Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “TAILS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed1995

Regulation of Na(+)-pump activity by dopamine in rat tail arteries.

We investigated the effect of dopamine on the vascular Na+-pump activity in isolated rat tail artery sections. Effect of dopamine on vascular tone was also assessed using a perfused tail artery preparation. Dopamine inhibited the Na+-pump activity in isolated rat tail arteries in a dose-dependent manner. Both SKF-38393 HCl, a selective dopamine D1 receptor agonist, and quinpirole HCl, a selective dopamine D2 receptor agonist inhibited the Na+-pump activity. The inhibition of the Na+-pump activity. The inhibition of the Na+-pump by dopamine was accompanied with a transient increase in the vascular tone. SKF-38393, but not quinpirole produced a sustained increase in the vascular tone. Tissues preincubated simultaneously with SCH-23390 HCl, a selective dopamine D1 receptor antagonist, and sulpiride, a selective dopamine D2 receptor antagonist, prevented the dopamine inhibition of the Na+-pump activity. Pertussis toxin blocked the Na+-pump inhibition produced by the dopamine D1 receptor agonist but not by the dopamine D2 agonist. Similarly, the dopamine D1 receptor but not dopamine D2 agonist increased the rate of phosphoinositide hydrolysis in rat tail artery sections. Our results indicate that dopamine inhibition of the Na+-pump is mediated by a pertussis toxin-sensitive mechanism and may be coupled to the activation of the phospholipase C system in rat tail arteries. The modulation of the Na+-pump by dopamine may contribute to the vascular tone.

Animals↗
PubMed1983

Studies on corticoid action on the toad tadpole tail in vitro.

The effect of adrenal corticoids on the shrinkage of tail segments from Bufo bufo japonicus tadpoles was studied in vitro. Deoxycorticosterone acetate (DCA) was effective in accelerating the shrinkage of tail segments if thyroxine (T4) or triiodothyronine (T3) was present in the medium. The shrinkage caused by DCA was dose dependent. In the absence of thyroid hormone, DCA did not induce tail resorption. Shrinkage of tail segments induced by DCA and T4 was blocked by prolactin. Among the steroid hormones testes in vitro, aldosterone and corticosterone exhibited a potent activity in accelerating shrinkage of tail segments in the presence of T4. The nature of the corticoid action is discussed.

Adrenal Cortex Hormones↗
PubMed1986

Observations on the interaction of prolactin and thyroxine in the tail of the bullfrog tadpole.

Explants of tail fin from tadpoles of Rana catesbeiana maintained in tissue culture underwent resorption when exposed to a medium containing 150 nM thyroxine (T4). Increases in the specific activity of hexosaminidase (Hex) and of acid phosphatase (AP) were associated with this response. Ovine prolactin inhibited resorption of explants in a dose-responsive manner; however, prolactin had no influence on the specific activity of either Hex or AP cultured explants. This result contrasted with the effect of prolactin in vivo, where it inhibited both the resorption of the tail and the increase in specific activity of hydrolytic enzymes induced by T4. The actions of both hormones, when applied in vivo, were more pronounced in the tail fin than in the muscular core of the tail at the stage of regression tested, indicating that the failure of prolactin to influence enzyme induction in vitro did not result from an incapacity of the fin to respond to prolactin in this fashion. It is suggested that the inhibition of T4-induced enzymic activity by prolactin which is observed in the intact animal may come about in response to some related but indirect systemic action of prolactin that is lacking when explants are cultured in vitro. It is concluded that inhibition of the induction of hydrolytic enzymes is not an essential factor in the inhibitory effect of prolactin on the resorption of the tail fin.

Acid Phosphatase↗
PubMed1987

A quantitative study on the tail flick test in the rat.

Tail flick latency and response temperature were measured in awake rats. Both of these parameters varied with the change in rate of increase of radiant heat stimulus and the area of skin irradiated. The caloric factor applied to the tail before the response occurred was calculated approximately from the time-temperature curves monitored over the tail and the response latencies. The magnitude of the caloric factor over a tentative threshold temperature was the crucial factor for the induction of tail flick response, because it was similar for the various irradiating conditions. It was proposed that analgesic effects in the tail flick test may be expressed using this caloric factor which allows direct comparison of studies in which different base-line latencies are used.

Analgesia↗
PubMed1995

Tail-flick test. I: Impact of a suprathreshold exposure to radiant heat on pain reactivity in rats.

Radiant heat applied to the tail elicits a vigorous tail-flick response in rats. This tail-flick reflex is frequently used to measure pain reactivity. Prior research has shown that a suprathreshold exposure to the radiant heat used to elicit this reflex causes a reduction in tail-flick latencies in pentobarbital anesthetized rats. Experiment 1 replicated this observation and showed that the effect is not due to a change in tail temperature. Experiment 2 showed that reduced latencies (hyperalgesia) are not observed if the spinal cord is transected prior to testing. Experiment 3 revealed that pentobarbital anesthesia is required to observe thermal-induced hyperalgesia, for this effect is not observed in awake subjects. Experiments 4 and 5 extended this observation by showing that awake rats also fail to exhibit hyperalgesia if others measures of pain reactivity are employed (shock-induced vocalization and motor reactivity). Implications of the results are discussed.

Animals↗
PubMed1983

Role of gene T in phage lambda tail assembly.

We have studied the phenotype of a heat-sensitive mutation that defines lambda tail gene T. Induction and growth at the nonpermissive temperature of a lambda Tts40 prophage results in production of morphologically normal but biologically inactive tails, which can be activated in vitro by lysates supplying the products of genes T, U, and Z. Thus, gene T acts between genes V and U in the tail assembly pathway or immediately after the completion of tail shaft polymerization. lambda Tts40 lysates also contain a substantial number of morphologically normal phage particles which are deficient in cleavage of the minor tail protein gpH. This result is consistent with the fact that gpH cleavage normally occurs later in the assembly pathway than the time found for gene T action. Purified lambda Tts40 virions that were produced at the permissive temperature are normal with respect to gpH cleavage. However, they are more sensitive to heat inactivation than are wild-type virions, suggesting that the T gene product is in the virion. At the permissive temperature, the mutant protein made by lambda Tts40 is active in vivo even if it has been synthesized at the nonpermissive temperature.

Bacteriophage lambda↗
PubMed1993

Reduced density of dopamine D2 receptors in the rat tail artery as a function of age.

The present study was designed to investigate the influence of aging on noradrenaline content and the density and pattern of prejunctional dopamine D2 receptors in the tail (ventral caudal) artery of male Sprague-Dawley rats. Tail artery is frequently used as a model for investigating mechanisms of sympathetic vascular control and contains prejunctional dopamine receptor belonging to the D2 subtype. Noradrenaline levels were reduced in rats of 12 months of age in comparison with 3-month-old animals. A further reduction in catecholamine concentration was found in 24-month-old rats. The density of prejunctional D2 receptors, which was measured in frozen sections of the tail artery by using both radioligand binding and autoradiographic techniques, was reduced by about 35% in 12-month rats in comparison with 3-month rats. A decrease by about 55% versus 3-month rats and by about 20% versus 12-month rats was observed in 24-month-old rats. Neither the pharmacological profile nor the anatomical localization of prejunctional D2 receptors was changed in the rat tail artery as a function of age. The parallel decrease in noradrenaline content and in the density of prejunctional dopamine D2 receptor sites in the tail artery of Sprague-Dawley rats of different ages probably accounts for the lack of an age-related change of prejunctional dopamine D2 receptor-linked responses reported in functional studies.

Aging↗
PubMed1978

Morphine-induced tail erection: site of action.

Acute ablation techniques were used to localize morphine-induced tail erection (MITE) within the central nervous system of mice. Morphine produced no elevation of tails in mice whose spinal cord had been transected at the lower thoracic or lumbar levels. Decortication and high-level precollicular decerebration did not prevent MITE while morphine caused no tail response at all in low-level inferior collicular decerebrate mice. Lesions in various portions of the mesencephalon revealed that the degree of MITE was closely related to the size of the lesions of the central gray matter. The larger the lesion, the smaller the degree of tail elevation. MITE could not be elicited in mice when the mesencephalic central gray matter had been completely destroyed. Results indicate that morphine acts on the mesencephalic central gray matter producing tail erection and the pathway responsible for the reaction descends from the midbrain downward to the spinal cord.

Animals↗
PubMed1984

Length determination in bacteriophage lambda tails.

We have isolated viable mutants of bacteriophage lambda that have in-frame deletions in gene H, which codes for a minor tail protein. They produce correspondingly smaller but active gene H protein products and assemble shorter-tailed phage particles. The deficiency in tail length for each mutant corresponds to the calculated shortening of the gene H protein caused by the deletion. These results show that the H protein determines tail length and argue strongly for a scheme in which the H protein is a ruler or template that measures length during tail assembly.

Bacteriophage lambda↗
PubMed1993

Effect of the tail ganglion on swimming activity in the leech.

In the medicinal leech, Hirudo medicinalis, isolated segmental nerve cords are capable of generating swimming activity. The role played by the head and tail ganglia in regulating the expression of swimming activity by the segmental nerve cord was evaluated by comparing swimming activity in nerve cord preparations with and without the head and tail ganglia attached. Several swim properties were examined, including length of induced swim episodes, ability to initiate swim episodes, swim cycle period, and phase. We found that, in general, the presence of the tail ganglion attached to isolated nerve cords countered the effects produced by the head ganglion on swimming activity. Moreover, we observed that the tail ganglion itself provides excitatory drive to the swim generating system. Thus, the inputs from the head and tail ganglia influence significantly the expression of swimming activity.

Animals↗
PubMed1990

In vivo neurochemical effects of tail pinch.

Tail pinch in the rat gives rise to a well characterised pattern of behaviour which includes gnawing, licking and eating. We have used both in vivo voltammetry and microdialysis to monitor neurochemical changes which accompany the behavioural response to a 5-min tail pinch. Tail pinch resulted in a increase of extracellular 5-hydroxytryptamine and a smaller and more delayed increase of 5-hydroxyindole acetic acid in the hippocampus. In the striatum there was a rise of both extracellular dopamine and ascorbate. With a recently developed constant potential voltammetric technique we can continuously monitor changes in extracellular ascorbate. Using this technique we found a very rapid rise in ascorbate current during a 5-min tail pinch; the current began to decline as soon as the clip was removed. The high time resolution of the technique also allowed us to record similar ascorbate changes during a 0.5-s tail pinch.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Age-related changes in the sensitivity of sympathetic nerves to altered extracellular calcium in tail arteries of F-344 rats.

There is a significant age-related increase in stimulation evoked norepinephrine release from adrenergic nerves in tail arteries of F-344 rats, that is not accounted for by a change in function of prejunctional alpha 2-adrenergic receptors. To further explore the mechanism of this age-related change in transmitter release, we investigated the effect of altered extracellular calcium. With short stimulation trains the effects of altered extracellular calcium were significantly greater in 20-month-old tail arteries compared to 6 months. At the highest calcium concentration (7.5 mM) when alpha 2-adrenergic receptors were active or blocked, there was a significant decline in fractional norepinephrine release only in arteries of 20-month-old animals. With long stimulation trains the effects of altered extracellular calcium were not as pronounced as with short trains, but the effect of calcium was still significantly greater in 20 month old tail arteries. With alpha 2-adrenergic receptors blocked 6 month tail arteries were insensitive to altered calcium while 20-month tail arteries remained sensitive. One explanation for these findings may be an age-related change in the efficiency of intracellular calcium buffering mechanisms leading to greater calcium transients in the nerves of older animals.

Aging↗
PubMed1987

Physicochemical properties of the triiodothyronine nuclear receptor from tadpole liver, intestine and tail fin.

The binding of triiodothyronine (T3) to tadpole liver, intestine, and tail fin nuclei was consistent with a single class of binding sites. The KD for the binding of T3 to isolated nuclei from the liver (1.02 nM), intestine (1.40 nM), and tail fin (0.831 nM) nuclei were not significantly different. The number of binding sites for T3 in the nuclei isolated from each tissue were also not significantly different. Sucrose gradient centrifugation of the salt-extracted nuclear T3-receptor complex revealed that the S20,w was not significantly different for the complex from the liver (3.7 S), intestine (3.9 S), or tail fin (3.9 S). Similarly, the Stokes radii of the complex from the liver (3.65 nm), intestine (3.84 nm), and tail fin (3.99 nm) were not significantly different. Molecular weights of 57,000, 64,000, and 67,000 were calculated from the sedimentation coefficients and Stokes radii for the T3-receptor complex from the liver, intestine, and tail fin, respectively. The similarity of the physicochemical properties of the T3-receptor complex from each of the tissues studied is consistent with the hypothesis that the same receptor is capable of inducing tissue-specific biochemical changes.

Animals↗
PubMed1995

Contrasting patterns of expression of thyroid hormone and retinoid X receptor genes during hormonal manipulation of Xenopus tadpole tail regression in culture.

The precocious induction of amphibian metamorphosis is an ideal system for analyzing the developmental action of TH, while the hormonal activation of tadpole tail regression offers the further advantage of studying programmed cell death. One of the striking features of thyroid hormone (TH)-induced tail regression (as with morphogenetic responses of all tadpole tissues) in Xenopus is the rapid autoinduction of TRbeta gene, but it is not known how TH would affect the expression of the genes encoding TR's heterodimeric partner, retinoid X receptor (RXR). Here we first show that the synthetic glucocorticoid dexamethasone (Dex) potentiates and prolactin (PRL) suppresses, 3,3',5-triiodothyronine (T3)-induced regression of pre-metamorphic Xenopus tadpole tails in organ culture. T3 strongly upregulated (11-35-fold) the concentration of Xenopus TRbeta (xTRbeta) mRNA in these cultures while downregulating by 50% that of Xenopus RXRgamma (xRXRgamma) mRNA in the same samples of tail RNA. DEX and PRL enhanced or diminished the T3-regulated expression of these two transcripts, respectively, which parallels their other effects in whole tadpoles or cultured tails. The contrasting effects of the three hormones on the steady-state levels of xTRbeta and XRXRgamma mRNAs were time- and dose-dependent. T3 and DEX also strongly upregulated the transcription of xTRbeta gene transfected into Xenopus XTC-2 cells but PRL failed to prevent this autoinduction. The actions of these three hormones involved in amphibian metamorphosis, as judged by the expression of xTRbeta and xRXRgamma genes, reveal a new facet of hormonal interplay underlying their developmental actions.

Animals↗
PubMed1994

Effects of diabetes on the morphine-induced Straub tail reaction in mice.

The effects of diabetes on the morphine-induced Straub tail reaction were examined in mice. The Straub tail reaction induced by s.c. administration of morphine was significantly less in diabetic mice than in non-diabetic mice. The morphine-induced Straub tail reaction was significantly reduced following pretreatment with beta-funaltrexamine, a selective mu-opioid receptor antagonist, in both diabetic and non-diabetic mice. Furthermore, the morphine-induced Straub tail reaction was also significantly reduced in both diabetic and non-diabetic mice following pretreatment with naloxonazine, a selective mu1-opioid receptor antagonist. These results suggest that mice with diabetes are hypo-responsive to mu1-opioid receptor-mediated Straub tail reaction.

Animals↗
PubMed1988

Behavioral and thalamic nociceptive responses in rats following noxious ischaemia of the tail.

In rats anaesthetized with urethane, we have investigated the response of neurones in the ventrobasal complex of the thalamus to noxious ischaemia of the tail, and to graded noxious thermal stimulation of the tail before and after ischaemia. In behavioural experiments conscious rats were exposed to the same experimental procedure. After ischaemia the threshold tail temperature required to elicit both a neuronal response and aversive behaviour in conscious rats, to thermal stimulation, was decreased significantly (P less than 0.01 paired t tests). Threshold temperatures for the neuronal response and the behavioural response were not significantly different, either before or after ischaemia. The time course of recovery to pre-ischaemic threshold temperatures was the same for both the behavioural and neuronal responses. Most thalamic neurones responding to noxious thermal stimulation of the tail also increased firing rate during ischaemia. The latency of response of the thalamic neurones to ischaemia was 12.1 +/- 1.8 min and the latency of the behavioural response to the same stimulus was 11.9 +/- 2.1 min. Ventrobasal thalamic neurones, therefore, which responded to noxious thermal stimulation of the tail also responded to noxious ischaemia, and exhibited a neuronal correlate of post-ischaemic hyperalgesia which paralleled behavioural responses closely.

Action Potentials↗
PubMed1993

Modality-specific hypersensitivity of dorsal horn convergent neurones during reperfusion of their receptive fields on the rat's tail.

In rats anaesthetised with enflurane, we examined the responses of convergent neurones in the dorsal horn of the spinal cord to noxious thermal and mechanical stimulation and to innocuous brushing, during reperfusion of their receptive fields on the tail, following transient ischaemia. Neurones were included if they responded, before induction of ischaemia, to both pinching and brushing of receptive fields restricted to the tail. Ischaemia was induced by occluding the blood supply to the tail for 30 min using a tourniquet. Compared to their own responses before ischaemia, during reperfusion almost all the neurones (17 of 20) exhibited significantly increased activity to noxious pinching and innocuous brushing of their receptive fields, following 30 and 60 min of reperfusion. Receptive field size increased markedly in 16 of 20 of the neurones tested. Only 13 of 35 of the neurones responded to noxious thermal stimulation of the tail before induction of ischaemia, and of these only two exhibited enhanced sensitivity to thermal stimulation during reperfusion. Our results indicate that there is a population of convergent neurones that demonstrates hypersensitivity to mechanical stimulation of the rat's tail, but not to noxious thermal stimulation, during reperfusion of their receptive fields following transient ischaemia.

Animals↗
PubMed1994

Central delay of the laser-activated rat tail-flick reflex.

The latency of the heat-activated rat tail-flick (TF) reflex is dependent upon 4 variables, none of which has previously been determined: activation of cutaneous nociceptors (TN); afferent conduction to the dorsal horn (TA); conduction within the central nervous system (CNS) (central delay); and conduction from the ventral horn (VH) to, and activation of, tail muscles (TE). Using a CO2 infrared laser (10 W, 45 msec) to produce synchronous activation of tail-skin nociceptors, TF latency (EMG response) was measured in 10 awake rats. Based on shifts in response latency from points of stimulation near the tip and base of the tail, conduction velocity in the afferent limb of the reflex was estimated to be 0.76 +/- 0.11 m/sec. This indicates that the response is mediated by C fibers. The rats were then anesthetized with pentobarbital and multiple-unit activity and evoked potentials (EPs) were recorded from the superficial dorsal horn at spinal segments S3-CO1 during laser or high-intensity electrical (10 mA, 1 msec) stimulation of the tail. Unit activity and EPs elicited by both stimuli consisted of two distinct components, corresponding to activation of A and C fibers. The difference in latency between laser and electrical evoked activity indicated that 60.00 +/- 7.33 msec was required for activation of nociceptors by the laser. Electrical stimulation of the VH at S3-CO1 in 3 rats produced a TF (EMG) response in 4 msec. Central delay, calculated as total TF time minus (TN+TA+TE), was 82.3 +/- 13.08 msec. This represents the time frame during which modulation of the reflex by an intrinsic, pain-activated, supraspinal system could occur.

Animals↗