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Biomedical subjects

R N Carter

Publications and source records attributed to R N Carter.

At least 19 recordsLinked to original sources
PubMed2005

Central responsiveness to a ghrelin mimetic (GHRP-6) is rapidly altered by acute changes in nutritional status in rats.

The hypothalamus appears to be more responsive to ghrelin and growth hormone secretagogues (GHS) in fasting, as reflected by a two- to three-fold increase in the number of cells detected that express Fos protein in the arcuate nucleus, in 48-h fasted rats compared to fed controls. Moreover, this increased hypothalamic responsiveness to GHS in fasting is regulated by the central action of exogenous leptin and insulin, although it is unknown whether these hormones mediate the changes in hypothalamic responsiveness to GHS associated with the fasting/fed state. In the present study, we show that refeeding with normal rat chow for only 2 h at the end of a 48-h fast reversed the potentiation of the Fos response to GHRP-6 observed in fasted rats. Circulating leptin and insulin levels remained significantly lower in refed rats compared to ad lib-fed rats, suggesting that the change in the hypothalamic sensitivity brought about by refeeding was independent of these hormones. By contrast, 2 h of chow refeeding at the end of a fast restored plasma glucose levels to those of the fed state. Refeeding with sugar alone for 2 h at the end of a 48-h fast also reduced the potentiated Fos response in fasting, indicating that elevated blood glucose can influence the central responsiveness to ghrelin/GHS. By contrast, infusion of the ileal satiety factor, PYY(3-36) (known to increase postprandially) did not alter the central responsiveness to GHRP-6, although it suppressed feeding and body weight as expected. This study highlights the importance of nutritional status in regulating the action of exogenous GHS (and presumably endogenous ghrelin) on the hypothalamic circuits controlling food intake.

Animal Feed↗
PubMed2004

Does the amygdala modulate adaptation to repeated stress?

Exposure of the rat to restraint results in activation of the hypothalamic-pituitary-adrenal (HPA) axis, a characteristic pattern of c-fos expression in the brain and increased cardiovascular function. These responses adapt with repeated exposure of an individual to the same stress. Corticosterone secretion habituates, and c-fos mRNA expression in the paraventricular nucleus of the hypothalamus (PVN) decreases. The increased expression of corticotropin releasing hormone mRNA in the PVN also becomes less prominent, whereas vasopressin mRNA progressively increases. The neural mechanisms responsible for this adaptation remain obscure. Because of its role in conditioned learning, we have hypothesised that the amygdala might be involved in this adaptive process. Here we show that large neurotoxic lesions of the amygdala in male rats do not prevent acute stress activation of the HPA axis following 30 min restraint, whilst more discrete lesions of the central nucleus actually exacerbate the acute response. Rats with large amygdala lesions demonstrate delayed habituation of corticosterone and c-fos to repeated restraint, an affect not apparent with central nucleus lesions. Furthermore we show that neither type of lesion significantly reduced tachycardiac responses to single or repeated restraint as measured by telemetry. We conclude that the amygdala and the central nucleus are not necessary for HPA and cardiovascular activation in response to stress (though the central nucleus may modulate it), and that adaptation to repeated stress is only modestly dependent upon the amygdala.

Acute Disease↗
PubMed2003

Acute effects of PYY3-36 on food intake and hypothalamic neuropeptide expression in the mouse.

It has recently been suggested that gut-derived PYY(3-36) may be involved in the central mediation of post-prandial satiety signals. We have examined the acute effects of peripherally administered PYY(3-36) on food intake and hypothalamic gene expression of neuropeptides in mice. A single intraperitoneal injection of PYY(3-36) to mice that had been fasted for 24h resulted in a highly significant reduction in food intake at 6 and 24h post-injection but not at 48h. However, in freely fed mice, food intake was unaltered by PYY(3-36) administration. In the arcuate nucleus POMC mRNA expression was significantly elevated at 6h and remained elevated at 24h following PYY(3-36) injection. By contrast NPY mRNA expression in the arcuate nucleus was suppressed at 6h but not at 24h post-injection. In the lateral hypothalamus there were no differences in MCH mRNA expression at either time point. In conclusion, peripherally administered PYY(3-36) has a suppressive effect on food intake that is more prominent in recently fasted mice and lasts up to 24 h. This is associated with a short-lived suppression of NPY mRNA, a longer lasting increase in POMC mRNA but no change in MCH mRNA expression.

Adaptation, Physiological↗
PubMed1999

Plasma lactate decline during passive recovery from high-intensity exercise.

PURPOSE: An athlete's ability to repeatedly perform at high intensities during intermittent exercise could be related to an accelerated plasma lactate removal ability during recovery periods. METHODS: We determined the decline in plasma lactate levels during passive recovery after an incremental exercise test to exhaustion on a bicycle ergometer in five trained and five untrained male subjects. Venous blood samples were taken during exercise and recovery for the analysis of plasma lactate concentration. The endurance fitness of the subjects was characterized using a variable known as the maximum turn point power output (MTP), measured in W x kg(-1). MTP describes the workload at which lactate levels rise significantly above resting concentrations. RESULTS: The decline in plasma lactate levels during recovery was determined at selected intervals from the exponential recovery curve plotted as a percentage of peak plasma lactate versus time. No significant relationships were found between the recovery parameters measured from the curve and the MTP values of these subjects (Spearman's rank order correlation; r(s) values from -0.042 to -0.31). CONCLUSIONS: Therefore, we can conclude that training confers no advantage to the decline in plasma lactate while recovering passively from exercise at equivalent relative maximal work intensities.

Adult↗
PubMed1998

Brain and abdominal temperatures at fatigue in rats exercising in the heat.

We measured brain and abdominal temperatures in eight male Sprague-Dawley rats (350-450 g) exercising voluntarily to a point of fatigue in two hot environments. Rats exercised, at the same time of the day, in three different trials, in random order: rest 23 degrees C, exercise 33 degrees C; rest 23 degrees C, exercise 38 degrees C; and rest 38 degrees C, exercise 38 degrees C. Running time to fatigue was 29.4 +/- 5.9 (SD), 22.1 +/- 3.7, and 14.3 +/- 2.9 min for the three trials, respectively. Abdominal temperatures, measured with intraperitoneal radiotelemeters, at fatigue in the three trials (39.9 +/- 0.3, 39.9 +/- 0.3, and 39.8 +/- 0.3 degrees C, respectively) were not significantly different from each other. Corresponding brain temperatures, measured with thermocouples in the hypothalamic region (40.2 +/- 0.4, 40.2 +/- 0.4, and 40.1 +/- 0.4 degrees C), also did not differ. Our results are consistent with the concept that there is a critical level of body temperature beyond which animals will not continue to exercise voluntarily in the heat. Also, in our study, brain temperature was higher than abdominal temperature throughout exercise; that is, selective brain cooling did not occur when body temperature was below the level limiting exercise.

Abdomen↗
PubMed1994

Cellular location and temporal expression of the Plasmodium falciparum sexual stage antigen Pfs16.

The temporal expression during gametogenesis and the cellular location of the sexual stage specific protein Pfs16, a putative integral membrane protein of Plasmodium falciparum, was investigated using two monoclonal antibodies, 2G7 and 93A3A2. Using sorbitol synchronised, in vitro gametocyte cultures along with immunofluorescence assays, the time at which Pfs16 is first expressed during gametogenesis has been estimated to 35 hours post merozoite invasion. By immunofluorescence assays on thin blood smears monoclonal antibodies specific for Pfs16 react strongly with the gametocyte and also with vesicles within the red blood cell cytoplasm, many of which connect with the gametocyte cell. Purification of parasitophorous vacuole membranes from mature and immature gametocytes and immunoelectron microscopy on gametocytes during gametogenesis have allowed us to locate Pfs16 to the parasitophorous vacuole membrane. During gametogenesis this membrane is shed along with the red blood cell membrane. Immunofluorescence assays and immunoelectron microscopy studies of emerged gametes indicate that in a minority of cases the parasitophorous vacuole membrane along with Pfs16 can be retained to some extent on the gamete surface.

Animals↗
PubMed1981

Salivary control.

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Dental Bonding↗