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PubMed2003

Whisking as a "voluntary" response: operant control of whisking parameters and effects of whisker denervation.

The rat's ability to vary its whisking "strategies" to meet the functional demands of a discriminative task suggests that whisking may be characterized as a "voluntary" behavior--an operant--and like other operants, should be modifiable by appropriate manipulations of response-reinforcer contingencies. To test this hypothesis we have used high-resolution, optoelectronic "real-time" recording procedures to monitor the movements of individual whiskers and reinforce specific movement parameters (amplitude, frequency). In one operant paradigm (N = 9) whisks with protractions above a specified amplitude were reinforced (Variable Interval 30 s) in the presence of a tone, but extinguished (EXT) in its absence. In a second paradigm (N = 3), rats were reinforced on two different VI schedules (VI-20s/VI-120s) signaled, respectively, by the presence or absence of the tone. Selective reinforcement of whisking movements maintained the behavior over many weeks of testing and brought it under stimulus and schedule control. Subjects in the first paradigm learned to increase responding in the presence of the tone and inhibit responding in its absence. In the second paradigm, subjects whisked at significantly different rates in the two stimulus conditions. Bilateral deafferentation of the whisker pad did not impair conditioned whisking or disrupt discrimination behavior. Our results confirm the hypothesis that rodent whisking has many of the properties of an operant response. The ability to bring whisking movement parameters under operant control should facilitate electrophysiological and lesion/behavioral studies of this widely used "model" sensorimotor system.

Animals↗
PubMed2000

The uncoupling protein-3 gene is transcribed from tissue-specific promoters in humans but not in rodents.

Uncoupling protein-3 (UCP3), a mitochondrial membrane transporter, is a candidate effector of thermogenesis. Even though mice with targeted disruption of the UCP3 gene are not obese, indirect evidence suggests that this protein contributes to the control of energy expenditure in humans. We therefore characterized the human UCP3 gene and compared it with its rodent homologues with respect to tissue-specific expression and regulatory regions. Like rodent UCP3, human UCP3 was expressed in skeletal muscle and brown adipose tissue (BAT). The short mRNA isoform, UCP3(S), which is absent in rodents, was relatively more abundant in human skeletal muscle in comparison to human BAT. Two tissue-specific transcription start sites for each skeletal muscle and BAT were delineated for human UCP3. Tissue-specific transcript initiation was maintained in both tissues and cultured cells over a wide range of expression levels. In contrast, rodent transcripts were initiated at the same site in BAT and muscle tissue. Comparison of human and rodent promoters indicated a rapid phylogenetic evolution suggesting functional diversification. The transcription from tissue-specific promoters in humans is a novel finding that may provide the basis for therapeutic interventions aimed at regulating energy expenditure in a tissue-specific fashion.

Adipose Tissue, Brown↗
PubMed1996

The Harderian gland: perspectives.

This is the three-hundred and second anniversary of the first description of Harderian glands by Johann Jakob Harder. Despite more than three centuries of study, many features of these glands, including their definition and function, are not yet established to everyone's satisfaction. Some topics of Harderian biology will be reviewed. Morphology, ontogeny: Mammalian Harderian glands secrete largely by exocytosis, which is unusual in a lipid-secreting exocrine gland. Polytubular complexes are features of male hamster glands; their significance is unknown. Porphyrins: High levels of porphyrin in rodent Harderian glands have made this an attractive organ for research on the control of porphyrin synthesis. Attempts to use it as a model of human porphyria, however, have been disappointing. We do not know the function of Harderian porphyrin. The golden (hamster) age: Syrian (golden) hamster Harderian glands show marked sexual differences, including porphyrin levels. This has made them a very useful experimental animal for endocrine studies. The pineal connection: Rodent Harderian glands contain melatonin. Pinealologists often also study Harderian glands, and Harderianologists also often study the pineal. This relationship has contributed valuable insights to our knowledge of both systems. Lipids: Rodent Harderian glands are about 20% lipid by wet weight, and the main secretory product is lipid. The main lipid in many animals is 1-alkyl-2, 3-diacylglycerol. Harderian gland lipid is extensively studied for insights into lipid biochemistry; less has been done on understanding the function of lipids in the physiology of the glands. Behavior: Lipids may function as vehicles for pheromone secretion. In addition, the possible use of Harderian secretion during cold temperatures by gerbils has been noted. Immunology: Bird Harderian glands are probably lymphoid organs. This does not seem to be true of mammals, though the female Syrian hamster shows large numbers of mast cells. Harderian glands of amphibians and reptiles: Research on nonmammalian Harderian glands has been limited, though important insights continue to emerge from these studies.

Amphibians↗
PubMed1992

Induction of peroxisomes by treatment with perfluorooctanoate does not increase rates of H2O2 production in intact liver.

Increases in acyl coenzyme A (CoA) oxidase activity due to peroxisome proliferation are postulated to cause oxidative stress via elevated production of H2O2, leading to DNA damage. These changes are suspected to be responsible for tumor formation caused by non-genotoxic carcinogens which do not bind to DNA but cause proliferation of peroxisomes. However, the activity of the peroxisomal enzyme acyl CoA oxidase assayed in vitro in the presence of excess fatty acyl CoA substrate may not reflect rates of H2O2 generation in intact liver where fatty acid supply is carefully controlled in part by delivery of substrate. The purpose of this work was to determine if rates of hepatic H2O2 generation were altered in perfused liver and in vivo following induction of H2O2-generating acyl CoA oxidase activity. Injection of the potent peroxisome proliferating agent perfluorooctanoate into rats 5 days prior to sacrifice caused an expected 4-fold increase of H2O2-generating acyl CoA oxidase activity measured in hepatic homogenates. In contrast, rates of H2O2 generation in perfused liver measured spectrophotometrically (660-640 nm) through a lobe of the liver were not altered by perfluorooctanoate treatment (7.3 +/- 1.5 vs. 7.8 +/- 0.5 mumol/g/h in livers from untreated control rats). Similar treatment with perfluorooctanoate also increased in vitro acyl CoA oxidase activity 9-fold in livers from deermice; however, rates of elimination of methanol, a selective substrate for catalase in rodents whose oxidation is limited by the supply of H2O2, were not altered significantly in vivo (control, 110 +/- 11 mumol/g/h vs. perfluorooctanoate, 112 +/- 32 mumol/g/h). Taken together, these data demonstrate that elevation of H2O2 formation by acyl CoA oxidase activity measured in vitro is not necessarily associated with increases in rates of H2O2 generation in intact perfused liver or in vivo, most likely due to rate-limitation in intact cells by fatty acid supply. These data do not support the hypothesis that the induction of peroxisomes leads to excessive H2O2 production and oxidative stress. It follows that alternative hypotheses to explain carcinogenesis caused by peroxisome-proliferating agents need to be considered.

Animals↗
PubMed1997

Effect of basic fibroblast growth factor on perforated chinchilla tympanic membranes.

Basic fibroblast growth factor (bFGF) is a polypeptide mitogen which stimulates proliferation of epidermal and connective tissue cells. When applied to tympanic membrane perforations it has been reported to enhance healing and produce connective tissue hyperplasia. Previous work with animal models has shown that hyperplastic alterations of the tympanic membrane play an essential role in cholesteatoma development. This study was designed to further investigate the hyperplastic effects of bFGF and to determine if it might induce cholesteatoma formation during the healing process. Ten chinchillas received bilateral tympanic membrane perforations. In each animal, three doses of bFGF (400 nanograms per dose) were applied to the perforated tympanic membrane on one side; the opposite (control) ear received saline alone. The animals were terminated at either two or four weeks and studied histologically. Although the dosage and administration schedule used were consistent with previous studies utilizing other rodent species, there was little evidence that bFGF affected tympanic membrane healing in chinchillas. In both control and bFGF-treated ears, dense connective tissue occupied the lamina propria of the tympanic membrane, providing an effective barrier against ingrowth of skin toward the middle ear. No cholesteatomas developed in any animals included in the study. The results of this work indicate that the risk of cholesteatoma formation following administration of bFGF is minimal when it is applied short-term to acute perforations.

Animals↗
PubMed2003

Patterns of functional activity associated with cocaine self-administration in the rat change over time.

RATIONALE: Although imaging studies in human addicts have been valuable for identifying the neural substrates of the effects of abused drugs, few studies have used this approach in animal models where conditions can be carefully controlled. OBJECTIVE: To define the substrates that mediate the effects of cocaine in a rodent model of cocaine self-administration using the 2-[(14)C]deoxyglucose method and to assess changes in these patterns over the course of drug exposure. METHODS: Male Sprague-Dawley rats self-administered cocaine (0.75 mg/kg per injection; FR2; 21 injections/session) and control rats received saline infusions in the same pattern as the cocaine rats for 5 or 30 days. Metabolic mapping was applied immediately after the final session. RESULTS: Following 5 days of self-administration, rates of glucose utilization were decreased in the nucleus accumbens, and increased in autonomic brainstem structures and in sensorimotor regions. After 30 days of cocaine exposure, self-administration reduced glucose utilization throughout the dorsal and ventral striatum, central nucleus of the amygdala, medial forebrain bundle, and infralimbic and prelimbic prefrontal cortices. In addition, at this time point glucose utilization was no longer elevated in any autonomic or sensorimotor brain regions. CONCLUSIONS: These data demonstrate that the distribution of functional activity associated with self-administered cocaine undergoes considerable change over the course of drug exposure. While increases in metabolic rates were largely found in autonomic and sensorimotor structures after short-term cocaine access, decreases were prominent in mesocorticolimbic regions after prolonged exposure. These differences in the patterns of brain activity that develop with long-term cocaine self-administration may play a role in the transition to habitual drug seeking behavior.

Animals↗
PubMed1999

Linkage analysis of candidate obesity genes among the Mexican-American population of Starr County, Texas.

Recent advances in the molecular basis of body fat regulation have identified several genes in which genetic variation may influence obesity and related measures in human populations. Genes that have been shown to have a regulatory function in the control of body fat utilization, eating behavior, and/or metabolic rate in rodent models of obesity include leptin (LEP), leptin receptor (LEPR), neuropeptide Y (NPY), NPY Y1 receptor (NPYY1), glucagon-like peptide-1 (GLP-1), GLP-1 receptor (GLP1R), and uncoupling protein 1 (UCP1). We have typed microsatellite markers located within or near these seven candidate obesity genes in 302 non-diabetic individuals from 59 Mexican-American families from Starr County, Texas. Sib pair linkage analysis was used to examine linkage between these genes and obesity status (obese siblings only; n = 170 pairs) and several obesity-related quantitative variables (all siblings; n = 545 total sibling pairs). Significant linkage (P = 0.042) was found between obesity and NPY within the obese sibling pairs. No other candidate gene was linked to obesity status in this subsample. Consistent with the obese sib pair linkage results, NPY showed evidence of linkage to body weight (P = 0.020), abdominal circumference (P = 0.031), hip circumference (P = 0.012), diastolic blood pressure (P = 0.005), and a composite measure of body mass and size (P = 0.048) in the entire sibling sample. Other significant linkages observed were between LEP and waist/hip ratio (P = 0.010), total cholesterol (P = 0.030), and HDL cholesterol (P = 0.026) and between LEPR and fasting blood glucose (P = 0.018) and diastolic blood pressure (P = 0.003). These results support further investigation of NPY, LEP, and LEPR to identify genetic variation that may influence obesity status, glucose and lipid metabolism, and blood pressure in Mexican Americans.

Adult↗
PubMedDate not supplied

Early markers of ventilator-induced lung injury in rats.

Positive pressure ventilation with hyperdistention of the lungs (PPVHDL) causes microscopic lung injury in rats and in mice. This study compared lung lavage and serum levels of lactate dehydrogenase (LDH), aspartate aminotransferase (AST), creatinine phosphokinase (CPK), lung lavage and plasma endothelin-1 (ET-1) concentration, lung tissue ET-1 mRNA expression, angiotensin converting enzyme (ACE) activity of lung homogenates, and histology of the lung structure in control and PPVHDL rats. Rats were anesthetized with pentobarbital. While control rats were breathing spontaneously, the PPVHDL rats were ventilated with a rodent ventilator delivering 30 percent oxygen, a tidal volume of 18.6 +/- 4.5 ml/kg, and a respiratory rate of 55 to 60 per minute. End-tidal CO2 was maintained at 38-40 mm Hg. After seven hours, rats were killed and the lungs were lavaged. Red blood cells were present in the sediment of lavage fluid in PPVHDL rats and their lung structure showed severe congestion, alveolar septa filled with red cells, and extravasation of red blood cells and inflammatory cells into the alveolar space. Lung lavage fluid AST and LDH were significantly higher in the PPVHDL compared with the control group (P < 0.03 and P < 0.001, respectively). Electrophoresis of the lung lavage LDH showed increased peak-5 in the PPVHDL group. Serum LDH, CPK, AST, and potassium concentrations [K]+ were significantly higher in the PPVHDL rats whereas their serum total protein level was significantly lower than the control group (P < 0.001). Electrophoretic patterns of serum and lung lavage protein were similar in both groups indicating a transmural passage of serum protein from the intravascular to the intra-alveolar space. No significant difference was found in lung tissue ET-1 mRNA expression and lung protein concentration between the two groups. Lung ACE activity, in contrast, was significantly lower in PPVHDL rats. This study demonstrated that moderate alveolar hyperdistention caused significant structural lung damage accompanied by decreased ACE activity after seven hours of mechanical ventilation and that elevated lung lavage and serum LDH and AST levels in lung lavage and in serum might be early markers of ventilator-induced lung injury in this rat model.

Animals↗
PubMed1992

Age-related alterations in gonadotropin, adrenocorticotropin and growth hormone secretion.

This review addresses some relevant aspects of the aging of the neuroendocrine system, particularly the reproductive and the adrenocortical axis. Deterioration of the reproductive function, one of the most striking endocrine alterations occurring in aging, is related to a complex interplay of factors. They comprise alterations occurring at the level of all the three components of the reproductive axis, the gonads, the pituitary and the brain, acting synergistically to disrupt the normal pulsatile release of gonadotropins. Particular relevance is given to the neurotoxic action of estrogens during the constant estrous phase occurring in aged female rodents, at the level of hypothalamic nuclei regulating gonadotropin secretion. This effect, to be found also in women during the anovulatory period of the perimenopause, would worsen the dysregulation of the central mechanisms controlling the reproductive function. The activity of the adrenocortical (HPA) axis increases with advancing age in rodents but also, although less strikingly, in humans. The main alteration which can be evidenced in both species is a delayed post-stimulus decline in plasma corticosteroid levels, indicating a diminished sensitivity to glucocorticoids of HPA axis feedback regulation in the elderly. Increased exposure to the highly catabolic adrenal glucocorticoids appears to be associated to a loss of cerebral neurons, particularly in the hippocampus, and the emergence of cognitive deficits in the aged rats. The relevance of experimental data performed in rodents to healthy and pathological human aging is extensively discussed. Finally, this chapter considers the age-related impairment in growth hormone secretion, a common finding of all the animal species investigated so far. The etiology of the hyposomatotropism of aging is namely linked to a progressive defect in growth hormone releasing hormone-producing hypothalamic neurons, although alterations of somatostatin-producing neurons have also been described. This background knowledge makes the use of neuroactive compounds aimed at restoring the physiologic function of hypothalamic hypophysiotropic hormones a rational approach to rectify the alterations of the neuroendocrine system occurring in elderly individuals.

Adrenocorticotropic Hormone↗
PubMed1998

Cloning experiments and developmental expression of both melatonin receptor Mel1A mRNA and melatonin binding sites in the Syrian hamster suprachiasmatic nuclei.

The suprachiasmatic nuclei (SCN) are implicated in the control of circadian biological rhythms, and especially the melatonin nocturnal synthesis. In numerous rodents, melatonin has been shown to feed back on the SCN activity through high affinity receptors. In contrast, Syrian hamster SCN activity is unresponsive to melatonin injections. As this lack of effect could be linked to a developmental loss of SCN melatonin receptors, the goals of the present study were 1) to report in Syrian hamster SCN, and pars tuberalis (PT) as a control, a complete pattern of the postnatal (PN) development of the melatonin receptor density and 2) to investigate whether the regulation of the Mel1a mRNA expression could be implicated in the post natal variations of the melatonin binding capacities. We first subcloned by PCR a partial cDNA encoding the Mel1a receptor from Syrian hamster SCN. Subsequent quantification of Mel1a mRNA expression and melatonin receptor density revealed that in the PT and SCN, both Mel1a mRNA expression and melatonin binding capacities declined abruptly between PN 0 and PN 8. Afterwards, in the PT, both parameters went up until they got stabilized in adulthood. Therefore, in the PT, post natal melatonin receptor density variations were highly correlated with post natal variations of the Mel1a mRNA expression. In the SCN, after PN 8, the melatonin receptor density followed its drop and then declined by more than 92% between post natal day 0 (PN 0) and PN 60 (12.11+/-0. 27 vs. 0.94+/-0.08 fmol/mg protein at PN 0 and PN 60 respectively). In contrast, Mel1a mRNA expression only slightly went down after PN 8 and got stabilized in adult age at 42% of the birth day expression level. These results show that Syrian hamster SCN undergo a dramatic post natal loss of their melatonin receptors that could explain the lack of effect of melatonin injections on SCN circadian activity. Furthermore, this SCN binding capacities decline could not be attributed to an inhibition of the mRNA expression, but rather to a post transcriptional blockade of the Mel1a receptor expression.

Aging↗
PubMed1985

Conservation from rat to human of cytosolic phosphoenolpyruvate carboxykinase and the control of its gene expression.

Structural conservation of cytosolic phosphoenolpyruvate carboxykinase protein and mRNA sequence was found in all species examined from rodents to human. The mitochondrial isoenzyme, in all species tested, represents a distinct protein. Moreover, irrespective of the ratio of cytosolic to mitochondrial isoenzyme, cytosolic phosphoenolpyruvate carboxykinase activity in the human as in the rat is controlled at the level of gene expression and through the same multiple hormonal stimulation. This evolutionary conservation of the cytosolic phosphoenolpyruvate carboxykinase structure and mode of regulation supports the enzymes' physiological importance in mammals.

Animals↗
PubMed1991

Bypassing the Saccadic Pulse Generator: Possible Control of Head Movement Trajectory by Rat Superior Colliculus.

Saccades produced by electrical stimulation of the superior colliculus in primates are influenced primarily by the location of the stimulating electrode, with the suprathreshold intensity or frequency of the stimulating pulse train having little effect. Any given collicular site produces a characteristic movement of relatively fixed amplitude and velocity. In accordance with this finding, in models of the saccadic eye movement system the superior colliculus specifies the change of eye position: the velocity of movement components are determined by 'pulse generators' located between the superior colliculus and the oculomotor neurons. Previous findings in rodents, however, have suggested that eye and head movements induced by stimulation at some collicular sites may be critically dependent on stimulation parameters, implying that in these animals the superior colliculus has access to a non-saccadic control system. To investigate this possibility, rats with electrodes implanted into the lateral intermediate layers were stimulated with pulse trains of varying frequency and duration, and the resultant head movements analysed from video tape. At seven of the nine sites studied, amplitude of the horizontal component of the head movement was linearly related to stimulating frequency for fixed-duration trains, in some cases over a ten-fold range. Subsequent variation of train duration showed that amplitude was affected not by frequency as such, but by the number of pulses in the train; frequency was related to the mean velocity of the movement. By appropriate setting of these parameters, independent control of head movement amplitude and velocity could be achieved. These results suggest that the rodent superior colliculus may be able to control head movement without recourse to a pulse generator, and thus influence the trajectory of the movement directly. If so, it may prove to be a useful preparation for testing theories of trajectory formation.

Journal Article↗
PubMed2000

[An anesthesia technique for experimental studies and microsurgical ear interventions in newborn rodents].

BACKGROUND: Experimental investigations on laboratory animals usually require sufficient anesthesia with adequate analgesia and sedation. The technique used should be reliable and easily controllable by the investigator. Here, we present a technique for anesthesia to facilitate invasive and noninvasive investigations in newborn rats and mice. METHODS: Using a custom made breathing mask, anesthesia was induced in these animals with inhalation of gaseous nitrous oxide-oxygen (equal volume at 1 l/min) and halothane (3% by volume). To maintain anesthesia, halothane insufflation was reduced to 1-1.5% by volume. After completion of the experimental procedure, the application of the inhalative gases was determined and substituted by oxygen at 2 l/min. Anesthesia was performed in spontaneously breathing animals. Heart frequency and oxygenation were monitored using a commercially available pulse oximeter. RESULTS: Using the above described technique in neonatal rodents, microsurgery of the ear was performed without signs of pain or major bleeding. Auditory brain stem responses were recorded clearly and reproducible. CONCLUSIONS: This method represents a noninvasive, well tolerated and easy controllable anesthetic procedure which has proven to provide a sufficient and reliable sedation in neonatal rodents for surgical and nonsurgical investigations.

Anesthesia, Inhalation↗
PubMed1991

Evidence that the relative densities of afferents from both eyes control laminar distribution and binocular segregation of retinotectal projections in rats.

In the superior colliculus of normal rodents the crossed retinal projection overlaps the uncrossed projection. The present study describes an abnormal laminar distribution and binocular segregation of the retinotectal afferents induced after the experimental enlargement of the uncrossed retinotectal pathway in pigmented rats. Intraocular injections of anterograde tracers were used to investigate the topographic and laminar organization of retinotectal projections in adult rats given unilateral optic tract lesions at birth. These lesions are known to increase the number of ipsilaterally projecting ganglion cells in the opposite retina. The uncrossed retinal projection to the remaining superior colliculus forms an abnormal band of terminal labeling at the superficial half of the stratum griseum superficiale, markedly different from the laminar distribution of this pathway in unoperated controls. This abnormal uncrossed projection has its maximum density at the rostrolateral quadrant of the tectum. Within this region, the crossed retinotectal projection retracts from the surface of the superior colliculus, leading to partial binocular segregation. The results suggest that both the laminar distribution and the experimental binocular segregation of retinotectal afferents depend on the balance of the densities of the converging pathways from both eyes in the superior colliculus.

Animals↗
PubMed2000

A double dissociation between the rat hippocampus and medial caudoputamen in processing two forms of knowledge.

Rats with hippocampus, medial caudoputamen (CPU), lateral CPU, or control lesions were trained on declarative and procedural knowledge variants of a novel rodent sequential learning task. Medial CPU lesions impaired rats' ability to learn the procedure of running through a sequence of open maze arms but did not disrupt their capacity to explicitly generate (i.e.. "declare") maze arm sequences. Hippocampus lesions produced the opposite set of results. Rats with lateral CPU lesions were not impaired on either version of the task. Transfer tests indicated that control rats predominantly used egocentric cues to solve the procedural task and allocentric spatial cues to solve the declarative task. These findings suggest a double dissociation between the medial CPU and hippocampus in processing egocentric-procedural and allocentric-declarative sequential information, respectively.

Animals↗