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Breed assignment has proved to be useful to control meat trade and protect the value of special productions. Meat-related frauds have been detected in China; therefore, 95 SNPs selected from the ISAG core panel were evaluated to develop an automated and technologically updated tool to screen breed label fraud in the Chinese meat market. A total of 271 animals from four Chinese yellow cattle (CYC) populations, six Bos taurus breeds, two Bos indicus and one composite were used. The allocation test distinguished European, Japanese and Zebu breeds, and two Chinese genetic components. It correctly allocated Japanese Black, Zebu and British breeds in 100, 90 and 89% of samples, respectively. CYC evidenced the Zebu, Holstein and Limousin introgression. The test did not detect CYC components in any of the 25 samples from Argentinean butchers. The method could be useful to certify Angus, Hereford and Japanese Black meat, but a modification in the panel would be needed to differentiate other breeds., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Methods for individual identification are usually employed for traceability, whereas breed identification is useful to detect commercial frauds. In this study, Chinese Yellow Cattle (CYC) samples plus data from six Bos taurus breeds, two Bos indicus breeds, and one composite breed were used to develop an allocation test based on 22 microsatellites. The test allowed discriminating all foreign breeds from the CYC, although some CYC individuals were wrongly allocated as Limousin or Holstein, probably due to the recent introduction of these breeds into China. In addition, CYC evidenced a previously reported Zebu cline (south-north) and a possible structure within the B. taurus component that should be confirmed. An independent test performed with meat samples of unknown breed origin from Argentina allocated 92% of them to either Angus, Hereford, or their crossbreed, but none was identified as CYC. We conclude that the test is a suitable tool to certify meat of foreign breed origin and to detect adulterations of CYC beef labeled as imported meat., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Acute (45 min) exposure to pulsed (2 microseconds pulse width, 500 pulses per second) 2450-MHz microwaves at a power density of 1 mW/cm2 (whole body specific absorption rate 0.6 W/kg) microwaves caused a decrease in cholinergic activity in the hippocampus of the rat as measured by the sodium-dependent high-affinity choline uptake. Microinjection of beta-funaltrexamine (1 microgram) into the septum before microwave exposure blocked this effect. These data indicate that mu-opioid receptors in the septum mediate a microwave-induced decrease in cholinergic activity in the hippocampus and support our hypothesis that microwaves at a whole body SAR of 0.6 W/kg can activate endogenous opioids in the brain.

Cocaine (5-40 mg/kg, intraperitoneally) enhanced locomotion and rearing accompanied with head circling and body shaking. Although at 40 mg/kg typical stereotypy licking occasionally appeared, 40% of the rats died. At doses that did not affect physiologic locomotion and rearing, the D1-receptor antagonist SCH23390 but not D2 antagonist raclopride inhibited locomotion and rearing stimulated by cocaine (20 mg/kg). All behavioral responses of cocaine were abolished with increasing doses of raclopride and SCH23390. Sulpiride, a D2 antagonist, exerted a biphasic effect on locomotor activity (i.e., a low dose of sulpiride increased and a high dose decreased cocaine-induced locomotor activity). Sulpiride enhanced head circling, body shaking, and increases of rearing induced by cocaine. D2-receptor agonists quinpirole and bromocriptine inhibited these responses, presumably by activating the typical stereotyped behaviors such as sniffing at low doses, and licking and gnawing at high doses. The lowest dose of bromocriptine inhibited all behaviors induced by cocaine without producing typical stereotyped behaviors in itself. SK+F38393, a D1-receptor agonist, in combination with cocaine did not induce typical stereotype, which results in a synergistic effect of D1 and D2-receptor activities. The increases of locomotion and rearing, head circling, and body shaking induced by cocaine may involve the indirect activation of postsynaptic D1 and D2 receptors, presumably via dopamine release, resulting from inhibition of the presynaptic D2 receptors. These results also provide evidence that the indirect stimulation of postsynaptic D2 receptors by cocaine (20 mg/kg) is insufficient to induce stereotyped behaviors, and that the role of dopamine D1 receptors in mediating the behavioral actions of acute cocaine appears to be more important than that of D2 receptors. Our results also suggest that bromocriptine may be useful for the treatment of acute cocaine poisoning.

Acute (20 min) exposure to 100-dB white noise elicits a naltrexone-sensitive decrease in sodium-dependent high-affinity choline uptake in the frontal cortex and hippocampus of the rat. In the present study, the subtypes of opioid receptors involved were investigated by pretreating rats with microinjection of specific opioid-receptor antagonists into the lateral cerebroventricle before noise exposure. We found that the noise-induced decrease in high-affinity choline uptake in the hippocampus was blocked by pretreatment with either mu-, delta-, or kappa-opioid-receptor antagonists, whereas the effect of noise on frontal cortical high-affinity choline uptake was blocked by a mu- and delta- but not by a kappa-antagonist. These data further confirm the role of endogenous opioids in mediating the effects of noise on central cholinergic activity and indicate that different neural mechanisms are involved in the effects of noise on the frontal cortical and hippocampal cholinergic systems.

SKF 38393 (2-15 mg/kg, IV), but not quinpirole, shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rabbits. This effect was blocked by atropine (2-5 mg/kg, IV), but not by atropine methylbromide, suggesting that a central cholinergic mechanism was involved. The analeptic effect was also blocked by SCH 23390 (0.1 mg/kg, IV) or raclopride (5 mg/kg, IV). These results indicate that SKF 38393 activates central cholinergic neurons, which in turn initiate the analeptic effect. However, the fact that raclopride also blocked the SKF 38393 analeptic effect, but quinpirole did not exert any analeptic effect, suggests that a D-1/D-2 modulation of cholinergic systems may be involved in the SKF 38393-induced analeptic effect. These results also support our earlier findings and view that cocaine-induced analeptic activity is mediated by a dopaminergic-cholinergic mechanism.

SKF 38393 (5 mg/kg), but not quinpirole, shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rats. This effect was blocked by atropine (2 mg/kg), but not by atropine methylbromide, suggesting involvement of central cholinergic mechanisms. The analeptic effect was also blocked by SCH 23390 (0.2 mg/kg) or raclopride (2 mg/kg). SKF 38393 also increased sodium dependent high affinity choline uptake (HACU) in cortical and hippocampal synaptosomes that had been depressed by pentobarbital. SCH 23390 or raclopride prevented the SKF 38393 reversal of the depressed HACU, indicating that both D1 and D2 mechanisms were involved mediating the analeptic effect. These results provide neurochemical evidence that cortical and hippocampal D1-mediated cholinergic activation results in a behavioral arousal (analeptic) response. They also suggest that DA mechanisms may be involved in regulation of cortical and hippocampal cholinergic neurons.

Cocaine (1-5 mg/kg, IV) shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rabbits. This effect was completely blocked by scopolamine (1 mg/kg, IV), but not by scopolamine methylbromide, suggesting that a central cholinergic mechanism was involved. In urethane-anesthetized rats cocaine (1 mg/kg, IV) consistently generated hippocampal EEG theta rhythm lasting about 40 min. This effect was also abolished by scopolamine. These results suggest that cocaine produced behavioral and EEG arousal responses that involved the septohippocampal cholinergic system.

Rats were acutely (45 min) exposed to 100-dB white noise, and benzodiazepine receptors in the cerebral cortex, hippocampus, and cerebellum were studied immediately after exposure by the receptor-binding assay using 3H-flunitrazepam as the ligand. An increase in the concentration of receptors was observed in the cerebral cortex, whereas no significant change in receptor concentration was seen in the hippocampus and cerebellum. No significant effect of noise on receptor binding affinity was detected in the three brain regions studied. Experimental handling also did not significantly affect the benzodiazepine receptor properties. These data confirm previous reports that acute exposure to stressor can cause rapid changes in benzodiazepine receptors in the brain.

Bilaterally injected thioridazine (10 micrograms) into the striata of rats augmented the stereotypic behavior elicited by apomorphine. The enhancing effect was attenuated by pretreatment with alpha-methyl-p-tyrosine. At 48 hr postinjection of thioridazine (1.0 mg/kg, IP), motor suppression from a low dose of apomorphine (0.2 mg/kg, IP) was enhanced; however, motor response to a high dose of apomorphine (1 mg/kg, SC) was not affected. Possible mechanisms of action of thioridazine are discussed.

Stereotaxic microinjection of thyrotropin releasing hormone (TRH) into 16 brain areas revealed that only three sites, the medial septum and the lateral and anterior hypothalami, were sensitive to a 1.0 ug dose in stimulating intestinal transit in anesthetized rats. The medial septum and anterior hypothalamus also responded to 0.1 ug, but not to 0.01 ug, of TRH. Because TRH and its receptors are distributed in these brain areas, the present results suggest a possible role for this peptide in the central regulation of gastrointestinal activity.

Our previous research showed that 45 min of exposure to low-level, pulsed microwaves (2450-MHz, 2-microseconds pulses, 500 pps, whole-body average specific absorption rate 0.6 W/kg) decreased sodium-dependent high-affinity choline uptake in the frontal cortex and hippocampus of the rat. The effects of microwaves on central cholinergic systems were further investigated in this study. Increases in choline uptake activity in the frontal cortex, hippocampus, and hypothalamus were observed after 20 min of acute microwave exposure, and tolerance to the effect of microwaves developed in the hypothalamus, but not in the frontal cortex and hippocampus, of rats subjected to ten daily 20-min exposure sessions. Furthermore, the effects of acute microwave irradiation on central choline uptake could be blocked by pretreating the animals before exposure with the narcotic antagonist naltrexone. In another series of experiments, rats were exposed to microwaves in ten daily sessions of either 20 or 45 min, and muscarinic cholinergic receptors in different regions of the brain were studied by 3H-QNB binding assay. Decreases in concentration of receptors occurred in the frontal cortex and hippocampus of rats subjected to ten 20-min microwave exposure sessions, whereas increase in receptor concentration occurred in the hippocampus of animals exposed to ten 45-min sessions. This study also investigated the effects of microwave exposure on learning in the radial-arm maze. Rats were trained in the maze to obtain food reinforcements immediately after 20 or 45 min of microwave exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

The intravenous administration of codeine to diazepam-narcotized rabbits resulted in a shortened duration of loss of righting reflex. Coadministration of naltrexone plus codeine enhanced this analeptic effect and was also effective in shortening the duration of pentobarbital narcosis. The analeptic effect was blocked by atropine, but not by methylatropine, indicating involvement of a central cholinergic mechanism. In rats the analeptic activity correlated with the reversal of the diazepam-induced fall in sodium dependent high affinity choline uptake in hippocampal and cortical synaptosomes. These findings may represent the pharmacological basis of the recently reported antinarcoleptic action of codeine in man.

Supersensitivity developed in the central dopaminergic system of the rat after 21 days of chronic haloperidol injection. This was indicated by a higher level of apomorphine-elicited stereotypic behavior and by higher concentrations of striatal 3H-spiroperidol binding sites in haloperidol-treated rats compared to saline-treated controls. The chronic haloperidol treatment did not affect the baseline body temperature but potentiated both apomorphine- and ethanol-induced falls in core temperature. Such potentiation may also be related to dopamine supersensitivity. However, no significant correlation was found between apomorphine- or ethanol-induced hypothermia and apomorphine-elicited stereotypic behavior or the concentration of striatal 3H-spiroperidol binding sites. Hence, the nigrostriatal dopamine system does not appear to be involved in the development of hypothermic responses to these agents.

Thyrotropin releasing hormone (TRH) administered intraventricularly to rabbits produces tachypnea, hyperthermia, behavioral excitation and, with larger doses, compulsive scratching. These effects of TRH were unaffected by various catecholamine and serotonin antagonists or depleting agents. When TRH was administered to pentobarbital-narcotized animals, tachypnea and rapid recovery of the righting reflex occurred. The antagonism of narcosis or sedation was evident against other barbiturates, diazepam, chlorpromazine, and reserpine, but not against morphine. Morphine actually appeared to antagonize the excitatory actions of TRH. Scopolamine pretreatment prevented the arousal from pentobarbital narcosis, but not the tachypnea or hyperthermia. TRH represents a new class of psychoactive chemical which may play a role in brain function.