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At least 955 records · Page 53Linked to original sources
PubMed2001

Central antiemetic effects of AS-8112, a dopamine D2, D3, and 5-HT(3) receptor antagonist, in ferrets.

The involvement of a central mechanism in the antiemetic effect of AS-8112 ((R)-5-bromo-N-(1-ethyl-4-methylhexahydro-1H-1,4-diazepin-6-yl)-2-methoxy-6-methylamino-3-pyridinecarboxamide x 2 fumarate), a novel and potent dopamine D2, D3, and 5-HT(3) receptor antagonist, was investigated in ferrets. Intracerebroventricularly administered AS-8112 dose dependently inhibited R(+)-7-OH-DPAT (R(+)-7-hydroxy-2-(N,N-di-n-propylamino) tetraline)-induced emesis (ID(50); 0.11 microg/kg, i.c.v.). In addition, AS-8112 (10 microg/kg, i.c.v.) significantly inhibited emesis induced by cisplatin. Ondansetron (10 microg/kg, i.c.v.) also inhibited cisplatin-induced emesis, but did not inhibit R(+)-7-OH-DPAT-induced emesis. S(-)-eticlopride (10 microg/kg, i.c.v.) did not inhibit emesis induced by cisplatin. However, racemic CP-99,994 ((+/-)-(2S, 3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine) (10 microg/kg, i.c.v.) inhibited both cisplatin- and R(+)-7-OH-DPAT-induced emesis. These results suggest that the antiemetic effects of AS-8112 are centrally mediated via dopamine D3 and 5-HT(3) receptors in ferrets.

Animals↗
PubMed1997

Gastrointestinal motor activity in conscious ferrets.

Gastrointestinal motility was measured with force transducers in conscious ferrets. The gastrointestinal motility pattern in both the interdigestive and digestive states was similar to that reported for humans. The activity front, phase III contractions of the migrating motor complex, occurred cyclically in the antrum and migrated to the duodenum and ileum in the interdigestive state, and relatively low-amplitude contractions were sustained in the antrum, duodenum and ileum in the digestive state. Colonic motility was characterized by basal relatively low-amplitude contractions and a single high-amplitude contraction preceding defecation. Cisapride (0.3-3 mg/kg s.c.) enhanced antral and colonic motility. This ferret model will help the investigation and evaluation of drug effects on gastrointestinal motility in humans.

Animals↗
PubMed1999

Effect of non-peptide tachykinin NK(1) receptor antagonists on non-adrenergic, non-cholinergic neurogenic mucus secretion in ferret trachea.

We investigated, in ferret trachea in vitro, the binding characteristics and the inhibition of non-adrenergic, non-cholinergic (NANC) neural mucus secretion of four tachykinin receptor antagonists: the non-peptide tachykinin NK(1) receptor antagonists CGP 49823 ((2R,4S)-2-benzyl-1-(3, 5-dimethylbenzoyl)-4-(quinolin-micro-ylmethyl amino) piperidine), CGP 55000 ((2R,4S)-2-benzyl-1-(3, 5-bistrifluoromethyl-benzoyl)-4-(quinolinyl-methylamino)piperidine ) and CP 99,994 ((+)-(2S,3S)-3-methoxybenzyl amino)-2-phenylpiperidine), and the peptide tachykinin NK(2) receptor antagonist MEN 10,627 (cyclo(Met-Asp-Trp-Phe-Dap-Leu)cyclo(2beta-5beta)). CGP 49823, CGP 55000 and CP 99,994 concentration-dependently displaced [125I]Bolton-Hunter substance P binding in tracheal membranes with Hill coefficients not different from unity and IC(50) values of 1.4, 1.7 and 1.3 nM, respectively. In contrast, MEN 10,627 displaced binding according to a two-site model, with IC(50)s of 0.2 nM and 1. 3 microM. Electrical stimulation of tracheal segments with adrenoceptor and cholinoceptor blockade increased output of the mucus marker 35SO(4) by 59% above baseline (representing the NANC neural secretory response). CGP 49823, CGP 55000 or CP 99,994 concentration-dependently inhibited NANC neural secretion with IC(50) values of 30, 8 and 120 nM, respectively. In contrast, MEN 10, 627 (3 microM) did not inhibit secretion. The NK(1) antagonists, but not the NK(2) antagonist, inhibited [Sar(9)]substance P-induced secretion, while none of the antagonists affected acetylcholine-induced secretion. We conclude that NANC neural secretion in ferret trachea in vitro is a useful test system for tachykinin NK(1) receptor antagonists with therapeutic potential in conditions of the airways in which tachykininergic mechanisms and mucus hypersecretion are implicated in pathophysiology, for example asthma and chronic bronchitis.

Acetylcholine↗
PubMed1995

Acetylcholinesterase in the developing ferret retina.

The function of acetylcholinesterase (AChE) is to terminate the action of acetylcholine at the cholinergic synapse. Recent evidence suggests additional roles for acetylcholinesterase as a peptidase and/or a protease which is expressed by growing neurites as part of their invasion of developing neural structures. We report the localization of acetylcholinesterase in developing ferret retina. AChE histochemical staining is seen in the developing inner plexiform layer (IPL) of ferret retina at birth (post-natal day zero, PO), the earliest developmental stage examined. Transient expression is seen at the border between the ganglion cell layer and the nerve fiber layer at P14 and P21. A small amount of transient expression is seen in the outer plexiform layer (OPL) at this age as well. By P28, the transient expression in the OPL is at its peak, and is found at photoreceptor terminals and associated with apparent horizontal cell axons. Labeling is also seen intracellularly in the inner nuclear layer (INL), at the OPL/INL border, suggesting that horizontal cells are the source of the transient AChE expression in the OPL. Overt synaptic profiles also appear in the inner plexiform layer (IPL) at P21 and P28. About 2 days layer, the eyes open and the photoreceptor outer segments are fully developed. By 2 weeks later, at P42, the AChE staining pattern in the retina has taken on its adult appearance: no reaction product in the outer retina; intracellular reaction product in the Golgi apparatus of a subset of amacrine and displaced amacrine cells which manufacture AChE; and extracellular reaction product at both synaptic and non-synaptic sites in the IPL. These data are consistent with a role for AChE as a peptidase early in development, and as an enzyme essential in the termination of synaptic action at mature synapses.

Acetylcholinesterase↗
PubMed1985

Regional myocyte size in compensated right ventricular hypertrophy in the ferret.

The effect of pressure-induced right ventricular hypertrophy on regional myocyte size and shape and regional myocardial wet weight was studied by comparing 20 ferrets which underwent pulmonary artery banding at a weanling age to 19 non-operated siblings. Using isolated myocyte preparations from six myocardial regions in 10 banded and seven non-banded ferrets, a 60% increase in cell volume in the right ventricular outflow tract and the right ventricular free wall was shown to be due primarily to an increased cross-sectional area of individual myocytes. The right side of the interventricular septum exhibited an intermediate increase in cell volume, while the left side of the interventricular septum did not respond to the pulmonary artery banding procedure. These findings confirm that localized hemodynamic changes produce hypertrophy of individual myocytes in selected regions of the heart and that a pressure-induced model of hypertrophy involves an increased cross-sectional area of myocytes, with minimal change in cell length.

Animals↗
PubMed1978

The histochemistry of mucosubstances in ferret salivary glands.

The mucosubstances of the major salivary glands of the ferret were analysed using different histochemical reactions. Almost all the parotid acinar cells had sialic acid-containing mucus. There were a very few cells, the granules of which gave reactions for sulphated mucins. Submandibular gland mucus was sulphated in the major parts of the gland. There were occasional cells which gave reactions to carboxylated mucin. The sublingual and the molar glands had tubules which had 2 types of mucous cells. The central cells contained sulphated mucins and the peripheral ones had carboxylated mucins. The mucus in the tubules of the zygomatic gland was predominantly sulphated. In the sublingual, molar as well as in the zygomatic, there were granulated cells scattered among the tubules. Some of these granules were found to contain carboxylated and the others neutral mucins. No sexual dimorphism was observed in any of the glands among the 4 male and 4 female ferrets used in this study.

Animals↗
PubMed1997

Biphasic emetic response of cyclophosphamide in the ferret.

Cyclophosphamide (177 mg/kg, IV: n = 8) produced a biphasic emetic response in the ferret with a mean +/- SE of 23.3 +/- 4.0 emetic episodes during a 4-h observation period. The emetic profile of cyclophosphamide showed a first phase with 18.6 +/- 3.9 episodes and a second phase with 4.7 +/- 1.2 episodes. Ondansetron (0.07 and 0.13 mg/kg, IV) and droperidol (0.25 and 0.79 mg/kg, IV) significantly reduced the number of emetic episodes in the first phase. Metoclopramide (2.24, 4.08, and 7.07 mg/kg, IV) also significantly reduced the number of emetic episodes in the first phase, and the dose of 7.07 mg/kg completely prevented emetic episodes in the second phase. In addition, ondansetron-treated ferrets (0.04, 0.07, and 0.13 mg/kg, IV) had a significant increase in the number of emetic episodes in the second phase.

Animals↗
PubMed2004

Human monoclonal antibody as prophylaxis for SARS coronavirus infection in ferrets.

SARS coronavirus continues to cause sporadic cases of severe acute respiratory syndrome (SARS) in China. No active or passive immunoprophylaxis for disease induced by SARS coronavirus is available. We investigated prophylaxis of SARS coronavirus infection with a neutralising human monoclonal antibody in ferrets, which can be readily infected with the virus. Prophylactic administration of the monoclonal antibody at 10 mg/kg reduced replication of SARS coronavirus in the lungs of infected ferrets by 3.3 logs (95% CI 2.6-4.0 logs; p<0.001), completely prevented the development of SARS coronavirus-induced macroscopic lung pathology (p=0.013), and abolished shedding of virus in pharyngeal secretions. The data generated in this animal model show that administration of a human monoclonal antibody might offer a feasible and effective prophylaxis for the control of human SARS coronavirus infection.

Animals↗
PubMed1977

Behaviour in ferrets of swine influenza virus isolated from man.

After intranasal instillation into ferrets, the "swine" influenza virus A/New Jersey/8/76(Hsw1 N1) had a 50% minimal infectious dose similar to that of previously tested A/PR/8-A/England (H3 N2) recombinants virulent and attenuated for man. A/New Jersey produced only a mild upper respiratory tract infection. However, higher titres of virus were recovered from the lungs over a longer period than experienced previously with Asian and Hong Kong virus strains. There was a diphasic pyrexia the second and higher peaks of which correlated with peak titres of virus in lung macerates. These results suggest that A/New Jersey has a pneumotropic potential in ferrets and, if the animal model is valid, possible in man.

Animals↗
PubMed2000

Molecular cloning of a ferret angiotensin II AT(1) receptor reveals the importance of position 163 for Losartan binding.

A complementary DNA for the angiotensin II (AngII) type 1 (AT(1)) receptor from Mustela putorius furo (ferret) was isolated from a ferret atria cDNA library. The cDNA encodes a protein (fAT(1)) of 359 amino acids having high homologies (93-99%) to other mammalian AT(1) receptor counterparts. When fAT(1) was expressed in COS-7 cells and photoaffinity labeled with the photoactive analogue (125)I-¿Sar(1), Bpa(8)AngII, a protein of 100 kDa was detected by autoradiography. The formation of this complex was specific since it was abolished in the presence of the AT(1) non-peptidic antagonist L-158,809. Functional analysis indicated that the fAT(1) receptor efficiently coupled to phospholipase C as demonstrated by an increase in inositol phosphate production following stimulation with AngII. Binding studies revealed that the fAT(1) receptor had a high affinity for the peptide antagonist ¿Sar(1), Ile(8)AngII (K(d) of 5. 8+/-1.4 nM) but a low affinity for the AT(1) selective non-peptidic antagonist DuP 753 (K(d) of 91+/-15.6 nM). Interestingly, when we substituted Thr(163) with an Ala residue, which occupies this position in many mammalian AT(1) receptors, we restored the high affinity of this receptor for Dup 753 (11.7+/-5.13 nM). These results suggest that position 163 of the AT(1) receptor does not contribute to the overall binding of peptidic ligands but that certain non-peptidic antagonists such as Dup 753 are clearly dependent on this position for efficient binding.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1997

Adrenal gland disease in ferrets.

Adrenocortical disease is a frequent problem affecting pet ferrets in the United States. This article describes the typical history, signs, and diagnostic test results to be expected in ferrets with this disease. Treatment options are discussed. A newly developed diagnostic technique is also described.

Adrenal Cortex Function Tests↗
PubMed2002

DNA vaccination of ferrets with chimeric influenza A virus hemagglutinin (H3) genes.

Recently a technology was established based on homologous recombination that allowed the rapid generation of chimeric HA genes of influenza viruses, containing the antigenic determinants obtained from various influenza virus A (H3N2) viruses. In the present report plasmids were generated using a H3 HA vector handle and the hypervariable regions of two genetically distinct influenza A H3N2 viruses, A/Stockholm/7/97 and A/Netherlands/18/94. In a ferret model it was shown that immunisation with plasmid DNA encoding chimeric HA indeed elicited antibody responses specific for the virus from which the hypervariable region with the antigenic determinants were obtained. After DNA-immunisation of the ferrets, protective immunity against infection with influenza virus A/Netherlands/18/94 was evaluated.

Animals↗
PubMed1999

The effect of fentanyl on c-fos expression in the trigeminal brainstem complex produced by pulpal heat stimulation in the ferret.

We have previously shown that Fos-like immunoreactivity (Fos-LI) is evoked in the brainstem of ferrets following stimulation of pulpal A delta and C fibers originating from the maxillary canine. This study evaluated the effects of the mu-opioid receptor agonist fentanyl on Fos expression evoked by noxious thermal stimulation of the right maxillary and mandibular canines in pentobarbital/chloral hydrate anesthetized adult male ferrets. Pulpal heating evoked Fos expression in two distinct regions of the spinal trigeminal nuclear complex: the transitional region between subnucleus interpolaris and caudalis (Vi/Vc) and within the subnucleus caudalis (Vc). More Fos positive cells were expressed in both regions ipsilateral to the site of stimulation compared with the contralateral side (P < 0.05, ANOVA). Pretreatment with fentanyl significantly and dose-dependently suppressed the number of Fos positive cells in both the Vi/Vc transitional region and Vc (P < 0.05, ANOVA). The suppressive effect of fentanyl on Fos expression was blocked by the intravenous administration of naloxone, an opioid antagonist, indicating a specific opioid receptor effect. In addition, opioid receptor antagonism with naloxone alone enhanced Fos expression in Vi/Vc and Vc in response to heat stimulation. The administration of naloxone without heat stimulation failed to evoke Fos expression in Vi/ Vc and Vc. These findings suggest that the activation of trigeminal Vi/Vc and Vc neurons by noxious dental heat stimulation is controlled by a naloxone sensitive endogenous opioid system as indicated by Fos expression. Collectively, these results suggest that neuronal populations in Vi/Vc and Vc regions may contribute to pain responses to noxious dental stimulation and these responses can be modulated by both endogenous and exogenous opioids.

Analgesics, Opioid↗
PubMed1998

Fos expression in the ferret trigeminal nuclear complex following tooth pulp stimulation.

The aim of this study was to establish which regions of the trigeminal nucleus are activated by tooth pulp stimulation in the normal ferret. The distribution of Fos-like immunoreactivity was examined following electrical stimulation of the tooth pulp in the awake and anaesthetized ferret. Stimulus-specific labelling was found in subnuclei caudalis and oralis of the trigeminal spinal nucleus. Three groups of chronically prepared animals; conscious, anaesthetized (alphaxolone/alphadolone) and anaesthetized-paralysed (alphaxolone/alphadolone with gallamine triethiodide), received electrical stimuli to both the upper and lower left canine teeth (1 Hz train of 3 x 0.5 ms at 200 Hz) at an amplitude of 10 times the threshold of the jaw opening reflex. Three control groups were treated identically except no stimulus was given. In stimulated anaesthetized and anaesthetized-paralysed animals, Fos-positive profiles were seen in laminae I and II of subnucleus caudalis and in the medial part of subnucleus oralis. There was no labelling evident in subnucleus interpolaris or the main sensory nucleus, or contralaterally in any of the subnuclei. In all conscious stimulated animals there was additional bilateral Fos-positive labelling, mainly in the deeper laminae of subnucleus caudalis. This bilateral labelling was not stimulus-specific as it was also seen in conscious non-stimulated animals. After correction for this bilateral labelling no significant difference was found between conscious, anaesthetized and anaesthetized-paralysed groups of stimulated animals or between the different groups of control animals. These results support the concept that the rostral parts of the trigeminal spinal nucleus are involved in processing of nociceptive input. They also demonstrate that light alphaxolone/alphadolone anaesthesia has no effect on stimulus-specific Fos expression following tooth pulp stimulation. The second aim of this study was to develop a clearly defined model for future studies in which Fos expression is no different to that seen in the conscious state. As in the conscious animal, labelling not associated with the stimulus is difficult to distinguish from stimulus specific labelling, further studies using this model of trigeminal nociceptive pathways would be best carried out in lightly anaesthetized animals.

Anesthesia, General↗
PubMed1998

F2-isoprostane generation in isolated ferret lungs after oxidant injury or ventilated ischemia.

Pulmonary edema develops when pulmonary blood flow is interrupted, then restored. Because the lung is not always hypoxic when ischemic, mechanisms of pulmonary ischemia-reperfusion injury are likely to differ from systemic organs, where reactive oxygen species generated during reperfusion mediate organ dysfunction. We previously showed that pulmonary vascular permeability of isolated ferret lungs increased prior to reperfusion, if ventilation was maintained while blood flow was impaired. To determine whether reactive oxygen metabolites generated during ischemia mediated ischemic injury, we measured tissue levels of F2-isoprostanes as an index of lipid peroxidation, 30 min after administration of glucose (5 mM)-glucose oxidase (GOX, 0.1 U/ml), or after short (45 min) or long (180 min) ventilated ischemia, in isolated ferret lungs. Osmotic reflection coefficient for albumin (sigma alb), an estimate of vascular protein permeability, was measured in the same lungs. Tissue F2-isoprostanes increased 375% after exposure to glucose-GOX in association with a 42% decrease in sigma alb, and administration of catalase (CAT, 100,000 U) and superoxide dismutase (SOD, 25,000 U) completely attenuated this lipid peroxidation. In contrast, tissue F2-isoprostanes increased only 60% following 45 min of ischemia, then did not increase additionally. sigma alb was not altered by 45 min of ischemia, but decreased 72% following 180 min of ischemia. CAT+SOD did not alter F2-isoprostane formation during ischemia, but partially attenuated vascular injury. These results suggest that tissue levels of F2-isoprostanes reflect lung lipid peroxidation, but that F2-isoprostane generation does not directly increase vascular permeability following ventilated pulmonary ischemia.

Animals↗
PubMed1989

Beta 2-adrenoceptor stimulation inhibits ganglionic transmission in ferret trachea.

To study the effect of beta-adrenoceptor stimulation on the transmission through airway parasympathetic ganglia, we used an in vitro nerve-muscle preparation of ferret trachea. Isometric muscle contractions were induced for 20 s every 2 min alternating with postganglionic activation by electrical field stimulation (EFS) or with preganglionic activation by direct nerve stimulation (DNS). The pulse frequency was always 12 Hz. A possible modulation of ganglionic transmission was assessed by comparing contractions induced by DNS to contractions induced by EFS. In 9 experiments isoprenaline initially reduced the response to EFS and DNS to the same extent, indicating an effect on postganglionic structures. After 20-30 min exposure the response to preganglionic activation by DNS was further reduced indicating an inhibition of ganglionic transmission. The concentration/response relationship for the ganglionic effect of isoprenaline was shifted about ten times to the right by 0.1 microM propranolol (n = 5) and by a beta 2-adrenoceptor-antagonist (0.1 microM ICI 118.551) (n = 8), whereas a beta 1-adrenoceptor-antagonist (10 microM practolol) had no, or only slight, effect. In two experiments pretreatment by 0.1 microM phenoxybenzamine for 20 min did not prevent ganglionic inhibition by 0.3 microM isoprenaline. We conclude that parasympathetic ganglia in ferret trachea have beta-adrenoceptors mediating inhibition of ganglionic transmission, and that these probably are of the beta 2 type. Tentatively these receptors could be operated upon by circulating catecholamines.

Adrenergic beta-Agonists↗
PubMed1989

Classification of beta-adrenoceptors in ferret tracheal smooth muscle by pharmacological responses.

Beta-adrenoceptors in ferret tracheal smooth muscle were classified into beta 1 or beta 2 by determination of (i) the potency rank order for isoprenaline, noradrenaline and adrenaline, and (ii) apparent pA2-values for a specific beta 1-antagonist (practolol) and a specific beta 2-antagonist (ICI 118.551) and (iii) concentration-inhibition curves for procaterol, a beta-agonist showing a biphasic concentration-response curve in organs with a mixed beta 1 and beta 2 adrenoceptor population. We used in vitro tracheal rings and assessed the responses to beta-adrenoceptor agonists as inhibition of phasic contractions elicited by electrical field stimulation (2 Hz for 20 s) or relaxation of tonic contractions elicited by acetylcholine (0.5 microM). The potency rank order for the agonists was isoprenaline greater than noradrenaline approximately adrenaline indicating action through beta 1-receptors. Apparent pA2-values for the antagonists were for 1, 3 and 10 microM practolol 6.0 (SE 0.27), 6.1 (SE 0.21) and 6.3 (SE 0.03), respectively. Apparent pA2 for 0.1, 1 and 10 microM ICI 118.551 were 6.8 (SE 0.25), 6.7 (SE 0.12) and 6.1 (SE 0.14), respectively. These values agree well with published pA2-values for the action of these drugs on beta 1-adrenoceptors. However, the Schild plot for ICI 118.551 was alinear indicating a possible heterogeneity of the beta-adrenoceptors in ferret trachea. The concentration-response curve for procaterol showed the biphasic form typical for organs with a mixed beta 1 and beta 2 population. However, the lower part of the curve, reflecting stimulation of beta 2-adrenoceptors reached only 17.5% (SE 1.4) of the maximally achieved inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Ocular disorders of pet ferrets.

Ocular disorders in pet ferrets are becoming more widely recognized as the popularity of these animals as companions increases. Knowledge of the anatomy of ferrets and a thorough examination are critical to accurately diagnosing ocular disease. If recognized early, some conditions can be managed successfully. Veterinarians should continue to report ocular conditions that are encountered in this species to help increase knowledge about these disorders.

Animals↗