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PubMed1994

Opposite responses of mesolimbic dopamine system to controllable and uncontrollable aversive experiences.

It has been previously shown that rodents exposed to stressful experiences show a biphasic response of the mesolimbic dopamine (DA) system, that is, initial increase of DA release followed by a decrease below control levels (Puglisi-Allegra et al., 1991). Evidence is now presented showing that mice exposed to a series of foot shocks show an increase of DA release in the nucleus accumbens septi (NAS) if they are allowed to control the shock experience (shocked condition) and a decrease of DA release in this brain area if they are not allowed to exert any control (yoked condition). These results indicate that escapable/controllable and inescapable/uncontrollable aversive experiences elicit opposite responses from the mesolimbic DA system. Mice exposed to the apparatus without receiving shock (sham condition) show a time-dependent biphasic evolution mesolimbic DA release in line with previous reports indicating that confinement in an unknown environment represents a stressful experience for mice. Moreover, exposure to the sham condition for a time comparable to the duration of shock and yoked exposure induces a mesolimbic DA response only quantitatively different from the response of the yoked group but qualitatively different from the response of the shocked mice. These results suggest that in environmental conditions that allow behavioral control, enhanced mesolimbic DA release is maintained regardless of the intensity of the aversive stimuli. On the other hand, evaluation of changes in acid DA metabolites levels in the frontal cortex (FC) of mice exposed to the shocked, yoked, and sham conditions suggests that stressful experiences characterized by a different intensity of the aversive stimuli could elicit graded responses in the FC DA system.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

PubMed1987

Somatostatin release from dispersed hypothalamic cells: effects of diabetes.

We examined the release of growth hormone-release inhibiting factor (somatostatin) from dispersed hypothalamic cells obtained from mature diabetic rodents and normal age-matched controls, in an attempt to demonstrate a possible hypothalamic defect which might underlie some of the reported abnormalities in somatotrophic function in diabetes mellitus. Insulinopoenic diabetes was induced by either streptozotocin or alloxan. Somatostatin release from cells from diabetic rats was diminished both basally and after stimulation by membrane depolarisation. Stimulated release was calcium dependent in cells from both normal and diabetic animals. The defect was present in both streptozotocin and alloxan induced diabetes. We also compared hypothalamic somatostatin release from cells obtained from obese hyperinsulinaemic C57 BL/Ks db/db diabetic mice and non diabetic lean litter mates (db/-). Despite longstanding marked hyperglycaemia, no significant alteration in somatostatin release was apparent. Likewise, starvation of rats for 5 days did not result in significant diminution of somatostatin release. These observations document a defect in hypothalamic somatostatin release in experimentally induced insulinopoenic diabetes, which is not apparent in the db/db mouse, suggesting that glucose per se is not responsible. Rather than the anticipated increase in hypothalamic somatostatin release in insulinopoenic diabetes, a reduction in release was observed. These observations are compatible with the hypothesis that increased hypothalamic somatostatin release is not responsible for abnormal growth hormone secretion in this model.

Animals↗

PubMed1999

Impulsivity resulting from frontostriatal dysfunction in drug abuse: implications for the control of behavior by reward-related stimuli.

Drug abuse and dependence define behavioral states involving increased allocation of behavior towards drug seeking and taking at the expense of more appropriate behavioral patterns. As such, addiction can be viewed as increased control of behavior by the desired drug (due to its unconditioned, rewarding properties). It is also clear that drug-associated (conditioned) stimuli acquire heightened abilities to control behaviors. These phenomena have been linked with dopamine function within the ventral striatum and amygdala and have been described specifically in terms of motivational and incentive learning processes. New data are emerging that suggest that regions of the frontal cortex involved in inhibitory response control are directly affected by long-term exposure to drugs of abuse. The result of chronic drug use may be frontal cortical cognitive dysfunction, resulting in an inability to inhibit inappropriate unconditioned or conditioned responses elicited by drugs, by related stimuli or by internal drive states. Drug-seeking behavior may thus be due to two related phenomena: (1) augmented incentive motivational qualities of the drug and associated stimuli (due to limbic/amygdalar dysfunction) and (2) impaired inhibitory control (due to frontal cortical dysfunction). In this review, we consider the neuro-anatomical and neurochemical substrates subserving inhibitory control and motivational processes in the rodent and primate brain and their putative impact on drug seeking. The evidence for cognitive impulsivity in drug abuse associated with dysfunction of the frontostriatal system will be discussed, and an integrative hypothesis for compulsive reward-seeking in drug abuse will be presented.

Animals↗

PubMed2000

Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury.

A characteristic feature of severe diffuse axonal injury in man is radiological evidence of the "shearing injury triad" represented by lesions, sometimes haemorrhagic, in the corpus callosum, deep white matter and the rostral brain stem. With the exception of studies carried out on the non-human primate, such lesions have not been replicated to date in the multiple and diverse rodent laboratory models of traumatic brain injury. The present report describes tissue tears in the white matter, particularly in the fimbria of Sprague-Dawley rats killed 12, 24, and 48 h and 7 days after lateral fluid percussion brain injury of moderate severity (2.1-2.4 atm). The lesions were most easily seen at 24 h when they appeared as foci of tissue rarefaction in which there were a few polymorphonuclear leucocytes. At the margins of these lesions, large amounts of accumulated amyloid precursor protein (APP) were found in axonal swellings and bulbs. By 1 week post-injury, there was macrophage infiltration with marked astrocytosis and early scar formation. This lesion is considered to be due to severe deformation of white matter and this is the first time that it has been identified reproducibly in a rodent model of head injury under controlled conditions.

Amyloid beta-Protein Precursor↗

PubMed1976

Neural control of blood flow in gastric mucosa.

The innervation of the small vessels in the fundic mucosa of the rat and the effects of vagotomy on this innervation were studied ultrastructurally. The capillaries and arterioles, but not the venules, were found to receive direct innervation. Vagotomy causes degeneration of the nerve endings that innervate these vessels, confirming their vagal origin. This finding, and the fact that some morphologic changes in the capillaries were observed after vagotomy, provides morphologic evidence for the neural control of blood flow in the rodent gastric mucosa.

Animals↗

PubMed1990

Transforming growth factor-alpha messenger RNA localization in the developing adult rat and human mammary gland by in situ hybridization.

Transforming growth factor-alpha (TGF alpha) has been implicated in the autocrine growth control of a number of different rodent and human tumor cells, including breast cancer cells. Although TGF alpha has been detected in a limited number of normal tissues, its distribution and physiological function in the mammary gland are relatively unknown. TGF alpha mRNA expression was detected by in situ hybridization with a labeled TGF alpha antisense RNA probe and quantitated by application of computer-assisted digital image processing in both the ductal and alveolar epithelial cells in the virgin rat and nulliparous and parous human mammary glands. During pregnancy and lactation, the level of TGF alpha mRNA expression in the ductal and alveolar epithelial cells increased two- to threefold, while a heterogeneous yet strong expression of TGF alpha mRNA could also be detected in approximately 10-15% of the surrounding stromal cells in the pregnant mammary gland.

Animals↗

PubMed1994

Neonatal infraorbital nerve damage and the development of eating behavior in the rat.

It has been previously shown that bilateral infraorbital nerve (ION) transection in adult rats has little effect upon body weight regulation or eating behavior. However, in neonatal mouse, unilateral ION cut produces a profound decrease in body weight, beginning around the time of weaning. To help clarify the role of the ION in the development and sensorimotor control of eating solid food in rodents, the present experiment examined the effects of unilateral, neonatal ION transection in rats, upon body weight regulation and post-weaning eating behaviors. Comparison of normal and lesioned groups of rats, up to postnatal day (PND) 61, revealed no significant difference in mean adjusted (for sex) body weight. In addition, no significant differences were detected between the groups on post-weaning (PND 26 to PND 61) measures of mean adjusted (for weight) food intake, responsiveness to food, biting ability or inefficiency of mandibulation. At the end of the experiment, the effectiveness of the lesion was histologically evaluated. A significant 48.5% mean reduction in the cross-sectional area of the ophthalmic-maxillary portion of the trigeminal ganglion was observed on the lesioned side, relative to the intact side. There appears to be a differential influence of unilateral, neonatal ION cut upon eating in rat and mouse.

Afferent Pathways↗

PubMed1996

An endpoint, descriptive, and kinematic comparison of skilled reaching in mice (Mus musculus) with rats (Rattus norvegicus).

The forelimb and paw movements of mice were compared with those of rats in two skilled reaching for food tasks. Both species could use a single forelimb to reach for food, as measured in two different tasks, although performance was better and more consistent in rats than in mice. Both species located the food using olfaction, and moved from a diagonal supporting pattern in which support and postural adjustments came mainly from the contralateral to reaching forelimb and the ipsilateral to reaching hindlimb. Forelimb movements in both species could be divided into 3 components: (1) a transport component in which the limb is lifted, aimed, advanced, and pronated over the food using mainly movements of the upper limb; (2) a manipulatory component in which the digits are pronated over the food in an arpeggio movement and in which the digits grasp the food using grips that are scaled to the size of the food; and (3) a withdrawal component, in which the paw is supinated by adduction by the upper arm and by a movement about the wrist, as the food is withdrawn and presented to the mouth. Kinematic measures showed that the initial velocity of reaching in mice was slower than for rats, but otherwise the shape of the velocity curve and the trajectory of the limb movement, above and beyond the food pellet, were similar in both species. The results suggest that the motor control of reaching in the two rodent species is almost the same despite an evolutionary divergence that occurred about 20 million years ago. This profile of movement could be useful for investigating motor systems in normal mice and it could be applied to the analysis of motor systems in mutant and transgenic mice suspected of having motor abnormalities.

Animals↗

PubMed1993

Selected immune responses of adult cotton rats (Sigmodon hispidus) to dietary restriction.

1. We examined the influence of moderate to severe dietary restriction on immune system function in adult cotton rats. Animals (N = 80) were fed ad lib. (controls) or restricted [moderate = 80% ad lib. for 1 or 2 weeks; severe = 80% ad lib. for 1 or 2 weeks followed by 40% ad lib. for one (week 3) or two (week 4) additional weeks] amounts of food for 1-4 weeks. 2. Average body weight loss for severely restricted animals in week 4 was 17%; dietary treatments had no measurable effect on hematological parameters (hematocrit, white blood cell count), lymphoid organ weights (thymus gland, spleen, popliteal lymph nodes), and mononuclear cell yields from lymphoid organs. 3. Cell-mediated immune function was assessed in vitro by a lymphoproliferative response assay and in vivo by a delayed-type hypersensitivity response assay. 4. Proliferative responses of spleen cell cultures stimulated with concanavalin A (Con A, Canavalia ensiformis) and pokeweed (PWM, Phytolacca americana) were normal or significantly greater among moderately restricted than control cotton rats during week 1 and week 2. 5. Lymphoproliferative responses of severely restricted animals were normal or reduced during week 3 and week 4. 6. Delayed-type hypersensitivity responses to the contact antigen oxazolone were significantly depressed among severely restricted animals in week 4 compared to controls. 7. In comparison with laboratory rodent strains, our initial results indicate that immune system function in adult cotton rats is not as sensitive to short term (1-4 weeks) periods of dietary restriction. 8. Immune system function was related to changes in body weight as a result of feed restriction.

Animals↗

PubMed2000

Differential regulation of CD8+ T cell senescence in mice and men.

The cytotoxic CD8+ T cell population expands considerably during acute immune infection with virus. Most of these cells are removed by apoptosis at the end of the immune response. However, a balance has to be attained between clearance and retention of a memory population of cells, which respond more rapidly and efficiently to secondary encounter with the antigen. In this article, the role of apoptosis and in particular the development of replicative senescence as mechanisms which control this homeostatic balance are discussed. Although similar mechanisms regulate apoptosis in both humans and rodents, the available data suggests that replicative senescence may be controlled differently in these species, suggesting the there may be different constraints in the regulation of CD8+ T cell memory between different species.

Acute Disease↗

PubMed2001

A review of mechanisms controlling ovulation with implications for the anovulatory effects of polychlorinated dibenzo-p-dioxins in rodents.

Polychlorinated dibenzo-p-dioxins (PCDDs) can impinge on female fertility by preventing ovulation. In this review, the aspects of normal ovulatory physiology most relevant to our current understanding of PCDD action on the ovary are briefly reviewed. This is followed by a comprehensive assessment of data relevant to the effects of PCDDs during ovulation in the rat. PCDDs interrupt ovulation through direct effects on the ovary in combination with dysfunction of the hypothalamo-hypophyseal axis.

Animals↗

PubMed2002

Network and pharmacological mechanisms leading to epileptiform synchronization in the limbic system in vitro.

Seizures in patients presenting with mesial temporal lobe epilepsy result from the interaction among neuronal networks in limbic structures such as the hippocampus, amygdala and entorhinal cortex. Mesial temporal lobe epilepsy, one of the most common forms of partial epilepsy in adulthood, is generally accompanied by a pattern of brain damage known as mesial temporal sclerosis. Limbic seizures can be mimicked in vitro using preparations of combined hippocampus-entorhinal cortex slices perfused with artificial cerebrospinal fluid containing convulsants or nominally zero Mg(2+), in order to produce epileptiform synchronization. Here, we summarize experimental evidence obtained in such slices from rodents. These data indicate that in control animals: (i) prolonged, NMDA receptor-dependent epileptiform discharges, resembling electrographic limbic seizures, originate in the entorhinal cortex from where they propagate to the hippocampus via the perforant path-dentate gyrus route; (ii) the initiation and maintenance of these ictal discharges is paradoxically contributed by GABA (mainly type A) receptor-mediated mechanisms; and (iii) CA3 outputs, which relay a continuous pattern of interictal discharge at approximately 1Hz, control rather than sustain ictal discharge generation in entorhinal cortex. Recent work indicates that such a control is weakened in the pilocarpine model of epilepsy (presumably as a result of CA3 cell damage). In addition, in these experiments electrographic seizure activity spreads directly to the CA1-subiculum regions through the temporoammonic pathway. Studies reviewed here indicate that these changes in network interactions, along with other mechanisms of synaptic plasticity (e.g. axonal sprouting, decreased activation of interneurons, upregulation of bursting neurons) can confer to the epileptic, damaged limbic system, the ability to produce recurrent limbic seizures as seen in patients with mesial temporal lobe epilepsy.

4-Aminopyridine↗

PubMed2000

Inhibition of leptin secretion by insulin and metformin in cultured rat adipose tissue.

Leptin's role in the regulation of food intake, energy expenditure and weight control are widely recognized, especially in rodents. Likewise, the potential regulation of leptin secretion by insulin (and vice versa) has been of particular interest insofar as these nutrient signals may have meaningful, even adverse (inter)actions, in diabetes. We used a freshly isolated rat adipose tissue culture model to examine the effect of insulin, metformin and glibenclamide on basal and steroid-stimulated leptin secretion. This model was selected because of its physiologic rates of leptin formation and preservation of potentially significant cell-cell interactions compared to isolated cells. The basal rate of leptin secretion was 3. 4+/-1.2 ng/100 mg tissue/24 h. The addition of 100 nM dexamethasone or 400 nM hydrocortisone stimulated leptin secretion by 3-4 fold over basal (no steroid). Insulin inhibited both basal and steroid-activated leptin secretion by 35-50%. This inhibition was present with either 1 mM pyruvate or 5 mM glucose as a substrate suggesting that glycolysis was not required. Metformin inhibited basal and dexamethasone-stimulated leptin secretion in a dose dependent manner (50% inhibition occurred at 1 mM metformin) while glibenclamide was ineffective. The effect of insulin on isolated fat cells versus fat tissue was tested in parallel. After 24 h in culture, insulin inhibited leptin secretion similarly in both adipose preparations. The addition of 200 nM (-)N6-(2-phenylisopropyl)-adenosine did not alter the results.

Adipose Tissue↗

PubMed1977

Myxomatosis: the transmission of a highly virulent strain of myxoma virus by the European rabbit flea Sphilopsyllus cuniculi (Dale) in the Mallee region of Victoria.

The European rabbit flea Spilopsyllus cuniculi (Daley was introduced into Australia to act as a vector of myxoma virus. It was first released in the semi-arid Mallee region of Victoria in 1970 where epizootics cuased by field strains of myxoma virus occur each summer. Introductions of the readily identified Lausanne strain were made annually following the release of the flea. The introductions were successful and the strain persisted for up to 16 weeks despite competition from field strains. The Lausanne strain is more readily spread by fleas than the Glenfield strain which has been widely used in rabbit control. The ability of the Lausanne strain to persist and its effective transmission compared with the Glenfield strain may be due in part to the more florid symptoms of the disease.

Animals↗

PubMed1977

Innate resistance to myxomatosis in wild rabbits in England.

Wild rabbits (Oryctolagus cuniculus) from one study area in England have been used over a period of 11 years to investigate the possible appearance of innate resistance to myxomatosis. Rabbits of 4-6 weeks old were captured alive, retained in the laboratory until at least 4 months old, and then infected with a type of myxoma virus which kills 90-95% of laboratory rabbits. Observations were made of symptoms, mortality rate and survival times.In the first 4 years of the study (1966-9), mortality rates were not significantly different from those of laboratory rabbits, although survival times of wild rabbits were appreciably longer. In 1970, the mortality rate amongst wild rabbits was 59%, in 1974 it was 17%, and in 1976 it was 20%, thus showing that a considerable degree of inherited resistance to myxomatosis has developed.The types of myxoma virus most commonly isolated from wild rabbits in Great Britain in recent years have been those which cause 70-95% mortality in laboratory rabbits. Therefore, if the degree of innate resistance demonstrated is widespread in Great Britain, there are serious implications regarding the size of the rabbit population, because myxomatosis has been an important factor in holding rabbit numbers at a relatively low level.

Animals↗

PubMed1999

Lung injury following pulmonary resection in the isolated, blood-perfused rat lung.

Lung resection may be complicated by postpneumonectomy pulmonary oedema. Oxidant generation following surgery-induced ischaemia-reperfusion may be responsible. This hypothesis was tested utilizing isolated, in situ, blood perfused rodent lungs subjected to continuous perfusion (control subjects); one lung ventilation followed by pneumonectomy (group 1); or one lung ventilation followed by reinflation of the collapsed lung (group 2). In control subjects, no significant changes in markers of oxidant damage, oxygenation, pulmonary artery pressure or extravascular albumin extravasation were detected. In group 1 lungs, hydroxyl radical-like damage was detected in association with impaired oxygenation (p<0.05), and increased pulmonary artery pressure and extravascular albumin accumulation in both lungs. In group 2, there was evidence of hydroxyl radical-like damage, and a fall in oxygenation (p<0.05) occurred during one lung ventilation. There was a transient rise in pulmonary artery pressure following lung reinflation and extra vascular albumin accumulation was significantly increased in both lungs (right>left, p<0.05). Both changes were attenuated (p<0.05) following treatment with the reactive oxygen species (ROS) scavenger superoxide dismutase (group 2a) and the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (group 2b). Hydroxyl radical-like damage was undetectable following nitric oxide synthase inhibition. Oxidant stress may contribute to the pathologies seen in this model of lung injury.

Animals↗

PubMed2000

Regulated hepatic insulin gene therapy of STZ-diabetic rats.

Effective and safe insulin gene therapy will require regulation of transgenic insulin secretion. We have created a liver-targeted insulin transgene by engineering glucose responsive elements into a hepatic promoter containing an inhibitory insulin response sequence. In this work, we demonstrate application of this transgene for the treatment of diabetes mellitus in vivo, by administering a recombinant adenovirus vector, Ad/(GIRE)3BP-1 2xfur, to rats made diabetic with streptozotocin. We verified hepatic expression of transgenic insulin by RT-PCR, and confirmed glucose responsive stimulation of transgenic insulin secretion in vivo by serum RIA. Following a portal system injection of either Ad/(GIRE)3BP-1 2xfur, or an empty adenoviral vector, animals made diabetic with either low (120 mg/kg), or high (290 mg/kg) dose streptozotocin (STZ) were monitored for changes in body weight, and blood glucose. Without subcutaneous insulin injections, blood glucose values of sham-treated animals (n = 8) remained elevated, and animals failed to gain weight (n = 4), or died (n = 4). In contrast, body weight of Ad/(GIRE)3BP-1 2xfur-treated animals (n = 13) increased, and blood glucose remained at near normal levels from one to 12 weeks. Glucose values <50 mg/dl were infrequently observed, and no Ad/(GIRE)3BP-1 2xfur-treated animal succumbed to hypoglycemia. Treatment with the insulin transgene enabled diabetic animals to reduce blood sugars following a glucose load, and to maintain blood sugar levels during a 10-h fast. Hepatic production of human insulin produced near normal glycemia, and weight gain, without exogenous insulin, and without lethal hypoglycemia. In conclusion, we have demonstrated the feasibility of utilizing transcription to control transgenic insulin production in a rodent model of diabetes mellitus.

Adenoviridae↗

PubMed1999

Leptin receptor and neuropeptide Y gene expression in the sheep brain.

Leptin, a protein secretory product of adipocytes, is important in appetite control, energy balance and reproduction. In rodents, the physiological effects of leptin are centrally mediated, in part via the neuropeptide Y (NPY) system in the hypothalamus. The role of leptin in ruminants, where appropriate nutrition and reproductive status are of major economic concern, is largely unknown. To elucidate the function of leptin in sheep we have investigated putative sites of action for leptin in the brain and pituitary gland using both in-situ hybridization to detect expression of the signalling form of the leptin receptor (OB-Rb) and in-vitro autoradiography using (125I)leptin to detect sites of specific leptin binding. OB-Rb gene expression occurred in the hippocampus, cerebral cortex, preoptic area, stria terminalis and choroid plexus, and within the hypothalamus in the paraventricular (PVN), ventromedial (VHM) and arcuate (ARC) nuclei. OB-Rb gene expression in the ovine pituitary gland was not detected by in-situ hybridization. Sites of OB-Rb and NPY gene expression were compared using both in-situ hybridization on adjacent sections containing the arcuate and ventromedial nuclei, and dual in-situ hybridization on sections containing these areas. In serial sections, OB-Rb expression was found to correspond closely with that of NPY over the arcuate nuclei. Using dual in-situ hybridization, NPY expressing neurones in the arcuate nuclei were also positive for OB-Rb gene expression. Therefore, it appears that leptin may partly act via OB-Rb located on NPY neurones in the sheep hypothalamus as in the rodent.

Animals↗