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At least 19 recordsLinked to original sources

PubMed1996

Heterosynaptic facilitation of tail sensory neuron synaptic transmission during habituation in tail-induced tail and siphon withdrawal reflexes of Aplysia.

In cellular studies of habituation, such as in the gill and siphon withdrawal reflex to tactile stimulation of the siphon of Aplysia, a mechanism that has emerged as an explanation for response decrement during habituation is homosynaptic depression at sensory neurons mediating the behavioral response. We have examined the contribution of homosynaptic depression to habituation in sensory neurons that contribute to two reflex behaviors in Aplysia, tail withdrawal and siphon withdrawal, both elicited by threshold-level tail stimulation. In a companion paper (this issue), we reported that repeated tail stimulation, identical to that producing habituation in siphon withdrawal in freely moving animals, also produces habituation in reduced preparations. In this paper, we extend these behavioral findings by showing that in reduced preparations, identical tail stimulation also produces habituation of the tail withdrawal reflex. In addition, our cellular experiments show that (1) identified sensory and motor neurons in both reflex systems respond to identical repeated tail stimulation; in sensory neurons it produces a progressive decrease in spike number and increase in spike latency, and in motor neurons it produces progressive decrement in complex EPSPs and spike output. (2) Homosynaptic depression of the tail sensory neuron to tail motor neuron synapse does occur when the sensory neurons are activated repetitively by intracellular current. (3) Homosynaptic depression at this synapse does not occur when the sensory neurons are activated repetitively by threshold-level tail stimuli that elicit the behavioral reflex and cause habituation; rather, the sensory neurons exhibit significant heterosynaptic facilitation. Thus, in these reflexes, habituation is not accompanied by homosynaptic depression at the sensory neurons, suggesting that the plasticity underlying habituation occurs primarily at interneuronal sites.

Animals↗

PubMed2000

The effect of the acidic tail on the DNA-binding properties of the HMG1,2 class of proteins: insights from tail switching and tail removal.

The high-mobility group (HMG) proteins HMG1, HMG2 and HMG2a are relatively abundant vertebrate DNA-binding and bending proteins that bind with structure specificity, rather than sequence specificity, and appear to play an architectural role in the assembly of nucleoprotein complexes. They have two homologous "HMG-box" DNA-binding domains (which show about 80 % homology) connected by a short basic linker to an acidic carboxy-terminal tail that differs in length between HMG1 and 2. To gain insights into the role of the acidic tail, we examined the DNA-binding properties of HMG1, HMG2b and HMG2a from chicken erythrocytes (corresponding to HMG1, HMG2 and HMG2a in other vertebrates). HMG1, with the longest acidic tail, is less effective than HMG2a and 2b (at a given molar input ratio) in supercoiling relaxed, closed circular DNA, in inducing ligase-mediated circularisation of an 88 bp DNA fragment, and in binding to four-way DNA junctions in a gel-shift assay. Removal of the acidic tail increases the affinity of the HMG boxes for DNA and largely abolishes the differences between the three species. Switching the acidic tail of HMG1 for that of HMG2a or 2b gives hybrid proteins with essentially the same DNA-binding properties as HMG2a, 2b. The length (and possibly sequence) of the acidic tail thus appears to be the dominant factor in mediating the differences in properties between HMG1, 2a and 2b and finely tunes the rather similar DNA-binding properties of the tandem HMG boxes, presumably to fulfill different cellular roles. The tail is essential for structure-selective DNA-binding of the HMG boxes to DNA minicircles in the presence of equimolar linear DNA, and has little effect on the affinity for this already highly distorted DNA ligand, in contrast to binding to linear and four-way junction DNA.

Amino Acid Sequence↗

PubMed2000

Tss (Tail-short Shionogi), a new short tail mutation found in the BALB/cMs strain, maps quite closely to the Tail-short (Ts) locus on mouse chromosome 11.

A spontaneous morphological mutation characterized by a short and kinky tail (Tail-short Shionogi: Tss) was observed in a BALB/cMs mouse breeding colony. The inheritance mode of the Tss mutation is semi-dominant, and homozygotes (Tss/Tss) are probably embryonic lethal. The viability of the Tss/+ heterozygotes appear to be influenced by the mating partner: 47.1% of the (BALB/cMs-Tss/+ x C57BL/6J)F1 embryos were the mutant phenotype, whereas there were no (BALB/cMs-Tss/+ x A/J)F1 embryos with the mutant phenotype. The Tss locus was mapped by linkage analysis between microsatellite markers D11Mit128 and D11Mit256 on mouse Chromosome 11. These results suggest that the Tss mutation is a new allele on the Tail-short (Ts) locus.

Animals↗

PubMed1993

Evidence that the antinociceptive tail-flick response is produced independently from changes in either tail-skin temperature or core temperature.

It has recently been hypothesized that tail-skin temperature may exert a profound influence on the latency of the tail-flick response to radiant heat. Several recent reports in the literature urge investigators to assess tail temperatures concurrently when using the tail-flick test and to adjust the tail-flick latency by a coefficient when a change in tail temperature is detected. Because much of the supporting evidence of this hypothesis was strictly correlational, the purpose of the present study was to determine whether tail-skin temperature is an important factor contributing to the latency of the tail-flick response to radiant heat. The effects of a series of pharmacological and non-pharmacological manipulations on tail-skin temperature and response latencies were assessed using either a low-intensity or high-intensity tail-flick stimulus. In addition, colonic temperature was evaluated. None of the drug treatments yielded a significant correlation between tail temperature and tail-flick latency. Of the seven drugs tested, only mecamylamine produced a consistent change in tail-skin temperature. Although mecamylamine significantly elevated tail temperature by more than 2 degrees C, it failed to alter response latencies. Similarly tail submergence into 5 degrees C water for 10 sec led to profound decreases in tail temperature ranging from -6.5 to -7.6 degrees C while producing only minimal increases in tail-flick latency. Conversely, submerging the tail in 38 degrees C water or placing the animals over a heating pad maintained at 38 degrees C increased tail temperatures at least 2 degrees C without affecting response latencies. Inverse correlations were found between tail-flick latency and colonic temperature after morphine, delta 9-tetrahydrocannabinal (delta 9-THC), and nicotine administration; however, these relationships do not appear to be causal. Sodium barbital produced far more hypothermia than any other agent, but did not produce any antinociception. Moreover, placing subjects in heated cages increased tail-skin temperature between 2 and 4 degrees C and blocked the hypothermic effects of morphine and delta 9-THC without reducing the antinociceptive potencies of these agents. These findings indicate that tail-skin and core temperatures have a negligible influence on the tail-flick response. We conclude that monitoring tail-skin or core temperatures when employing the tail-flick test is unnecessary and altering tail-flick latencies to account for changes in tail temperature is unwarranted.

Analgesics↗

PubMedDate not supplied

Structural and physicochemical analysis of the contractile MM phage tail and comparison with the bacteriophage T4 tail.

The three-dimensional (3-D) structure of the bacteriophage MM extended tail has been determined from electron micrographs of negatively stained specimens and compared with 3-D models of coprocessed extended bacteriophage T4 tails. Accordingly, the phage MM extended tail exhibits an axial repeat of 3.8 nm and can be indexed according to the integer helical selection rule l = -3n + 7m (n = 6n') compared to 4.1 nm and l = -2n + 7m (n = 6n') for the T4 phage tail. Compared to the T4 tail sheath, which reveals a stacked-disk-like appearance, the MM tail exhibits a more open structure, yielding an arrow-head-like appearance. Although the phage MM extended tail sheath is more stable than the T4 tail sheath under low-ionic-strength conditions, various chemical treatments of the MM tail sheath revealed responses, notably disassembly and contraction, similar to those previously described for the T4 tail sheath. Extended tails and their structural components contained in phage lysates or prepared by chemical degradation were compared in the EM, and the mass-per-length values of extended tails and tail tubes were determined by quantitative scanning transmission electron microscopy and compared to the corresponding values computed from the respective 3-D mass density maps. Accordingly, masses of 111 and 135 kDa/nm were obtained for the MM and T4 phage tail sheaths, respectively, with the corresponding tail tubes calculated at 19.3 and 25.5 kDa/nm, respectively. Although negative staining and freeze drying/metal shadowing of the two tails revealed different extended tail sheath structures, freeze-dried/metal-shadowed specimens of their contracted tails revealed very similar 6-fold symmetric axial repeats, with the subunits arranged on a pseudo-12-fold symmetric surface lattice following the integer helical selection rule l = n + 11m. In both cases tail contraction started at the baseplate and propagated headward as a wave forming a contraction gradient with a sharp boundary.

Bacteriophage T4↗

PubMed1988

Apparent hyperalgesia in the mouse tail-flick test due to increased tail skin temperature after lesioning of serotonergic pathways.

The relationship between tail skin temperature and responsiveness to noxious radiant heat in the tail-flick test was investigated in mice. A significant negative correlation between tail skin temperature and tail-flick latency was found when the tail skin temperature was increased by elevating the ambient temperature. After intracerebroventricular injection of the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT, 80 micrograms) tail skin temperatures were increased and tail-flick latencies reduced. In contrast, administration of the tryptophan hydroxylase inhibitor p-chlorophenylalanine (PCPA, 400 mg kg-1 for 5 consecutive days) lead to a slight lowering of tail temperatures and a tendency towards elevation of tail-flick latencies. The results show that factors which affect tail skin temperature also influence the tail-flick test in mice. The divergent effects of 5,7-DHT and PCPA on tail-flick responsiveness may be due to the different effects of these compounds on the tail skin temperature. The results suggest that the reduced tail-flick latency after partial destruction of serotonergic pathways by 5,7-DHT is due primarily to the increased tail skin temperature. The dependence of tail-flick latency on tail skin temperature limits the usefulness of the tail-flick test unless changes in tail skin temperature are controlled for.

5,7-Dihydroxytryptamine↗

PubMed1989

The role of tail skin temperature in the facilitation of the tail-flick reflex after spinal transection or interference with descending serotonergic neurotransmission.

We examined in mice whether tail skin temperatures and tail-flick reflexes were changed after spinal transection or intrathecal (i.th.) injection of the serotonin (5-HT) neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) or the 5-HT receptor antagonist metergoline. Transection of the spinal cord reduced tail-flick latency (the time needed to evoke the tail-flick reflex by radiant heat) and increased tail skin temperature 15-21 days after surgery. Analysis of covariance showed that the effect of tail skin temperature on tail-flick latency was far more pronounced than the effect of spinal transection. Intrathecal injection of 5,6-DHT (5 or 10 micrograms mouse-1), which extensively reduced the spinal levels of 5-HT, reduced tail-flick latency and increased tail skin temperature 1-5 days after treatment. Similarly, tail-flick latency was shortened and tail skin temperature elevated 15 min after i.th. injection of metergoline (0.5 micrograms mouse-1). Analysis of covariance showed no significant effect of i.th. 5,6-DHT or i.th. metergoline on tail-flick latency. Tail skin temperature, on the other hand, had a highly significant effect on tail-flick latency. The results show that the facilitation of the tail-flick reflex in spinally transected mice and mice injected i.th. with 5,6-DHT or metergoline is mainly caused by increased tail skin temperature. The data do not indicate that descending 5-HT pathways tonically inhibit the tail-flick reflex.

5,6-Dihydroxytryptamine↗

PubMed1998

Quinpirole-induced alterations of tail temperature appear as hyperalgesia in the radiant heat tail-flick test.

Several reports in the recent literature argue both for and against the importance of alterations of tail-temperature in the outcome of the tail-flick test. The data we present here support the assertion that drug-induced changes of tail-temperature may have a highly significant effect on tail-flick latency independent of drug-induced changes in nociception. We previously reported that peripherally administered injections of the dopamine agonist, quinpirole, produce significant reductions in the latency of response in the tail-flick test. This present work confirms our earlier findings; however, it indicates that the apparent hyperalgesia is an artifactual function of quinpirole-induced increases in tail temperature. Quinpirole (0.1-1.0 mg/kg I.P.) produced significant (p < 0.001), dose-dependent, and highly correlated increases in tail temperature and decreases in tail-flick latency 15 min following injection. When controls for the change in tail temperature were applied, there was no distinguishable effect of the drug on tail-flick latencies. Sixty minutes following the administration of quinpirole there was no observable effect of the drug on either tail-temperature or tail-flick latency. The results of this study indicate that a) peripherally administered quinpirole has no effect on nociception as measured in the tail-flick test apart from its ability to alter tail temperature; and b) alterations in tail temperature may significantly alter the outcome of the tail-flick test.

Analysis of Variance↗

PubMed2004

Differential gene expression between the embryonic tail bud and regenerating larval tail in Xenopus laevis.

The regeneration of the amputated tail of Xenopus laevis larvae is an excellent model system for regeneration research. The wound left by the amputated tail is covered with epidermis within 24 h. Then, the cell number increases near the amputation plane at the notochord, spinal cord and muscle regions. An apparently complete tail with notochord, muscle and spinal cord is regenerated within two weeks. To reveal whether the molecular mechanism underlying the tail regeneration is the same as that in embryonic tail development, the gene expression patterns of the embryonic tail bud and the regenerating tail were compared by in situ hybridization and reverse transcription-polymerase chain reaction. Most genes analyzed were expressed at similar levels in both tissues, whereas two bone morphogenetic protein (BMP)-antagonists, chordin and noggin, were detected only in the embryonic tail bud. The regenerating tail also lacked expression of Xshh in the floor plate and expression of Xdelta-1 in the spinal cord and presomitic mesoderm. These results show that there are some differences in gene expression between the two processes. Furthermore, when the tail of Xenopus larvae is amputated, the regenerating tail has a gene expression pattern similar to the distal portion of the larval tail rather than the embryonic tail bud, suggesting that the cut larval tail does not make a new embryonic tail bud, but rather a new larval tail tip for regeneration.

Animals↗

PubMed1989

An improved method for tail-flick testing with adjustment for tail-skin temperature.

The tail-skin temperature is an important factor in determining tail-flick latency to noxious radiant heat in rats and mice. A simple, non-invasive method for recording the tail-skin temperature during conventional tail-flick testing is described. The method is conveniently performed during conventional tail-flick testing. It does not require additional handling of the animals, and it is not stressful. The method utilizes a small-sized thermocouple which is brought in contact with the dorsal surface of the tail close to the area exposed to the radiant heat stimulus. A computer based system is used to record the temperature and control the tail-flick apparatus. Continuous monitoring of skin temperature showed that the temperature as measured 23 mm from the tip of the tail agreed well with skin temperature in the position where the beam was focused during tail-flick testing (13 mm from the tip). The skin temperature closer to the base of the tail (100 mm from the tip) showed considerably more deviation from the temperature 13 mm from the tip. Temperature measurements close to the heated area gave a higher degree of correlation between recorded temperature and tail-flick latencies than did temperature measurements closer to the base of the tail. These results provide further support for the contention that tail-skin temperature is an important factor when assessing nociception by means of the tail-flick test, and demonstrate that the temperature should be measured as close to the heated area as possible.

Animals↗

PubMed1992

How Listeria exploits host cell actin to form its own cytoskeleton. I. Formation of a tail and how that tail might be involved in movement.

After Listeria is phagocytosed by a macrophage, it dissolves the phagosomal membrane and enters the cytoplasm. The Listeria then nucleates actin filaments from its surface. These actin filaments rearrange to form a tail with which the Listeria moves to the macrophage surface as a prelude to spreading. Since individual actin filaments appear to remain in their same positions in the tail in vitro after extraction with detergent, the component filaments must be cross-bridged together. From careful examination of the distribution of actin filaments attached to the surface of Listeria and in the tail, and the fact that during and immediately after division filaments are not nucleated from the new wall formed during septation, we show how a cloud of actin filaments becomes rearranged into a tail simply by the mechanics of growth. From lineage studies we can relate the length of the tail to the age of the surface of Listeria and make predictions as to the ratio of Listeria with varying tail lengths at a particular time after the initial infection. Since we know that division occurs about every 50 min, after 4 h we would predict that if we started with one Listeria in a macrophage, 16 bacteria would be found, two with long tails, two with medium tails, four with tiny tails, and eight with no tails or a ratio of 1:1:2:4. We measured the lengths of the tails on Listeria 4 h after infection in serial sections and confirmed this prediction. By decorating the actin filaments that make up the tail of Listeria with subfragment 1 of myosin we find (a) that the filaments are indeed short (maximally 0.3 microns in length); (b) that the filament length is approximately the same at the tip and the base of the tail; and (c) that the polarity of these filaments is inappropriate for myosin to be responsible or to facilitate movement through the cytoplasm, but the polarity insures that the bacterium will be located at the tip of a pseudopod, a location that is essential for spreading to an adjacent cell. Putting all this information together we can begin to unravel the problem of how the Listeria forms the cytoskeleton and what is the biological purpose of this tail. Two functions are apparent: movement and pseudopod formation.

Actins↗

PubMed1999

Tail kinematics of the chub mackerel Scomber japonicus: testing the homocercal tail model of fish propulsion.

Scombrid fishes possess a homocercal caudal fin with reduced intrinsic musculature and dorso-ventrally symmetrical external and internal morphology. Because of this symmetrical morphology, it has often been assumed that scombrid caudal fins function as predicted by the homocercal tail model. According to that model, the caudal fin moves in a dorso-ventrally symmetrical manner and produces no vertical lift during steady swimming. To test this hypothesis, we examined the tail kinematics of chub mackerel, Scomber japonicus (24.8+/-1.3 cm total length, L). Markers were placed on the caudal fin to identify specific regions of the tail, and swimming chub mackerel were videotaped from lateral and posterior views, allowing a three-dimensional analysis of tail motion. Analysis of tail kinematics suggests that, at a range of swimming speeds (1.2-3.0 L s(-)(1)), the dorsal lobe of the tail undergoes a 15 % greater lateral excursion than does the ventral lobe. Lateral excursion of the dorsal tail-tip also increases significantly by 32 % over this range of speeds, indicating a substantial increase in tail-beat amplitude with speed. In addition, if the tail were functioning in a dorso-ventrally symmetrical manner, the tail should subtend an angle of 90 degrees relative to the frontal (or xz) plane throughout the tail beat. Three-dimensional kinematic analyses reveal that the caudal fin actually reaches a minimum xz angle of 79.8 degrees. In addition, there is no difference between the angle subtended by the caudal peduncle (which is anterior to the intrinsic tail musculature) and that subtended by the posterior lobes of the tail. Thus, asymmetrical movements of the tail are apparently generated by the axial musculature and transmitted posteriorly to the caudal fin. These results suggest that the caudal fin of the chub mackerel is not functioning symmetrically according to the homocercal model and could produce upward lift during steady swimming.

Journal Article↗

PubMed2025

Genomic insights into the population history of fat-tailed sheep and identification of two mutations that contribute to fat tail adipogenesis.

INTRODUCTION: Since their domestication, domestic sheep (Ovis aries) have been culturally and economically significant farming animals worldwide. Fat-tailed sheep serve as a unique genetic resource for understanding adipogenesis and adaptive evolution in livestock. OBJECTIVES: Several genomic analyses have been conducted on various sheep breeds to elucidate the genome and regulation mechanism of the fat tail trait, prior genomic studies have failed to reconcile conflicting evidence about the genetic basis of tail morphology, particularly regarding the roles of PDGFD and BMP2. METHODS: Here, we conducted whole-genome resequencing of 283 sheep, encompassing 66 domestic breeds and 5 wild ovine species, to investigate the domestication history and selection signatures of fat-tailed sheep. Additionally, we performed transcriptome sequencing on adipose tissue to identify differentially expressed genes and cellular assays to validate these results. RESULTS: Demographic analysis revealed that domestic sheep descended from Asiatic mouflon and fat-tailed sheep began to diverge from thin-tailed sheep approximately 4.4-7.5 thousand years ago in East Asia. Chinese indigenous sheep were classified into Mongolian, Kazakh, Tibetan, and Yunnan populations. The Yunnan population may have experienced more recent genetic introgression from wild species, rather than an independent domestication event. Moreover, many potential regions associated with the fat-tailed phenotype (DDI1, PDGFD, and BMP2) were identified by selective sweep and genome-wide association analyses. Additionally, a fine-scale analysis of fat-tailed and thin-tailed sheep revealed two novel mutations: a G/A missense variant of PDGFD (Chr15: 3900312) and a C/T missense variant of BMP2 (Chr13: 48462350), both of which were significantly associated with tail adiposity. Functional validation demonstrated that mutant A-PDGFD significantly activated PFGFD expression and reduced fat deposition compared to wildtype. The C-BMP2 mutant activated BMP2 expression and promoted preadipocyte fat deposition. CONCLUSION: Our study provides the first evidence that these genes jointly regulate fat tail development through complementary mechanisms: PDGFD promotes adipose expansion, whereas BMP2 modulates energy partitioning. These findings offer new insights into the evolutionary history of fat-tailed sheep and identify potential targets for precision breeding in small ruminants.

Animals↗

PubMed1999

Novel structural elements identified during tail resorption in Xenopus laevis metamorphosis: lessons from tailed frogs.

When the tail of the Xenopus laevis tadpole resorbs at the end of metamorphosis, various cell types, including muscle, fibroblasts, skin, and spinal cord, are lost at about the same time. However, feeding frogs with tails can be produced by inhibiting thyroid hormone production at the climax of metamorphosis with the goitrogen methimazole. These tails lose their fast muscle preferentially, showing that the different cell types of the tail have different fates and confirming that more than one cell death program is involved in tail resorption. Both normal and methimazole tails contain "cords," novel structures that consist of two dorsal and two ventral parallel rows of slow muscle bundles joined by collagen fibers that run the length of the tail. The cords persist until the very end of tail resorption, being the last structure to dissolve. When thyroid hormone induces expression of proteolytic enzymes in the notochord sheath, the notochord, a structural rod that runs the length of the tail, begins to buckle, demonstrating that the tail is under tension. When sections of the tail that contain cords are surgically separated from the notochord, they contract in vitro, suggesting that the cords contribute to the tension that augments tail resorption.

Animals↗

PubMed1989

Cell death in the anuran tadpole tail: thyroid hormone induces keratinization and tail-specific growth inhibition of epidermal cells.

The mechanism of thyroid hormone-induced and glucocorticoid-modulated death of tail epidermal cells from tadpoles of bullfrog, Rana catesbeiana, was investigated by comparing tail epidermal cells with dorsal body epidermal cells. From morphological and biochemical criteria, there were two types of epidermal cells: basal cells and skein cells. The abundance of these cells was different between the tail and the body skin. Fifty percent of body cells and more than 95% of tail cells were skein cells. Effects of 3,3',5-triiodo-L-thyronine (T3, 10(-8) M) and cortisol (5 X 10(-7) M) were investigated with cultured epidermal cells. T3 differently regulated the keratinization of the tail and body cells. The keratinization of the tail epidermal cells was not observed without T3. T3 induced the keratinization dramatically. On the other hand, body epidermal cells were constantly undergoing keratinization without the hormone: T3 merely accelerated the rate of keratinization. Cortisol generally did not show any significant effect on keratinization. T3 showed opposite effects on DNA synthesis of the tail and body cells: suppression of tail cells and stimulation of body cells. Cortisol weakened the inhibitory effect of T3 on DNA synthesis in tail cells. Immunofluorescent micrographs with anti-BrdU showed that T3 decreased the number of cells in the S phase of the cell cycle in the case of tail cells but not of body cells. Thus, thyroid hormone plays dual roles for the tadpole epidermal cells: one is an induction and a promotion of keratinization in tail and body cells, respectively, and the other is an opposite regulation for the proliferation of both epidermal cells. These roles seem to have crucial connections to a tail-specific cell death induced by thyroid hormone.

Animals↗

PubMed2002

A generalized female bias for long tails in a short-tailed widowbird.

Tail elongation in the polygynous widowbirds (Euplectes spp.) has evoked both adaptive and non-adaptive explanations. Female choice has been shown in the three longest tailed species (20-50 cm), whereas an agonistic function was proposed for a medium-tailed (10 cm) widowbird. To test the generality and directionality of sexual selection on tail length in widowbirds, we experimentally investigated selection in the relatively short-tailed (7 cm) red-shouldered widowbirds (E. axillaris). Prior to territory establishment, males were assigned to four tail-treatment groups; control, short, long and supernormal (similar to a sympatric long-tailed congener). No effects on male competition were detected as the groups were equally successful in acquiring territories of similar size and quality. However, mating success among the 92 territorial males was strongly skewed in favour of supernormal-tailed males (62% of active nests; 5.2 +/- 1.3 nests per territory). Long-tailed males also acquired more nests (1.9 +/- 0.7) than control (0.7 +/- 0.5) and short-tailed (0.5 +/- 0.3) males, while the latter two groups did not differ significantly. These results support a general, open-ended female preference for long tails in widowbirds and may represent a receiver bias that arose early in their divergence from the short-tailed weaverbirds (Ploceinae).

Animals↗

PubMed1989

The apparent hyperalgesic effect of a serotonin antagonist in the tail flick test is mainly due to increased tail skin temperature.

It has been suggested that reduced activity in raphe-spinal serotonergic systems induces hyperalgesia. In rats, the serotonin antagonist metergoline (0.5 mg/kg intraperitoneally) reduced tail flick latency by 0.92 sec (p less than 0.001) and increased tail skin temperature by 2.4 degrees C (p less than 0.001) when measured 50 min after injection. Multiple regression analysis with tail flick latency as dependent variable and tail skin temperature and metergoline/vehicle as independent variables revealed a highly significant effect of tail temperature on tail flick latency. The increase of tail skin temperature explained a reduction of tail flick latency of 0.64 of the 0.92 sec observed [B = -0.267 +/- 0.034, t(37)= -7.75, p less than 0.0001]. When the effect on tail skin temperature was taken into account, metergoline reduced tail flick latency by 0.28 sec [B = -0.284 +/- 0.114, t(37) = -2.50, p less than 0.05]. Metergoline (0.5 and 2.0 mg/kg) did not significantly alter plantar paw skin temperature or the response temperature in the increasing temperature hot plate test. Thus, the observed effect of metergoline on tail flick latency is primarily due to an effect on tail skin temperature. The possibility exists that the remaining effect of metergoline may be due to inadequate correction for the skin temperature change, and it is concluded that the study provide no clear evidence for a tonic inhibition of nociception by serotonergic systems.

Animals↗

PubMed1988

Effects of serotonin receptor antagonists and agonists on the tail-flick response in mice involve altered tail-skin temperature.

Tail-flick latency and tail-skin temperature were measured in mice after administration of serotonin (5-HT) receptor antagonists (metergoline and metitepin) and agonists [5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT)]. Metergoline (4 mg/kg) and metitepin (0.5 mg/kg) reduced the tail-flick latencies and increased the tail-skin temperatures, but the effect on the tail-flick latencies was non-significant when the effect of temperature was taken into account. Both 5-MeODMT (3 mg/kg) and 8-OH-DPAT (1 mg/kg) reduced the tail-skin temperature but only 5-MeODMT increased the tail-flick latencies. The effect of 5-MeODMT on tail-flick latencies was still highly significant when the effect of temperature was taken into account. The results show that the apparent hyperalgesia elicited by 5-HT receptor antagonists in the tail-flick test in the mouse is secondary to increased tail-skin temperature and not due to increased nociceptive sensitivity. The antinociceptive effect of 5-MeODMT in the tail-flick test can, however, not be explained by effects of temperature.

8-Hydroxy-2-(di-n-propylamino)tetralin↗