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Tail-pinch induced analgesia and immobility: altered responses to noxious tail-pinch by prior pinch of the neck.

Noxious pinch to the scruff of the neck using a metal clip produces profound immobility and analgesia. Noxious pinch delivered to the tail fails to induce immobility and results in nociceptive behavior directed at the pinched tail. However, when administered shortly after neck-clip removal, noxious tail-pinch reinstated immobility without any nociceptive response. Prior neck-clip also enhanced the antinociception induced by the tail-pinch as measured by nociceptive response to a leg pinch. Immobility, as well as antinociception, decreased as the time interval between neck-clip removal and the tail-pinch application increased. Pharmacological manipulations which reduce nociception produced a similar alteration in the response to tail-pinch. Thus, following local injections antinociceptive doses of lidocaine to the base of the tail and systemic morphine administration tail-pinch produced marked immobility. Transection of the brain at the intercollicular level provides evidence for supraspinal involvement in post-neck pinch effects. Not only was the ability of prior neck-pinch to confer antinociceptive properties on tail-pinch abolished, but increased responsiveness to noxious tail-pinch was seen. We, therefore, propose that prior neck-pinch confers new stimulus properties on noxious pinch of other body regions resulting in an enhanced antinociceptive effect, which affects both remote regions and the site of stimulation, and the ability to induce immobility.

Analgesia↗

Origin, development and ultrastructure of boar spermatozoa with folded tails and with two tails.

Spermatozoa from the three epididymal regions (head, body and tail) of healthy and sexually mature boars have been examined by light microscopy, and scanning and transmission electron microscopy. The origin, development and external and internal morphologies of aberrant spermatozoa with folded tails and spermatozoa with one or two heads and two fused tails have been established. A count carried out in each region of the epididymis indicated that significant differences (P less than 0.01) exist in the frequencies of each type of malformation and the epididymal region from which the spermatozoa come. Spermatozoa with folded tails at Jensen's ring originate in the cauda of the epididymis from immature spermatozoa that have not ejected the distal cytoplasmic droplet. The plasma membrane which covers the main piece is fused with the membranes of the midpiece, the connecting piece and the head. The fibrous sheath deforms the mitochondrial sheath and is placed between the plasma membrane and the postacrosomal dense lamina. Spermatozoa with one head and two fused tails originate in the epididymal body from spermatozoa with one head and two unfused tails coming from the cephalic region of the epididymis. Spermatozoa with two heads and two fused tails originate in the cephalic region of the epididymis by head-to-head agglutination of two spermatozoa and later fusion of their tails. The frequency of spermatozoa with two fused tails increases as they progress through the epididymal duct. Their tails, parallel in monocephalic spermatozoa and helicoid in bicephalic spermatozoa, have two complete axonemal axes. In their midpiece, the mitochondrial sheaths of the two axes are fused, producing an 8-shaped sheath.

Animals↗

Corticotropin-releasing factor is cytoprotective in Xenopus tadpole tail: coordination of ligand, receptor, and binding protein in tail muscle cell survival.

Upon metamorphosis, amphibian tadpoles lose their tails through programmed cell death induced by thyroid hormone (T3). Before transformation, the tail functions as an essential locomotory organ. The binding protein for the stress neuropeptide corticotropin-releasing factor (CRF; CRF-BP) is strongly up-regulated in the tail of Xenopus tadpoles during spontaneous or T3-induced metamorphosis. This finding led us to investigate physiological roles for CRF and CRF-BP in tadpole tail. We found CRF, CRF-BP, and functional CRF1 receptor in tail and CRF and functional CRF1 receptors, but not CRF-BP, in the tail muscle-derived cell line XLT-15. CRF, acting via the CRF1 receptor, slowed spontaneous tail regression in explant culture and caused a reduction in caspase 3/7 activity. CRF increased, but stable CRF-BP overexpression decreased, [3H]thymidine incorporation in XLT-15 cells. Overexpression of CRF-BP in vivo accelerated the loss of tail muscle cells during spontaneous metamorphosis. Lastly, exposure of tail explants to hypoxia increased CRF and urocortin 1 but strongly decreased CRF-BP mRNA expression. We show that CRF is expressed in tadpole tail, is up-regulated by environmental stressors, and is cytoprotective. The inhibitory binding protein for CRF is regulated by hormones or by environmental stressors and can modulate CRF bioactivity.

Animals↗

The inheritance of growth and form in the mouse. IV. Changes in the variance components of weight, tail length and tail width during growth.

A complete diallel cross, including inbreds and reciprocals, was made among six inbred lines of mice. Body weight, tail length and tail width were measured at ages of 1 through 12 weeks. The analysis described by Griffing (1956a, 1956b, 1958) as the modified diallel, method 3, model II was made for each trait at each age, a separate analysis being made for each sex. Inbreds did not contribute to estimates of the effects in the diallel model, but were used to estimate heterosis. Positive heterosis was observed for all three traits. Heritability increased with age for all three traits, although it remained small for tail width; for body weight it was larger in females than for males, while for tail length and width the opposite was true. Non-additive genetic variance was observed for all three traits. Maternal effects variance was virtually non-existent for tail length, but for body weight and tail width exhibited a marked peak around weaning, followed by a gradual decline for body weight and a rapid decline for tail width. Environmental variance exhibited a marked peak at weaning for all three traits and was larger for male body weight and tail length from four weeks onward. Residual reciprocal effects were important for tail length at all ages, but were small or negligible for body weight and tail width. It is concluded that the relative importance of the individual's genotype in determining size increases with age, while that of non-genetic factors declines.

Age Factors↗

The apparent antinociceptive effect of desipramine and zimelidine in the tail flick test in rats is mainly caused by changes in tail skin temperature.

Tricyclic antidepressants have shown antinociceptive properties in some, but not in all, animal studies using the tail flick test. Tail flick latency has been found to be strongly negatively correlated to tail skin temperature with its highest correlation found when the temperature is measured close to the heated spot. The selective 5-HT reuptake inhibitor zimelidine, as well as the noradrenaline reuptake inhibitor desipramine, increased tail flick latencies. However, this increase could largely be explained by a concomitant reduction in tail skin temperature. The highest dose of desipramine investigated (25 mg/kg) seemed to possess antinociceptive properties in this test also after correction for the fall in tail skin temperature. Lower doses of desipramine (5 and 15 mg/kg) and zimelidine (5, 20 and 30 mg/kg) were either inactive or their effect on tail flick latency could be explained by the fall in tail skin temperature. The apparent antinociceptive effect of zimelidine in the tail flick test thus seems to be due to an effect on tail skin temperature. Desipramine also seems to have its main effect due to a similar mechanism; however, the highest dose of desipramine used induced significant antinociception.

Analgesics↗

The concepts of tail moment and tail inertia in the single cell gel electrophoresis assay.

Single cell gel electrophoresis under alkaline conditions is a technique used to detect primary DNA damage in individual mammalian cells. Cells embedded in agarose on microscope slides are subjected to lysis, unwinding of DNA and electrophoresis at high pH. After staining with a fluorescent dye, cells with DNA damage display increased migration of genetic material from the cell nucleus. The damage is quantified by measuring the displacement between the genetic material of the nucleus ('comet head') and the resulting 'tail'. The torsional moment of the tail ('tail moment') has been suggested to be an appropriate index of induced DNA damage in considering both the migration of the genetic material as well as the relative amount of DNA in the tail. In the present paper it will be shown that the moment of inertia ('tail inertia'), a not previously described tail parameter, provides a more precise description of the distribution of individual DNA fragments within the tails. The tail inertia was also found to be the most sensitive indicator of the DNA damage induced in peripheral lymphocytes from mice given a single intraperitoneal injection of cyclophosphamide (150 mg/kg b.w.). It is concluded that the tail inertia is an important complement to other tail parameters when looking for damage of DNA with the single cell gel electrophoresis assay.

Animals↗

Environmentally safe design of tailing dams for the management of iron ore tailings in Indian context.

The need for the disposal of iron ore tailings in an enviornmentally firiendly manner is of great concern. This paper investigates the soil engineering properties for the construction of iron ore tailing dam, its foundation, construction materials and design data used for the construction analysis of the tailing dam. Geophysical investigations were carried out to establish the bedrock below the spillway. A computer programme taking into account the Swedish Slip Circle Method of analysis was used in the stability analysis of dam. It also focuses on the charactierstics of the tailings reponsible for the determination of optimum size of tailing pond for the containment of the tailings. The studies on the settling characteristics of tailings indicate much less area in comparison to the area provided in the existing tailing ponds in India. In the proposed scheme, it is suggested to provide an additional unit of sedimentation tank before the disposal of tailings to the tailing pond.

Computer-Aided Design↗

Ventral tail bud mesenchyme is a signaling center for tail paraxial mesoderm induction.

A large body of evidence from several systems indicates that formation of the vertebrate tail is morphogenetically continuous with gastrulation, including neural inducing activity in descendants of the gastrula organizer. However, the signaling centers and molecular events regulating tail mesoderm induction and its organized elongation remain poorly defined. In mammals, the ventral ectoderm ridge (VER) is essential to maintain ongoing formation of paraxial mesoderm and somitogenesis in cultures of intact tail. Avian tail buds contain a similar VER structure. Here, we report that the chick ventral tail bud operates as a signaling center for paraxial mesoderm induction. By using "organizer" style grafting assays to early host embryos, we found that ventral tail bud was able to induce elongated paraxial mesodermal extensions and that the ventral tail bud mesenchyme underlying the VER is both necessary and sufficient for the induction in this assay system. Our observations combined with those of others suggest that interplay between several different signaling centers in the amniote tail bud regulates the coordinate induction and elongation of axial and paraxial structures in the developing tail.

Animals↗

Biogenesis of the posterior-tail plasma membrane domain of the mammalian spermatozoon: targeting and lateral redistribution of the posterior-tail domain-specific transmembrane protein CE9 during spermiogenesis.

We used immunoperoxidase histochemistry and confocal immunofluorescence microscopy to examine the events involved in the compartmentalization of CE9 to the posterior-tail plasma membrane domain during spermatogenesis in the rat. We identified two major episodes of spermatogenesis during which CE9 appeared to accumulate in relatively large amounts intracellularly within elements of the secretory pathway. The first episode encompassed cells from preleptotene through early pachytene primary spermatocytes and was evident as intense intracellular labeling of the endoplasmic reticulum and the Golgi complex. The second episode encompassed spermatids in steps 8-12 of spermiogenesis and was evident as intense intracellular labeling of the Golgi complex and smaller vesicular structures observed within the cytoplasm of the spermatid. Between these two episodes, CE9 was detected in considerably reduced amounts. Although present within the Golgi complex and the acrosomic system throughout much of the first half of spermiogenesis, CE9 was not detected on the tail of the spermatid until steps 8-9 of spermiogenesis. Although detected initially in relatively small amounts along the entire length of the tail beginning at steps 8-9, there was no evidence for the presence of relatively large amounts of CE9 on the tail or anywhere else on the surface of the spermatid until after step 11 of spermiogenesis. Between step 11 and steps 13-14 of spermiogenesis, CE9 was observed to accumulate in relatively large amounts on the whole tail coincident with its apparent loss from the Golgi complex. CE9 was observed to then undergo further compartmentalization to the posterior-tail domain sometime between steps 13-14 of spermiogenesis and spermiation. Our results suggest that CE9 is synthesized and enters the secretory pathway throughout much of spermatogenesis, but that the site of accumulation of CE9 varies considerably as a function of development. With respect to the biogenesis of the posterior-tail plasma membrane domain, our results suggest that CE9 is targeted from the Golgi complex to the plasma membrane of the whole tail during mid to late spermiogenesis and then redistributes laterally into the posterior-tail domain coincident with the caudal migration of the annulus late in spermiogenesis. This proposed pathway has a number of important implications for the logistical capabilities of the mammalian spermatid.

Animals↗

Developmental study on reduction and kinks of the tail in a new mutant knotty-tail mouse.

The knotty-tail (knt/knt) mouse has a short and knotty tail. The tail deformity is caused by a decrease in the number of caudal vertebrae and a deformity of them in the distal part of the tail. The objective of the study was to determine how reduction and kinks of the tail region were formed during secondary body formation. By day 12.0 pc, the somitogenesis of knt/knt embryos was completed; the number of caudal somites more or less agreed with those of the caudal vertebrae in knt/knt mice and were similar to those of knt/+ embryos. On the other hand, the somitogenesis of knt/+ embryos continued up to day 12.5 pc. The somites below about the sixth caudal somite were wedge-shaped with a dorsal apex in knt/knt embryos. The location of abnormal somites also corresponded well to that of deformed caudal vertebrae. Abnormal somitogenesis was always preceded by abnormalities in the presomitic region. Under gross observation, this could be seen to become markedly thickened, and histologically its dorsoventral diameter increased in the transverse plane on days 10.5-12.0 pc. In the mesenchyme there was often obvious cell death at the boundary of the unsegmented area and the tail bud after day 10.5 pc. These results suggested that the shortness of tail was primarily caused by the agenesis of distal caudal vertebrae following the agenesis of distal caudal somites, and partly by the disappearance of the presomitic part due to cell death, while the tail kinks were caused by the deformation of each caudal vertebra following disturbances of the caudal somites. Also, it is highly probable that the prominent cell death at the boundary of the unsegmented area and the tail bud may involve a defect or deformity of somites in this mutant.

Animals↗

Plastic changes and nitric oxide synthase induction in neurons which innervate the regenerated tail of the lizard Gekko gecko. II. The response of dorsal root ganglion cells to tail amputation and regeneration.

The lizard tail regenerates after amputation, which severs the spinal cord and spinal nerves. Dorsal root ganglia (DRGs) do not regenerate in the regrowing tail, which is innervated by DRGs rostral to the amputation. With Nissl staining, NADPH-diaphorase histochemistry and nitric oxide synthase (NOS) immunohistochemistry, we investigated NOS expression and its relationship with structural changes in DRG neurons of caudotomized lizards. First, by horseradish peroxidase retrograde tracing we here provided evidence that the sensory innervation of the regenerated tail derives only from the three pairs of DRGs rostral to the amputation plane. These ganglia were then analyzed in control animals with original intact tail, at 5, 15 and 30 days after caudotomy, and at 8 months in lizards with mature regenerates. Caudotomy elicited in DRG neurons marked hypertrophy that persisted after tail regeneration. In control ganglia, most neurons were lightly NADPH-diaphorase-positive, a few were unstained or intensely stained. Tail transection elicited marked staining up-regulation, and an increase in the proportion of intensely positive neurons. The staining intensity peaked in DRG neurons at 15 days and was still significantly increased in respect to controls several months after complete tail regeneration. NOS immunoreactivity in DRGs matched the histochemical findings. NADPH-diaphorase positivity was also enhanced in the dorsal horn superficial laminae of the corresponding spinal segments. We demonstrate that transection of the lizard spinal nerves, provoked by tail loss, elicits in the axotomized primary sensory neurons marked NOS enhancement, which accompanies axon elongation in the regrowing tail and persists after the end of this process.

Amputation, Surgical↗

DNA sequences of the tail fiber genes of bacteriophage P2: evidence for horizontal transfer of tail fiber genes among unrelated bacteriophages.

We have determined the DNA sequence of the bacteriophage P2 tail genes G and H, which code for polypeptides of 175 and 669 residues, respectively. Gene H probably codes for the distal part of the P2 tail fiber, since the deduced sequence of its product contains regions similar to tail fiber proteins from phages Mu, P1, lambda, K3, and T2. The similarities of the carboxy-terminal portions of the P2, Mu, ann P1 tail fiber proteins may explain the observation that these phages in general have the same host range. The P2 H gene product is similar to the products of both lambda open reading frame (ORF) 401 (stf, side tail fiber) and its downstream ORF, ORF 314. If 1 bp is inserted near the end of ORF 401, this reading frame becomes fused with ORF 314, creating an ORF that may represent the complete stf gene that encodes a 774-amino-acid-long side tail fiber protein. Thus, a frameshift mutation seems to be present in the common laboratory strain of lambda. Gene G of P2 probably codes for a protein required for assembly of the tail fibers of the virion. The entire G gene product is very similar to the products of genes U and U' of phage Mu; a region of these proteins is also found in the tail fiber assembly proteins of phages TuIa, TuIb, T4, and lambda. The similarities in the tail fiber genes of phages of different families provide evidence that illegitimate recombination occurs at previously unappreciated levels and that phages are taking advantage of the gene pool available to them to alter their host ranges under selective pressures.

Amino Acid Sequence↗

Plastic changes and nitric oxide synthase induction in neurons that innervate the regenerated tail of the lizard Gekko gecko: I. Response of spinal motoneurons to tail amputation and regeneration.

The lizard tail regenerates after autotomy or amputation. After horseradish peroxidase injections in the regenerate, motoneurons were retrogradely labeled only in the three spinal segments rostral to the amputation, whose spinal nerves are severed by tail loss. The changes in these motoneurons, compared to those of lizards with original intact tails, were investigated 5, 15, and 30 days after caudotomy and at 8 months in lizards with mature regenerates. Morphometric analysis of Nissl-stained motoneurons rostral to the amputation revealed marked hypertrophy, peaking at 15 days, when chromatolysis and nuclear eccentricity were also evident; motoneuron perikarya remained significantly larger than in controls after tail regeneration. The dUTP nick-end labeling (TUNEL) stain for apoptotic neurons did not reveal labeled cells in the spinal cord 5 and 15 days after caudotomy. Nitric oxide synthase (NOS) expression was studied with nicotinamide adenine-dinucleotide phosphate (NADPH)-diaphorase histochemistry and evaluated quantitatively with densitometry. A few caudal spinal motoneurons were lightly stained in lizards with intact tails. Induction of NADPH-diaphorase positivity was evident in the vast majority of these cells 5 days after caudotomy and was very marked at 15 and 30 days, during tail regrowth. These data were confirmed by neuronal NOS immunohistochemistry. After tail regeneration, histochemical positivity was markedly down-regulated in the tail spinal motoneurons but persisted in the majority of these cells. The findings show that in the lizard caudotomy elicits in axotomized caudal spinal motoneurons NOS induction associated with plasticity phenomena and in particular with vigorous regeneration of axons that innervate the regrowing tail.

Amputation, Surgical↗

The nonessential H2A N-terminal tail can function as an essential charge patch on the H2A.Z variant N-terminal tail.

Tetrahymena thermophila cells contain three forms of H2A: major H2A.1 and H2A.2, which make up approximately 80% of total H2A, and a conserved variant, H2A.Z. We showed previously that acetylation of H2A.Z was essential (Q. Ren and M. A. Gorovsky, Mol. Cell 7:1329-1335, 2001). Here we used in vitro mutagenesis of lysine residues, coupled with gene replacement, to identify the sites of acetylation of the N-terminal tail of the major H2A and to analyze its function in vivo. Tetrahymena cells survived with all five acetylatable lysines replaced by arginines plus a mutation that abolished acetylation of the N-terminal serine normally found in the wild-type protein. Thus, neither posttranslational nor cotranslational acetylation of major H2A is essential. Surprisingly, the nonacetylatable N-terminal tail of the major H2A was able to replace the essential function of the acetylation of the H2A.Z N-terminal tail. Tail-swapping experiments between H2A.1 and H2A.Z revealed that the nonessential acetylation of the major H2A N-terminal tail can be made to function as an essential charge patch in place of the H2A.Z N-terminal tail and that while the pattern of acetylation of an H2A N-terminal tail is determined by the tail sequence, the effects of acetylation on viability are determined by properties of the H2A core and not those of the N-terminal tail itself.

Acetylation↗

The influence of colonic temperature changes in anaesthetised rats on tail skin temperatures and repeated testing of tail-flick latencies.

Tail-flick (TF) response latencies were measured in pentobarbitone-anaesthetized rats and variations with time, body and tail temperatures and 5 tail stimuli positions analysed with a mixed model analysis of variance. Variation with time was not significant. Highly significant differences (P < 0.001) were found between tail-flick latencies (TFLs) for tail temperatures and stimulus position. The most proximal tail position showed significantly different relationships for TFL with time and body temperature from other positions. The method described allows multiple TFLs to be measured in 1 animal with the potential of reducing the total number of animals in an experiment. Tail stimuli positions from proximal to distal sites showed a variation in response from 4.3 sec (95% CI: 4.2, 4.4) to 6.7 sec (95% CI: 6.6, 6.9). Rat tail stimulus position should therefore be standardised to allow reproducible measures of TFL and body temperature maintained within normal limits. TFLs were found to be abnormal at body temperatures above 39 degrees C.

Analysis of Variance↗

Responses of rats to noxious mechanical stimulation of their tails during tail reperfusion following transient ischaemia.

We investigated whether conscious rats exhibit hyperalgesia to noxious mechanical stimuli during tail reperfusion following transient tail ischaemia. Mechanical stimuli were delivered by three mechanical algometers, differing in contact area, geometry and rate of application. Tail ischaemia was induced by applying a pneumatic tourniquet to the base of the tail until the rats exhibited escape behaviour. Control animals had a sham tourniquet placed on their tails. During tail reperfusion, there was significant hyperalgesia when the noxious mechanical stimulus was applied by a narrow bar transverse to the tail, less when applied by a rubber piston, and there was no hyperalgesia when the stimulus was punctate, similar to a von Frey hair. Repeated application of the mechanical stimuli themselves, at 30-min intervals, did not induce hyperalgesia. Rats subjected repetitively to the combination of the bar algometer and tail ischaemia at intervals of at least 48 h, for a total period of three weeks, exhibited progressively enhanced hyperalgesia to the bar algometer, and also enhanced hyperalgesia to noxious ischaemic and thermal stimuli. Rats therefore do exhibit hyperalgesia to mechanical stimuli following conditioning ischaemia, but the nature of the hyperalgesia depends critically on the geometry of the algometer, and the time course of the hyperalgesia was different to that which manifests to a noxious thermal stimulus.

Animals↗

The induction of tail malformations in trisomy 16 mouse fetuses heterozygous for the curly tail recessive gene.

The mouse mutant curly tail is thought to be inherited as an autosomal recessive (ct/ct) with incomplete penetrance so that approximately 60% of ct/ct individuals exhibit the curly tail (CT) phenotype. By outcrossing ct/ct with mouse stock carrying specific heterozygous combinations of Robertsonian (Rb) chromosomes, trisomy 16 (Ts16) and Ts19 mouse fetuses (and their chromosomally balanced littermates) were derived which were heterozygous for the ct gene. All of the Ts16 (ct/Rb;Rb) fetuses, studied between days 14-19 gestation had tail malformations, 86% of which were tail flexion defects (TFD) apparently very similar to the curly tail phenotype. Neither Ts19 nor any of the chromosomally balanced (ct/Rb) littermates from both experimental crosses showed any type of tail or other spinal malformation. At the 27-29 somite stage of development, Ts16 (ct/Rb;Rb) fetuses did not show any significant delay in the closure of the posterior neuropore (PNP) compared with their littermate controls, suggesting that the tail malformation observed in Ts16 (ct/Rb;Rb) occur as a result of mechanisms which differ significantly from those thought to be responsible to causing the curly tail malformation.

Animals↗

Developmental interactions in the pigmentary system of the tip of the mouse tail: effects of coat-color genes on the expression of a tail-spotting gene.

The tails of agouti C3H/HeJmsHir mice are completely pigmented, whereas the tails of black C57BL/10JHir animals possess unpigmented tips. Genetic analysis indicates that white tail-tipping is due to an autosomal recessive gene, with incomplete penetrance, that segregates independently from the gene for agouti with a maternal influence in the F1 generation. To analyze the influence of specific coat-color genes on the expression of tail-spotting in mice, five congenic lines of C57BL/10JHir with different coat colors were prepared. No influence was observed on the occurrence of tail-spotting in agouti (A/A) or dilute (d/d) mice or in F1 mice from crosses between black and albino (c/c), or in F1 mice from crosses between black and pink-eyed dilution (p/p). However, the frequency of tail-spotting was dramatically decreased in brown (b/b) mice. These results suggest that the mutant allele (b) at the brown locus is involved in determining the extent of pigmented areas in the tail tips of mice through an interaction with the tail-spotting gene.

Animals↗