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Jennifer L Temple

Publications and source records attributed to Jennifer L Temple.

10 recordsLinked to original sources
PubMed2006

Habituation and recovery of salivation and motivated responding for food in children.

Salivary responses habituate to repeated presentations of food cues, and these responses recover when new food stimuli are presented. Research suggests that within-session changes in motivated responding for food may also habituate, and motivated responding may, therefore, recover when new foods are presented. The purpose of this study was to evaluate similarities in the pattern of salivation and motivated responding for a cheeseburger stimulus in children, followed by either a novel stimulus (French fries) or another cheeseburger trial. The order of the task (salivation or motivation) was counterbalanced over days. Salivation and motivated responding for cheeseburger were reliably reduced over seven trials, and responses recovered after presentation of French fries on trial 8. Random regression models showed a significant relationship between the rate of change in motivated responding and salivation. These results provide additional support for similarities in processes that regulate salivation and motivated responding for food and strengthen support for the hypothesis that changes in motivated responding can be understood by habituation theory.

Child↗
PubMed2004

Bovine serum albumin-estrogen compounds differentially alter gonadotropin-releasing hormone-1 neuronal activity.

Steroid hormones regulate a host of physiological processes and behaviors. These actions can occur by genomic mechanisms involving gene transcription or by nongenomic mechanisms proposed to involve receptors associated with the plasma membrane. BSA-conjugated steroid hormones have been extensively used to elucidate signal transduction pathways for these hormones. We have previously shown, using calcium imaging, that 17beta-estradiol (E2) significantly increases GnRH-1 neuronal activity. During the course of these experiments, it became apparent that three different BSA-estrogen compounds have been used in a variety of cell types: 17beta-estradiol 6-O-carboxymethyloxime-BSA (E2-6-BSA); 1,3,5(10)-estratrien-3,16alpha,17beta-triol-6-one 6-O-carboxymethyloxime-BSA (E-6-BSA); and 1,3,5(10)-estratrien-3,17beta-diol 17-hemisuccinate-BSA (E2-17-BSA). The effects of these compounds on GnRH-1 neuronal activity were compared using calcium imaging. E-6-BSA and E2-17-BSA, but not E2-6-BSA, significantly increased all parameters of GnRH-1 neuronal activity. In addition, the effects of these two BSA compounds were reversed by the estrogen receptor antagonist ICI 182,780 but not by inhibition of gene transcription. The effects of E2-17-BSA, but not E-6-BSA were reversed by treatment with pertussis toxin, which blocks G protein-coupled receptors. These data indicate that these compounds cannot be used interchangeably and clearly have different binding properties and/or different effects on target tissues.

Anesthetics, Local↗
PubMed2004

Direct action of estradiol on gonadotropin-releasing hormone-1 neuronal activity via a transcription-dependent mechanism.

Pulsatile secretion of gonadotropin-releasing hormone-1 (GnRH-1) is essential for reproduction. GnRH-1 induces gonadotropin release and is regulated by 17beta-estradiol (E2). Although a subpopulation of GnRH-1 neurons expresses estrogen receptor (ER) beta, it is unclear whether E2 acts directly on GnRH-1 neurons or indirectly through interneuronal connections. To test the hypothesis that E2 acts directly on GnRH-1 neurons to regulate neuronal activity, we used calcium imaging to monitor intracellular calcium oscillations in GnRH-1 neurons maintained in nasal explants. TTX was used to minimize synaptic input from other cells. Consistent with previous studies, TTX reduced the activity of individual GnRH-1 neurons to a basal level, while the population of cells maintained synchronized calcium oscillations. Exposure of GnRH-1 cells to TTX plus E2 increased the number of calcium peaks/cell, percentage of cells with > or =10 peaks, mean peak amplitude, and percentage of cells that contributed to each calcium pulse in explants maintained in vitro for 7 d (7 div) compared with TTX alone. These effects were induced within 30 min and were not mimicked by 17alpha-estradiol, E2 conjugated to BSA (which does not cross the plasma membrane), or seen at 21 div, when the percentage of GnRH-1 cells expressing ERbeta transcripts declines. In addition, these effects were inhibited by the ER antagonist ICI 182,780 and prevented by inhibition of gene transcription. These data suggest that, via ERbeta, E2 can rapidly act as a hormone-activated transcription complex and are the first to show that E2 directly increases GnRH-1 neuronal activity and synchronization.

Adenocarcinoma↗
PubMed2003

Lack of functional estrogen receptor beta gene disrupts pubertal male sexual behavior.

The estrogen receptor-beta (ERbeta) mediates estrogen action in the female gonads, reproductive tract, and central nervous system. In addition, in rats and mice, gonadotropin-releasing hormone (GnRH-I) neurons coexpress ERbeta. Here we asked if ERbeta plays a role in the onset of puberty and in hypothalamic-pituitary-gonadal (HPG) axis function in male mice. We examined mating behavior, testosterone concentrations, steroid negative feedback on gonadotropins, and GnRH-I function in male ERbeta knockout (ERbetaKO) and wild-type (WT) mice. Peripubertal ERbetaKO males displayed their first ejaculation at a significantly older age than WT littermates. Castrated, adult ERbetaKO mice had significantly higher plasma luteinizing hormone (LH) than WT counterparts. Estradiol (E2) treatment reduced LH and follicle stimulating hormone (FSH) concentrations to an equivalent degree in castrates of both genotypes. In three different measures of the adult GnRH-I system, no genotypic differences were observed. These data show that ERbeta plays an important role in the timing of male sexual behavior at puberty, but does not appear to be involved in adult HPG axis functioning. Furthermore, our data suggest that a primary role of ERbeta may be to regulate ejaculatory behavior.

Animals↗
PubMed2003

An evolutionarily conserved form of gonadotropin-releasing hormone coordinates energy and reproductive behavior.

GnRH is the master neuropeptide that coordinates and regulates reproduction in all vertebrates and in some nonvertebrate species. Sixteen forms of GnRH have been isolated in brain. In the vast majority of species, two or more forms occur in anatomically and developmental distinct neuronal populations. In mammalian brain, two GnRH forms, mammalian (GnRH-I) and chicken-II (GnRH-II), exist. The distribution and functions of GnRH-I have been well characterized and intensively studied. However, the function of GnRH-II, which is the most evolutionarily conserved form of GnRH, has been elusive. Here we demonstrate that in a primitive mammal, the musk shrew (Suncus murinus), GnRH-II activates mating behavior in nutritionally challenged females within a few minutes after administration. In addition GnRH-II immunoreactive cell numbers and fibers increase in food-restricted females. Furthermore, GnRH type II receptor immunoreactivity was detected in musk shrew brain in regions associated with mating behavior. Our results lead us to hypothesize that the role of the evolutionarily conserved GnRH-II peptide is to coordinate reproductive behavior as appropriate to the organism's energetic condition.

Animals↗
PubMed2002

Mating behavior is controlled by acute changes in metabolic fuels.

Mild food restriction for 48 h inhibits mating behavior in female musk shrews (Suncus murinus). However, mating behavior is restored after a 90-min feeding bout. In this series of experiments, we examined the role of metabolic fuels in this behavioral restoration. First, drugs reported to block glycolysis or fatty acid oxidation were given 2 h before mating. Both treatments inhibited mating in food-restricted females that were refed after treatment. Blood glucose levels were assessed in females that were fed ad libitum, food restricted, or food restricted and refed for 90 min. Food restriction significantly lowered blood glucose compared with ad libitum feeding or food restriction in combination with 90 min of refeeding. However, neither glucose nor fat alone could substitute for food and promote mating behavior in food-restricted females. In addition, analysis of ketone bodies and body composition in females demonstrated low or undetectable levels of these energy substrates. Our data suggest that musk shrews have relatively little stored energy. Therefore, female musk shrews rely on continuous food intake and monitor multiple cues acutely, including glucose availability and fatty acid oxidation. This ensures that mating does not occur when adequate energy is unavailable.

Adipose Tissue↗
PubMed1999

Estrous variations in behavioral responses to vaginal and uterine distention in the rat.

Response properties of peripheral afferent fibers supplying the vagina and uterus of the rat vary with estrous stage (Robbins A, Berkley KJ, Sato Y. Estrous cycle variation of afferent fibers supplying reproductive organs in the female rat. Brain Res 1992,596:353-356), suggesting that behavioral sensitivity to vaginal and uterine stimulation might similarly vary. To test this hypothesis, detection and escape responses of 12 rats to different volumes of distention of the vaginal canal or uterine horn (six rats each) were compared during each of the four estrous stages, proestrus (P), estrus (E), metestrus (M), and diestrus (D), using previously-published behavioral techniques (Berkley KJ, Wood E, Scofield SL, Little M. Behavioral responses to uterine or vaginal distention in the rat. Pain 1995;61:121-131). Estrous variations in vaginal or uterine tone (pressure-volume functions) were also measured in the same rats. Vaginal canal: escape response percentages increased significantly as vaginal distention volume increased, but neither escape nor detection responses varied with estrous stage. Vaginal tone, however, was greater in P and E than in M and D, with the greatest tone in E and the least in D. When escape responses to different pressures were analyzed, it was found that escape response percentages to the same vaginal pressure were lower during P and E than during M and D. One outcome of these estrous influences would be that a vaginal stimulus of a given volume (such as an erect penis) would exert higher pressures during P and E (i.e. the penis would be held within the vaginal canal more firmly) than during M and D, but would be less likely during P and E to provoke escape responses. This modification of nociceptive sensitivity has obvious reproductive advantages, because P and E constitute the rat's fertile period. Uterine horn: escape response percentages increased significantly as uterine distention volume increased only during M and D, with no differences between them. Detection responses also occurred only during M and D. Similarly, uterine tone was significantly greater in M and D than in P and E, with the greatest tone occurring during M and the least during P. Although these changes in uterine tone were opposite to those of the vaginal canal, escape response percentages to the same uterine pressures were, in a manner similar to vaginal pressures, lower during P and E than during M and D. The functional significance of these variations for the uterus is unclear, but does suggest that, under pathophysiological conditions, stimulation of the uterine horn, as well as the vaginal canal, would be more likely to provoke escape behaviors in M and D than in P and E. A similar increased sensitivity in rats during M and D to noxious stimulation of other pelvic organs has been observed by others. This situation resembles that in women, for whom many visceral pain conditions are exacerbated during a comparable part of their ovarian cycle, i.e. perimenstrually.

Animals↗
PubMed1999

Effects of hypogastric neurectomy on escape responses to uterine distention in the rat.

Anatomical data indicate that the rat uterine horn is innervated primarily by afferent fibers in the hypogastric nerves, suggesting that hypogastric neurectomy, but not pelvic or pudendal neurectomy, should eliminate behavioral responses to uterine horn stimulation. To test this hypothesis, detection and escape responses of rats to different volumes of uterine horn distention (via an indwelling intrauterine balloon) were compared before and after bilateral hypogastric (n = 9), sham-hypogastric (n = 3), pelvic (n = 3), or pudendal (n = 2) neurectomies. As predicted, sham-hypogastric, pelvic, and pudendal neurectomies had no effect on the rats' responses. However, although hypogastric neurectomy completely eliminated responses in five rats whose postmortem evaluation revealed no signs that the uterine balloons had evoked any pelvic pathophysiology, the neurectomy had no effect on the responses of an additional four rats. Postmortem evaluation of these rats revealed gross signs of severe pathology in the vicinity of the balloon in two rats, and evidence that the balloon had shifted caudally so that it was stimulating the cervix rather than the uterine horn in a third. In the fourth rat, pathophysiology had been deliberately induced by the prior implantation of a small pellet that released approximately 1 microg/day of prostaglandin PF2alpha over the uterine horn. Similar findings have been reported in clinical studies on the efficacy of hypogastric ('presacral') neurectomy for dysmenorrhea. Together, the findings support the hypothesis that the major source of afferent innervation of the uterine horn in healthy rats and women is the hypogastric nerve but that the situation changes under conditions of pelvic pathology. Such changes could include additional activation of afferent fibers in nerves that supply other pelvic organs, activation by the uterine pathophysiology of latent uterine innervation from afferent fibers in the pelvic, vagus or ovarian plexus nerves, or some form of central sensitization.

Animals↗