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Dexamethasone differentially alters naltrexone effects on vasopressin and oxytocin release during tail electroshock.

The origin of endogenous opioid peptides that inhibit release of vasopressin (VP) and oxytocin (OT) into the bloodstream after tail electroshock was investigated. We hypothesized that endogenous opioid peptides derived from the anterior pituitary reduced secretion of VP and OT during this stimulus. To test this hypothesis, dexamethasone (DEX) was used to preferentially suppress release of endorphins with ACTH from the anterior pituitary. We evaluated the effects of an opiate receptor antagonist, naltrexone, on the rise in plasma [VP] and [OT] after tail electroshock in male Sprague-Dawley rats given DEX either chronically or acutely before the shock. In the chronic study rats were injected SC daily with saline (3.2 ml/kg) or DEX (0.2 mg/kg) for 17 days. In the short term study, rats were injected IP with saline (5 ml/kg) or DEX (0.5 mg/kg) the day before and again 105 min prior to tail electroshock. Thirty min (chronic study) or 90 min (acute study) after saline or DEX was given on the last day, rats were injected SC with saline (1 ml/kg) or naltrexone (1 mg/kg). Fifteen min later, animals received tail electroshock (41 V, 30 sec) and were decapitated 15 sec after shock was completed. Control animals were treated similarly but not shocked. Amounts of VP and OT in plasma and the neurointermediate lobe were quantified by RIA. [VP] and [OT] were elevated in plasma of all rats given tail electroshock. Greater increases (p less than 0.05) in hormone concentrations were measured in plasma of shocked rats treated with DEX.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Disruption of thyroid hormone-mediated Xenopus laevis tadpole tail tip regression by hexabromocyclododecane (HBCD) and 2,2',3,3',4,4',5,5',6-nona brominated diphenyl ether (BDE206).

Thyroid hormone regulates amphibian metamorphosis, including the transformation of a tadpole into a froglet and regression of the tail. Xenopus laevis tadpole tail tips in organ culture (ex vivo) undergo regression when exposed to 3,3',5-triiodo-l-thyronine (T(3)) and interference by chemicals with this process was utilized as a bioassay to detect thyroid hormone disruption. In the present study the bioassay was further validated by investigating its response to compound induced T(3)-antagonism and - potentiation. Tadpole tail tips were exposed to two brominated flame retardants (BFRs) in presence or absence of T(3) at its EC(50) (20 nM). T(3)-induced tail tip regression was antagonized by 2,2',3,3',4,4',5,5',6-nona brominated diphenyl ether (BDE206) and potentiated by hexabromocyclododecane (HBCD) in a concentration dependent manner, which was consistent with results obtained with a in vitro T(3)-dependent proliferation bioassay termed the T-screen. Neither compound induced any effect in the absence of T(3). The results indicate that studying possible hormone disrupting effects of agonistic, antagonistic or potentiating compounds should include combined exposure with the natural hormone at around its EC(50) concentration. The results obtained with the tail tip exposures were in accordance with the T-screen predictions, and occurred at BFR-concentrations that were only 5-50 times those of T(3). The bioassay proved to be suitable not only for detecting T(3)-agonism, but also for antagonism and potentiation.

Animals↗

Compound action potential of sensory tail nerves in the rat.

Assessment of the conduction velocity of motor fibers of the rat tail nerves has been used by some authors in the past, but very little is known about the sensory fibers. In 10 adult rats, weighing between 320 and 380 g, responses from the nerves and muscles of the tail have been recorded after stimulation at its root and tip. It was found that stimulation of the tip involved mainly sensory fibers, of which two main groups could be identified. One faster group, conducting within the range of 38-27 m/s, and one slower group with range 14-7 m/s. The bipolar recording configuration was found to be optimal for sensory recording. Stimulation of the tail root evoked a motor response, which was preceded by a very small neurographic activity, due to the fastest sensory fibers conducting antidromically. The conduction velocity of motor fibers was calculated to be approximately 19 m/s. Distance traveled by the volley can be assessed with excellent precision on the tail nerves; hence the calculated conduction velocities are highly reliable and reproducible. We propose that the tail nerves may be a useful tool for evaluation of conduction velocity of Abeta and Adelta afferents. As the technique is just minimally invasive, the test can be repeated a number of times in animals under chronic experimental conditions.

Action Potentials↗

Effects of bisphenol A on thyroid hormone-dependent up-regulation of thyroid hormone receptor alpha and beta and down-regulation of retinoid X receptor gamma in Xenopus tail culture.

We investigated effects of different concentrations (10(-7) - 10(-5) M) of bisphenol A (BPA), which is known as an estrogenic and anti-thyroid hormonal endocrine disrupter, on the expression of thyroid hormone receptor (TR) alpha and beta and retinoid X receptor (RXR) gamma mRNA in tails of stage 52-54 Xenopus tadpoles in organ culture in the presence or absence of different concentrations of triiodo-thyronine (T(3)). In the absence of T(3), BPA at any concentration examined did not show remarkable effects on tail length but blocked 10(-7) M T(3)-induced tail resorption in a concentration-dependent manner. Semi-quantitative analyses of TRalpha and TRbeta mRNAs by RT-PCR in the tail specimens indicated that BPA shows an apparent antagonistic effect towards the receptors and reduced their mRNA levels relative to controls. When administered together with 10(-7) M T(3), the antagonistic effects of BPA were detected more clearly and dose-dependently. While BPA prevented the autoinduction of both TRalpha and TRbeta genes by T(3), the effect was less marked on TRalpha than on TRbeta. BPA also moderately suppressed RXRgamma gene expression. Gene expression of RXRgamma, a partner for heterodimer formation of TRs, was supressed by T(3) alone and also by BPA alone, but no additive effects were observed so far as studied. The present study indicates that a relatively low concentration of BPA, 10(-7) M, as compared with those examined previously (10(-5) to 10(-4) M) by us and other investigators, acts as an antagonist of T(3) through suppression of TRalpha and TRbeta gene expression in Xenopus tail in culture.

Animals↗

Effect of OS-0689, a novel SERM, on periarterial nerve function in tail arteries of ovariectomized rats.

OBJECTIVE: We have previously shown that OS-0689 attenuates the rise in tail skin temperature of ovariectomized rats, which is believed to be relevant to human symptoms of hot flush. In this study, we elucidate the mechanism underlying the ameliorating effects of OS-0689 on elevated tail skin temperature. METHODS: Female Sprague-Dawley rats were ovariectomized and orally treated with OS-0544 (1 mg/kg), OS-0689 (3 mg/kg; (+)-enantiomer of OS-0544) or 17beta-estradiol (3 mg/kg; E2) for 1 week. At 1, 3 or 6 weeks after ovariectomy, the vasoconstrictions and vasorelaxations induced by periarterial nerve stimulation (PNS), l-noradrenaline (NA), and rat calcitonin gene-related peptide (CGRP) in isolated tail arteries were compared between OVX and sham-operated rats. RESULTS: Three weeks after ovariectomy, vasoconstrictions in response to PNS and NA in the arteries of OVX rats were markedly less than those in the arteries of sham-operated rats. However, at 1 and 6 weeks after ovariectomy the stimuli-induced vasoconstrictions in the arteries of OVX rats were greater than those of sham-operated rats. Moreover, NA reactivity was not attenuated in the mesenteric arteries at 3 weeks after ovariectomy. OS-0544, OS-0689 and E2 prevented the decrease in vasoconstrictions in the tail arteries. Vasorelaxations in response to PNS and rat CGRP were significantly greater in the arteries of OVX rats than in those of the sham-operated rats. OS-0689 inhibited the increase in vasorelaxation induced by both stimuli, whereas E2 had no effects. CONCLUSIONS: Ovariectomy not only decreases adrenergic function but also enhances CGRPergic function in rats' tail arteries. OS-0689 improves both impairments and thereby improves on rat hot flush.

Analysis of Variance↗

Maternal PAN2 selectively maintains mRNA Poly(A) tail homeostasis to regulate RNA degradation during oocyte-to-early embryo transition in mice.

In mammals, the precise degradation of maternal mRNAs is essential for oocyte maturation and early embryonic development, as it facilitates the "maternal-to-zygotic transition (MZT)" by eliminating maternal transcripts and enabling zygotic genome activation (ZGA). However, the physiological role of the poly(A)-specific nuclease 2 (PAN2), a deadenylase that initiates cascade degradation of long-tailed transcripts, remains unknown. Here, we generated oocyte-specific Pan2 conditional knockout (cKO) mice to investigate its role. We found that Pan2 cKO females exhibit severe female subfertility despite normal oocyte maturation and ovulation, with embryos arresting at the 2-cell stage. PAIso-seq2 and transcriptome sequencing reveal that PAN2 coordinates maternal mRNA deadenylation and decay. Mechanistically, PAN2 recognizes its substrates through a PAN3-PABPC1 bridging complex, and it preferentially targets transcripts whose poly(A) tails lack guanosine (G) but are enriched for uridine (U). PAN2 deficiency causes poly(A) tail dyshomeostasis, leading to global accumulation of maternal mRNAs, impaired zygotic genome activation, and abnormal protein accumulation in 2-cell embryos. Overexpression of these proteins phenocopies developmental defects. Notably, the PAN2-regulated transcriptome is largely non-overlapping with the LC3B-mediated degradation pathway, highlighting the unique and non-redundant role of PAN2 in maternal mRNA clearance. Our study establishes maternal PAN2 as a critical regulator of poly(A) tail homeostasis, ensuring timely maternal mRNA clearance and proper ZGA, highlighting the stage-specific and tail-composition-dependent functions of the deadenylase cascade during the maternal-to-zygotic transition. These findings offer new perspectives on post-transcriptional regulatory mechanisms in early mammalian embryogenesis.

Deadenylation↗

Virion tails of Beet yellows virus: Coordinated assembly by three structural proteins.

Filamentous virions of Beet yellows virus contain a long body formed by a major capsid protein and a short tail that is assembled by a minor capsid protein (CPm), an Hsp70-homolog (Hsp70h), a 64-kDa protein (p64), and a 20-kDa protein (p20). Using mutation analysis and newly developed in planta assays, here we investigate the genetic requirements for the tail assembly. We show that the inactivation of CPm dramatically reduces incorporation of both Hsp70h and p64. Furthermore, inactivation of Hsp70h prevents incorporation of p64 into virions and vice versa. Hsp70h and p64 are each required for efficient incorporation of CPm. We also show that the tails possessing normal relative amounts of CPm, Hsp70h, and p64 can be formed in the absence of the major capsid protein and p20. Similar to the tails isolated from the wild-type virions, these mutant tails encapsidate the approximately 700 nt-long, 5'-terminal segments of the viral RNA. Taken together, our results imply that CPm, Hsp70h and p64 act cooperatively to encapsidate a defined region of the closterovirus genome.

Base Sequence↗

Role of G(i)-proteins in norepinephrine-mediated vasoconstriction in rat tail artery smooth muscle.

We showed, in rat de-endothelialised tail artery, that pertussis toxin (PTX) (1 microg/mL, 2 hr) attenuated norepinephrine (NE)-induced vasoconstriction without modifying intracellular calcium concentration [Ca2+](i) mobilisation. We suggested the existence of two NE-induced intracellular pathways: a first, which would be insensitive to PTX and lead to [Ca2+](i) mobilisation, and a second sensitive to PTX and involved in the [Ca2+](i) sensitivity of NE-induced contraction. The aim of this study was to demonstrate the existence of the second intracellular pathway. PTX-sensitive G(i/o)-proteins in rat tail artery SMC membrane were identified by immunoblot and ADP-ribosylation. [(32)P]ADP-ribosylation of alpha(i/o)-subunits was demonstrated in situ by perfusing rat de-endothelialised tail artery segments with PTX (1 microg/mL, 2 hr), which suggested that G(i/o)-protein inactivation was involved in the reduction by PTX of the [Ca2+](i) sensitivity of NE-induced contraction. Coupling between G(i/o)-proteins and NE receptors was confirmed by the NE-induced increase in G(i/o)-specific GTPase activity (24.1 +/- 1.9 vs 8.8 +/- 0.4 pmol P(i)/mg protein at 5 min; P < 0.05 vs basal). [(3)H]Prazosin-binding data showed the presence of a heterogeneous alpha(1)-AR population in rat tail artery smooth muscle cells. We demonstrated the in vitro coupling between alpha(1A)-AR subtype and alpha(i)-subunits. In conclusion, we identified, in rat de-endothelialised tail artery, a PTX-sensitive G(i/o)-protein-modulated pathway that is coupled to NE receptors via alpha(1A)-AR. We suggest that NE stimulates two alpha(1)-AR-mediated intracellular pathways: a first, which is mediated by a G(q)-protein and leads to [Ca2+](i) mobilisation and contraction, and a second, which is mediated by a G(i)-protein and is involved in the amplification of the [Ca2+](i) sensitivity of NE-induced tension.

Analysis of Variance↗

Intense peripheral electrical stimulation evokes brief and persistent inhibition of the nociceptive tail withdrawal reflex in the rat.

In a study of modulation of nociception by sensory inputs, electrical stimulation was applied to specific sites in the hindlimb and effects on the nociceptive tail withdrawal reflex were monitored in the lightly anaesthetized rat. Stimulation was applied to previously defined sites in the hindlimb, meridian points femur-futu (ST-32), fengshi (GB-31) and zusanli (ST-36). It consisted of a 4 Hz train of 2 ms square pulses given for 20 min at 20 x the threshold intensity required for muscle twitch. Tail withdrawal was provoked by application of a noxious heat stimulus applied to the tip of the tail. Results were expressed as a percentage of the maximal possible inhibition which is achieved when the post-treatment latency is 2 x the pre-treatment latency otherwise known as the cut off. During stimulation, the latency of the withdrawal increased to approximately 70% of the maximal possible inhibition. Following stimulation, the inhibition persisted for > 1 h. Stimulation at 2 or 6 Hz elicited similar effects but stimulation at 8 Hz evoked inhibition during the stimulation only. Stimulation applied to sites away from defined meridian points inhibited tail withdrawal during the stimulation; no post-stimulation effect was produced. In acutely transected animals (< or = 48 h), stimulation of meridian points elicited a small, brief increase in latency but during stimulation only. At 7 and 14 days after spinal transection, this response during stimulation was greater in magnitude and a brief post-stimulation increase was also observed. The return of this latter effect was coincident with the return of bladder function. These data suggest that high intensity, low frequency electrical stimulation of hindlimb meridian points in the lightly anaesthetized rat produces both brief and persistent inhibitory effects on the nociceptive tail withdrawal reflex. These effects appear to be elicited by different mechanisms. The persistent effect may represent a plastic change in central inhibitory mechanisms. Data from spinal animals indicate a major participation of supraspinal structures but that spinal mechanisms are also capable of sustaining both types of effect.

Animals↗

Involvement of 5-hydroxytryptamine(1A) receptors in nicotine-induced tail tremor in rats.

Involvement of the serotonergic system in tail tremor induced by repeated administration of nicotine was investigated in rats. Tail tremor induced by nicotine (0.5 mg/kg, s.c.) was suppressed by a 5-HT(1A) receptor antagonist, N-¿2-[4-(2-methoxyphenyl)-1-piperazinyl-]ethyl¿-N-(2-pyridinyl)cycloh exanecarboxamide trihydrochloride (WAY-100635; 0.3-3 mg/kg, i.p.), but not by a 5-HT(2) receptor antagonist, ketanserin (0.1-0.3 mg/kg, i.p). The 5-HT(1A) receptor agonists, buspirone (1-20 mg/kg, i.p.), gepirone (1-10 mg/kg, i.p.), tandospirone (1-10 mg/kg, i.p.) and (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.01-0.1 mg/kg, s.c.), enhanced the tail tremor. The enhancement of tail tremor by buspirone (10 mg/kg, i.p.) was blocked by WAY-100635 (0.3-3 mg/kg, i.p.). These findings suggest that nicotine-induced tail tremor is mediated by 5-HT(1A) receptors and that 5-HT(1A) receptor antagonists are effective in the treatment of tremor.

Animals↗

Uncompetitive NMDA receptor antagonists potentiate morphine antinociception recorded from the tail but not from the hind paw in rats.

We investigated the effects of pretreatment with low-affinity, uncompetitive NMDA receptor antagonists on morphine-induced antinociception in rats using the same intensity of thermal stimulus applied to the tail and the paws. Similar baseline responses to thermal stimuli of the same intensity were recorded from tails and hind paws. However, morphine produced equal antinociception from the tail and hind paw when used at doses of 2.5 and 6 mg/kg, respectively. These doses were used in further experiments. Thirty minutes before morphine, rats were administered the NMDA receptor antagonists dextromethorphan (2.5--30 mg/kg), memantine (2.5--15 mg/kg) and MRZ 2/579 (1-amino-1,3,3,5,5-pentamethyl-cyclohexane HCl) (1.25--10 mg/kg). All three compounds significantly and dose-dependently potentiated morphine-induced antinociception recorded from the tail. However, none of these NMDA receptor antagonists affected morphine antinociception recorded from the paw. These findings suggest that low-affinity NMDA receptor antagonists modulate differently morphine antinociceptive activity recorded from the tail and hind paws.

Analgesics↗

Comparison of relative potencies of i.v. and i.c.v. administered 8-OH-DPAT gives evidence of different sites of action for hypothermia, lower lip retraction and tail flicks.

8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT)-induced temperature reduction, lower lip retraction and tail flick responses are widely used models of 5-HT1A receptor function. To obtain information about the sites of receptors mediating these effects we measured these responses, parallel over wide dose ranges after intracerebroventricular (i.c.v., 0.6-67 micrograms/kg) and intravenous (i.v., 3-500 micrograms/kg) administration. Analysis of the dose-response curves provided evidence for a 9.8-fold ratio of the potency of 8-OH-DPAT following i.c.v. compared to i.v. administration on body temperature reduction (ED50 values are 5.1 and 50 micrograms/kg, after i.c.v and i.v. administration, respectively) and a 2.9-fold ratio in potency for lower lip retraction (ED50 values are 29 and 86 micrograms/kg, after i.c.v. and i.v. administration, respectively). 8-OH-DPAT was less potent in the induction of tail flicks than of the other responses and had a lower potency after i.c.v. than after i.v. administration (ED50 values, the first one extrapolated, are 526 and 246 micrograms/kg, after i.c.v. and i.v. administration, respectively). In addition, the i.c.v. ED50 for temperature reduction was significantly lower than those for lower lip retraction or tail flick responses. The relative potency, that is, the ratio of i.v. and i.c.v. ED50, was significantly higher for temperature reduction than for lower lip retraction or tail flick responses (ED50 i.v./ED50 i.c.v. values are 9.8, 2.9, and 0.47, respectively). These data provide evidence that distinct sites of action are involved in these models. Temperature reduction is mediated mainly by postsynaptic receptors in the close vicinity of the lateral ventricle. Receptors that mediate lower lip retraction are located more distantly in the brain, supporting previous evidence that they are somatodendritic autoreceptors, and receptors in the spinal cord are probably responsible for tail flick responses.

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

The structure of the receptor-binding domain of the bacteriophage T4 short tail fibre reveals a knitted trimeric metal-binding fold.

Adsorption of T4 bacteriophage to the Escherichia coli host cell is mediated by six long and six short tail fibres. After at least three long tail fibres have bound, short tail fibres extend and bind irreversibly to the core region of the host cell lipo-polysaccharide (LPS), serving as inextensible stays during penetration of the cell envelope by the tail tube. The short tail fibres consist of a parallel, in-register, trimer of gene product 12 (gp12).X-ray crystallography at 1.5A resolution of a protease-stable fragment of gp12 generated in the presence of zinc chloride reveals the structure of the C-terminal receptor-binding domain. It has a novel "knitted" fold, consisting of three extensively intertwined monomers. It reveals a metal-binding site, containing a zinc ion coordinated by six histidine residues in an octahedral conformation. We also suggest an LPS-binding region.

Amino Acid Sequence↗

Balance in the cat: role of the tail and effects of sacrocaudal transection.

To determine whether the tail of the domestic cat plays a role in balance during locomotion, four cats were trained to traverse a narrow beam. To challenge balancing ability, a sudden lateral displacement was imparted to the beam as the subject was crossing. Freeze-frame videotape analysis revealed that cats responded to beam movement by rapidly moving the tail in the opposite direction. Adjustment of the tail contributed to realignment of the hips over the beam and enabled the animal to remain aboard the beam. Following complete sacrocaudal spinal transection, that eliminated supraspinal control to only the tail, cats fell significantly more often in response to movements of the beam. The importance of the cat's tail for balance, and the utility of this system for modeling functional consequences of spinal cord injury and therapeutic interventions, are discussed.

Animals↗

A mouse model for peripheral neuropathy produced by a partial injury of the nerve supplying the tail.

We attempted to develop a mouse model for peripheral neuropathy by a partial injury of the nerve supplying the tail. Under enflurane anesthesia, the unilateral superior caudal trunk was resected between the S3 and S4 spinal nerves. Tests for thermal allodynia were conducted by immersing the tail into 4 or 38 degrees C water. The mechanical allodynia was assessed by stimulating the tail with a von Frey hair (1.96 mN, 0.2 g). After the nerve injury, the experimental animals had shorter tail withdrawal latencies to cold and warm water immersion than the presurgical latency, and exhibited an increase in tail response to von Frey stimulation. We interpret these abnormal sensitivities as the signs of mechanical, cold and warm allodynia following the superior caudal trunk injury in the mouse.

Animals↗

Comparative biochemical analysis of sea urchin peristome and rat tail tendon collagen.

We report here a biochemical comparison between type 1 rat tail tendon collagen and collagen isolated from sea urchin peristome tissue. The sea urchin collagen consisted of two species of apparent mol masses, 140 and 116 kDa. Amino acid compositional analysis of the 140 and 116 kDa species revealed the presence of hydroxyproline and hydroxylysine as well as a glycine content of 28.1 mol.%. In solubility experiments the rat tail tendon collagen was found to precipitate at sodium chloride concentrations between 1 and 2 M while peristome collagen remained soluble at salt concentrations as high as 4 M. Incubation of the peristome and rat tail tendon collagen preparations with a sea urchin collagenase/gelatinase resulted in cleavage of the former but not the latter collagen. Upon heat denaturation at 60 degrees C, however, the rat tail tendon collagen served as a substrate for the gelatinase. Cyanogen bromide cleavage of rat tail and peristome collagens generated largely unique peptide maps. Collectively, these results suggest that structural differences exist between echinoderm and vertebrate type 1 collagens.

Amino Acids↗

Involvement of EphA2 in the formation of the tail notochord via interaction with ephrinA1.

Eph receptors have been implicated in cell-to-cell interaction during embryogenesis. We generated EphA2 mutant mice using a gene trap method. Homozygous mutant mice developed short and kinky tails. In situ hybridization using a Brachyury probe found the notochord to be abnormally bifurcated at the caudal end between 11.5 and 12.5 days post coitum. EphA2 was expressed at the tip of the tail notochord, while one of its ligands, ephrinA1, was at the tail bud in normal mice. In contrast, EphA2-deficient notochordal cells were spread broadly into the tail bud. These observations suggest that EphA2 and its ligands are involved in the positioning of the tail notochord through repulsive signals between cells expressing these molecules on the surface.

Animals↗

Comparison of methods for the reduction of acute pain produced by rubber ring castration or tail docking of week-old lambs.

Behavioural and plasma cortisol changes were recorded for groups of eight Suffolk x Greyface lambs subjected to castration or tail docking using rubber rings with and without local anaesthetic treatment. Immediately after application of the rubber ring, local anaesthetic (2 x 0.2 ml 2% lignocaine) was administered either by needle and syringe or by high-pressure needleless injection into each side of the neck of the scrotum or tail at the site of the ring, or by high pressure needleless injection into the testes before ring application. In other groups, the innervation to the scrotum or tail was disabled by crushing with a powered bloodless castrator just proximal to the ring. Measurements were recorded in groups of control (handled) lambs, with and without local anaesthetic treatment. Application of local anaesthetic by high pressure needleless injection had little effect on either plasma cortisol values or behaviour of control lambs. For castration, application of the bloodless castrator and/or local anaesthetic at the ring site reduced the peak plasma cortisol concentration by 50% (P < or = 0.01), the incidence of active behavioural responses by 80 and 64% (P < or = 0.01) respectively, and the time spent in abnormal postures by 68 and 59% (P < or = 0.01) respectively. Both methods were effective in reducing pain for tail docking [active behavioural responses reduced by more than 80% (P < or = 0.01) and abnormal postures by 56% (P < or = 0.01)], although local anaesthetic was more effective, reducing the peak cortisol by 60% (P < or = 0.01) [crushing by 44% (P > 0.05)]. Injection of local anaesthetic into the testes was less effective than injection into the neck of the scrotum at the site of the ring [reduction in abnormal lying postures (P < or = 0.05), 45 vs 71%, respectively]. The rapid action, effectiveness, and ease of application of these experimental methods may provide the basis for commercially viable methods for reducing the acute pain produced by rubber ring castration and tail docking of lambs.

Anesthetics, Local↗