indicate that nervous activity, either spontaneous or induced, must be present for the cyclic fluctuations in transmural PD and motility. However, fluctuations in transmural PD associated with intestinal motility are not directly dependent on an intact vagal or sympathetic supply and involve coordination with the enteric nervous system.

Animals↗