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RL-37, an alpha-helical antimicrobial peptide of the rhesus monkey.

Rhesus monkey bone marrow expresses a cathelicidin whose C-terminal domain comprises a 37-residue alpha-helical peptide (RL-37) that resembles human LL-37. Like its human counterpart, RL-37 rapidly permeabilized the membranes of Escherichia coli ML-35p and lysed liposomes that simulated bacterial membranes. When tested in media whose NaCl concentrations approximated those of extracellular fluids, RL-37 was considerably more active than LL-37 against staphylococci. Whereas human LL-37 contains five acidic residues and has a net charge of +6, rhesus RL-37 has only two acidic residues and a net charge of +8. Speculating that the multiple acidic residues of human LL-37 reduced its efficacy against staphylococci, we made a peptide (LL-37 pentamide) in which each aspartic acid of LL-37 was replaced by an asparagine and each glutamic acid was replaced by a glutamine. LL-37 pentamide's antistaphylococcal activity was substantially greater than that of LL-37. Thus, although the precursor of LL-37 is induced in human skin keratinocytes by injury or inflammation, its insufficiently cationic antimicrobial domain may contribute to the success of staphylococci in colonizing and infecting human skin.

Amino Acid Sequence↗

Methyl alcohol poisoning. II. Development of a model for ocular toxicity in methyl alcohol poisoning using the rhesus monkey.

Rhesus monkeys were intoxicated with methyl alcohol, using an initial dose of 2 gm/kg and subsequent doses were administered in order to maintain an attenuated and prolonged state of intoxication. Arterial blood samples were drawn for methyl alcohol, formate, PO2, PCO2, and pH, which were monitored periodically throughout the course of the experiment. With the use of these procedures monkeys developed metabolic acidosis with the accumulation of formic acid in the blood and a corresponding decrease in blood bicarbonate. These animals served as models, which allowed for ocular evaluation for early signs related to methyl alcohol poisoning. A mechanism to explain toxicity is proposed and discussed.

Acidosis↗

Endocrine regulation of fetal development and its relation to parturition in the rhesus monkey.

Rhesus monkey fetuses were surgically prosencephalectomized (Type 2) or functionally hypophysectomized (Type 1) at 75 days gestation, then returned to the uterus until elective Caesarean section on day 145--150 (term 167 days). Deprivation of fetal hypothalamic releasing factors in Type 2 and fetal pituitary tropic hormones in Type 1 significantly delayed the ontogeny and functional development of fetal endocrine tissues. Bone ossification and growth were significantly retarded in Type 1 only, not in Type 2. In Type 1 the body and all organs except the endocrine glands were about half normal weight. The adrenals, thyroids, ovaries and testes were histologically abnormal and about one-tenth normal weight. Non-endocrine organs were histologically similar to 110-130-day fetuses. Thyroxine (T4) concentrations were significantly depressed in Type 1 fetal and maternal plasma at Caesarean section but normal in Type 2. Cortisol concentrations were normal in Type 1 fetal and maternal plasma. Types 1 and 2 plasma oestradiol concentrations were significantly lower in mothers but normal in fetuses. Type 1 placentas produced significantly less progesterone in vitro than normal. Fetal endocrine autonomy is indicated (thyrotropin-releasing factor excepted). Many of the hypothalamic and anterior pituitary hormones do not pass in effective amounts from mother to fetus. Fetal endocrine autonomy is a prerequisite for the control of both development and parturition.

Adrenal Glands↗

The effects of low dietary levels of polyunsaturates on alcohol-induced liver disease in rhesus monkeys.

Rhesus monkeys that were maintained on a diet containing low, yet adequate, amounts of vitamins C and E and in which linoleate and linolenate represented 1.4% and 0.08% of the total caloric intake, respectively, developed liver fibrosis after consuming alcohol (mean, 2.6 g kg(-1) d[-1]) over a period of 3 years. In the liver, several polyunsaturated fatty acids including 18:2n6, 20:4n6, and 22:6n3 decreased compared with dietary controls, and similar findings were also observed in plasma lipoproteins and erythrocytes. The amount of alcohol consumed correlated positively with plasma lipid peroxidation products, 4-hydroxynonenal (4-HNE) and 8-isoprostane F2alpha, and negatively with 20:4n6 and 22:6n3 levels. These findings imply that alcoholics who also have a marginal intake of essential fatty acids and antioxidants in their diets may be at an increased risk of developing liver disease.

Aldehydes↗

Hepatic and metabolic effects of ethanol on rhesus monkeys.

Rhesus monkeys were tube-fed 100 calories per kg of a liquid diet based on casein in which 41% of the calories were derived from grain alcohol. The alcohol intake was 5.8 g per kg per day. Control diets contained isocaloric amounts of glucose. The protein content of the diet was 15% and fat supplied 21% of the calories. After 28 days the animals which had been fed ethanol developed hepatic fatty change and serum L.D.H. levels were elevated. The most striking electron microscopic changes in the alcohol animals were mitochondrial swelling, focal cytoplasmic degradation, and dilatation of the rough endoplasmic reticulum. In the monkeys which had received ethanol the metabolism of alcohol increased from 17.4 mg per 100 ml per hour to 26.6 mg and antipyrene half-life decreased from 61.0 minutes to 49.9 minutes. The carbohydrate animals showed no significant change in alcohol metabolism or antipyrene half life. The ethanol animals lost weight significantly while the carbohydrate animals gained significantly. The metabolic effects of alcohol thus were not reproduced by glucose. Administration of phenobarbital at 30 mg per kg for 5 days increased alcohol metabolism from 16.5 mg per hour to 22.5 mg per hour and shortened antipyrene half life from 76.5 minutes to 33.6 minutes. Alcohol and phenobarbital both induced enhanced drug metabolism but alcohol was a more powerful inducer of its own metabolism than phenobarbital. Phenobarbital on the other hand was a better inducer of antipyrene metabolism than alcohol.

Animals↗

Effects of clonidine and morphine on opioid withdrawal in rhesus monkeys.

Rhesus monkeys undergoing opioid withdrawal either due to withholding morphine administration for 14 h or due to administration of naloxone, were treated with or due to administration of naloxone, were treated with either morphine or clonidine. Morphine eliminated all of the withdrawal signs that developed when morphine was withheld for 14 h. Clonidine also eliminated some but not all signs that developed when morphine was withheld. The frequencies of individual signs prior to drug administration were directly related to the minimal doses necessary to eliminate signs for morphine but not for clonidine. Morphine also eliminated most of the signs precipitated by naloxone, whereas clonidine did not eliminate as many of the naloxone-precipitated signs. Additionally, some of the naloxone-precipitated signs that were eliminated by clonidine were not eliminated by morphine. The present results are consistent with clinical findings indicating an efficacy of clonidine in the treatment of opioid withdrawal through a non-opioid mechanism.

Animals↗

Saccadic reaction times and activation of the prelunate cortex: parallel observations in trained rhesus monkeys.

Rhesus monkeys were trained to fixate a small spot and saccade to a second stimulus in the near periphery if the fixation spot went off. In different tests the target stimulus could occur at various delay times before or after the offset of the fixation spot. During periods of single unit recording from the prelunate cortex neural events were measured together with saccadic reaction times (SRT): If the stimulus was visible for a period of time (1 or 0.5 s) before the fixation spot disappeared (positive "delayed saccade" task) the SRT reached values of more than 300 ms. The SRTs were shorter when the target stimulus occurred simultaneously with the offset of the fixation spot ("saccade" task). SRT were shortest (approximately 150 ms) if the target stimulus appeared 100-250 ms after the offset of the fixation spot (negative "delayed saccade" task). Moreover, they decreased with the time of daily training. The different behavioural conditions resulted in different types of cortical activity with different latencies: In "saccade" and negative "delayed saccade" tasks the neurons on-responses could be enhanced in comparison to the passive visual on-responses during stationary fixation. The latencies of the on-response and the enhanced on-response were equal with approximately 80 ms. In striking contrast the latencies of the presaccadic activation (PSA) in the positive "delayed saccade" tasks were more than twice as long with about 200 ms. Daily training influences both the SRTs and the PSA: The SRTs become shorter by more than 150 ms in positive "delayed saccade" tasks (delay: 300-500 ms) and the percentage of PSA-neurons decrease from more than 70% to less than approximately 20% after 3 weeks of daily training and recording. The temporal aspects of events preceding visually guided eye movements are important to understand the serial and parallel processing in cortical and subcortical structures that are involved in the learning, initiation, and execution of goal directed movements.

Animals↗

Elevation of blood lead concentration by confinement in the rhesus monkey.

Rhesus monkeys were exposed to lead (Pb) acetate under various regimens during the first 12 months of life. At 30 months of age, these animals and unexposed controls were confined to an unfamiliar experimental chamber for one week. Serum cortisol concentration and Pb concentration in whole blood (PbB) were measured prior to, during, and after this confinement. Cortisol concentrations rose 60--90% within 2 hours of confinement, and declined to baseline levels after 98 hours of confinement. Mean baseline PbB levels reflected the state of clearance of the previously-ingested lead, rose 25--35% within 2 hours of confinement, and reached mean maximum levels as much as 100% above baseline after 98 hours of confinement. The data are discussed in terms of hormonal mobilization of Pb stored in bone, and subgest (1) that this storage is multicompartmental, (2) that more than one process is probably involved in its mobilization, (3) that cortisol probably does not directly affect PbB levels, and (4) that stress should be considered a potential factor in determining the PbB in studies of Pb metabolism.

Animals↗

Reinforcing effect of the D1 dopamine agonist SKF 81297 in rhesus monkeys.

Rhesus monkeys with IV catheters were allowed to self-administer cocaine for 1 h/day. When responding was stable, saline or the D1 dopamine agonist SKF 81297 (SKF; 0.001-0.3 mg/kg/inj) was substituted for cocaine. At least two doses of SKF maintained responding above saline levels in all monkeys. The D1 antagonist SCH 39166 (0.001-0.03 mg/kg, IM) was then administered 30 min before sessions of self-administration of the lowest dose of SKF that maintained behavior (0.01 mg/kg/inj). SKF-maintained responding decreased in a dose-related manner, suggesting antagonism of the reinforcing effect. These results suggest that stimulation of D1 receptors can initiate a reinforcing effect and further implicate D1 receptors in the reinforcing effects of drugs that increase dopamine neurotransmission.

Animals↗

Effects of increasing response requirement on choice between cocaine and food in rhesus monkeys.

Rhesus monkeys were trained in a discrete-trials choice procedure and allowed to choose between intravenous injections of cocaine (0.01-1.0 mg/kg/injection) and food presentation (1 or 4 pellets; 1 g/pellet) during daily 7-h experimental sessions. When each reinforcer was available under a fixed-ratio (FR) 30 schedule, the frequency of cocaine choice and the total drug intake increased in a dose-related manner for all monkeys. When the FR for cocaine was differentially increased, the frequency of cocaine choice decreased, shifting the cocaine dose-response function to the right and/or downward. When the FR for cocaine was at least 480, cocaine preference could not be recovered up to doses of 1.0 mg/kg/injection. In a second experiment, when the response requirement for food was differentially increased, the frequency of cocaine choice increased. These results demonstrate that altering the response requirement for cocaine or for alternative reinforcers that are available can substantially affect cocaine self-administration.

Animals↗

Localization and detection of visual stimuli following superior colliculus lesions in rhesus monkeys.

Rhesus monkeys were trained to fixate a central stimulus and to detect and localize a 50 msec light flash presented 6-80 degrees on either side of the central stimulus. Following large lesions of the superior colliculus, they showed persistent deficits in localizing flashes presented 43-80 degrees from the fixation stimulus. However, they were not consistently impaired when the flashes were presented more centrally, and their performance with peripheral stimuli improved when the stimulus duration was 1 sec. Thus, the superior colliculus appears to be necessary for the localization of brief visual stimuli in the far periphery.

Animals↗

Dorsolateral prefrontal cortex lesions and discrimination of movement-produced cues by rhesus monkeys.

Rhesus monkeys were trained on a conditional discrimination in which sequences of either 32 or 64 lever presses served as discriminative stimuli. For half the subjects, reinforcement was contingent upon choice of a red response key following a sequence of 32 presses (FR 32), and a white key after FR 64, with the position of the two key colors randomized across trials. The remaining subjects were reinforced for left key presses after FR 64, and right key presses after FR 32, with key color again randomized across trials. Ablation of dorsolateral prefrontal cortex resulted in postoperative deficits in all subjects, although 6 of 8 eventually remastered the task. This recovery was investigated in a second experiment, in which psychophysical functions were generated by varying the length of the shorter FR. Although dorsolateral lesions again produced a severe disruption in performance, the post-operative functions eventually obtained were identical to the preoperative functions. This pattern of marked impairment in retention of fixed ratio discriminations, but no change in asymptotic capacity, suggests participation of dorsolateral prefrontal cortex in processing kinesthetic information, possibly analogous to the role of inferior temporal cortex in processing visual information.

Animals↗

Central noradrenergic adaptation to long-term treatment with imipramine in rhesus monkeys.

Rhesus monkeys were treated with the antidepressant drug imipramine; cerebrospinal fluid norepinephrine and dopamine-beta-hydroxylase were measured to assess central noradrenergic activity. Large changes occurred after short-term, but not long-term, treatment. Biochemical stabilization occurs at the time when therapeutic effects are seen in patients.

Acclimatization↗

Cortical neural evoked correlates of somatosensory stimulus detection in the rhesus monkey.

Rhesus monkeys were trained to respond to constant-current electrical pulse stimuli to the hand which are known to elicit touch sensation in man. Simultaneously, recordings of somatosensory evoked potentials (SEPs) were made from postcentral gyrus of the performing monkeys. The prominent features of the SEP at most recording sites were a negative (N1) component peaking at 50-65 msec followed by a positive wave (P2) peaking at 105-130 msec. Primary evoked activity (P1) was minimal or absent at most sites at the intensities employed. Differences in N1 peak latency ranging from 4 to 9 msec were observed between the central member of a cluster of recording sites and those surrounding it. These differences are thought to reflect the propagation of evoked activity from some unidentified focus in postcentral gyrus to surrounding regions. N1 and P2 amplitude was found to decrease as a function of behavioral response latency at both the center and surrounding sites of the electrode clusters. The signal detection theoretical model, which provided the interpretative framework for neurophysiologic and psychophysical responses, suggested that N1 and P2 peak amplitude may reflect somatosensory information processing events necessary for psychophysical performance of the monkey. The propagation of evoked activity to different sites on postcentral gyrus could therefore signify the transmission of this sensory information to surrounding cortical regions. Since the psychophysical model is equally applicable to monkey or man, it is suggested that evidence presented here and in similar studies may be relevant to the question of the neural coding of conscious somatic sensory experiences of man.

Animals↗

Discriminative stimulus effects of monohydroxylated phencyclidine metabolites in Rhesus monkeys.

Rhesus monkeys were trained to discriminate saline from an injection of ketamine. In tests of stimulus generalization, phencyclidine (PCP) produced dose-related ketamine-appropriate responding in each monkey. Two monohydroxylated PCP metabolites also produced ketamine-like discriminative effects, although only at considerably higher doses than did PCP. A third monohydroxylated PCP metabolite produced only sham-appropriate responding. The results suggest that these PCP metabolites contribute little to the behavioral actions of PCP in the monkey.

Animals↗

Intermittent naloxone attenuates the development of physical dependence on methadone in rhesus monkeys.

Rhesus monkeys that received 15 daily injections of methadone (2 mg/kg i.m.) exhibited a characteristic opiate withdrawal syndrome after injection of naloxone (0.5 mg/kg i.m.) on the 16th day. In comparison, injection of naloxone (0.5 mg/kg i.m.) once every 2 days during a similar 15 day methadone treatment period in these same monkeys significantly attenuated the severity of the opiate withdrawal syndrome exhibited after naloxone injection on the 16th day. Each naloxone administration during the 15 day methadone treatment period elicited an opiate withdrawal syndrome that did not significantly differ on each of the 7 days it was given and was less severe than the syndrome precipitated by naloxone following 15 days of methadone without intermittent naloxone. The lack of increments in the withdrawal response to the seven naloxone injections during the 15 days of methadone treatment and the attenuation of the withdrawal response to naloxone on day 16 after intermittent naloxone administration during the 15 day methadone treatment period support the hypothesis that naloxone modifies opiate receptor mechanisms so that they revert to an agonist-naive state following antagonist exposure. These findings suggest that various agonist and antagonist opiate drug combinations or mixed agonist-antagonist drug could be clinically useful in the management of situations where physical dependence on opiates is a problem.

Animals↗

Discriminative and aversive properties of beta-carboline-3-carboxylic acid ethyl ester, a benzodiazepine receptor inverse agonist, in rhesus monkeys.

Rhesus monkeys were trained to discriminate injections of saline from those of beta-carboline-3-carboxylic acid ethyl ester (beta-CCE), a compound that binds to the benzodiazepine receptor, but often has actions opposite to those of the benzodiazepines. A benzodiazepine agonist midazolam and low doses of a specific benzodiazepine antagonist, Ro 15-1788, reversed the discriminative effects of beta-CCE. Higher doses of Ro 15-1788 produced stimulus effects similar to beta-CCE. In a separate experiment, monkeys responded to terminate intravenous infusions of beta-CCE, but not midazolam. This aversive effect of beta-CCE was reversed by Ro 15-1788. The behavioral effects of beta-CCE in these non-human primates are consistent with other data that have shown it to act on benzodiazepine receptors, and support the hypothesis that beta-CCE can be considered an inverse agonist at this receptor.

Animals↗