Biomedical subjects

Janine D Flory

Publications and source records attributed to Janine D Flory.

At least 19 recordsLinked to original sources

PubMed2006

Preference for immediate over delayed rewards is associated with magnitude of ventral striatal activity.

Discounting future outcomes as a function of their deferred availability underlies much of human decision making. Discounting, or preference for immediate over delayed rewards of larger value, is often associated with impulsivity and is a risk factor for addictive disorders such as pathological gambling, cigarette smoking, and drug and alcohol abuse. The ventral striatum (VS) is involved in mediating behavioral responses and physiological states associated with reward, and dysregulation of the VS contributes to addiction, perhaps by affecting impulsive decision-making. Behavioral tests of delay discounting (DD), which index preference for smaller immediate over larger delayed rewards, covary with impulsive tendencies in humans. In the current study, we examined the relationship between individual differences in DD, measured in a behavioral assessment, and VS activity measured with blood oxygenation level-dependent functional magnetic resonance imaging, in 45 adult volunteers. VS activity was determined using a task involving positive and negative feedback with monetary reward. Analyses revealed that individual differences in DD correlate positively with magnitude of VS activation in response to both positive and negative feedback, compared with a no-feedback control condition. Variability in DD was also associated with differential VS activation in response to positive, compared with negative, feedback. Collectively, our results suggest that increased preference for smaller immediate over larger delayed rewards reflects both a relatively indiscriminate and hyper-reactive VS circuitry. They also highlight a specific neurocognitive mechanism that may contribute to increased risk for addiction.

Adult↗

PubMed2006

Human choline transporter gene variation is associated with corticolimbic reactivity and autonomic-cholinergic function.

BACKGROUND: Our previous work has shown genetic variation in the human choline transporter gene (CHT1) to be associated with depressive symptoms and autonomic cardiac (cholinergic) dysregulation. Here, functional magnetic resonance imaging (fMRI) was used to examine the relation between a single nucleotide polymorphism (SNP) in CHT1 on regional brain reactivity relevant to autonomic (cholinergic) function. METHODS: Thirty-two participants of European ancestry (18 men, 14 women; age: 33-54 years) completed an fMRI protocol using corticolimbic reactivity and prefrontal inhibitory control paradigms. Resting cholinergic function, as measured by heart rate variability (HRV), was quantified from electrocardiogram. Subjects were genotyped for a CHT1 G/T SNP. RESULTS: GG homozygotes had greater right (R) dorsal amygdala (p < .008), bilateral anterior cingulate (p < .009), and R caudate reactivity (p < .015) than T-allele carriers. Heart rate variability was related to R frontal cortex (Brodmann Areas 6, 9, and 46), R hippocampal formation, bilateral caudate, and bilateral anterior cingulate reactivity (p's < .007). CONCLUSIONS: CHT1 variation is related to differences in a distributed corticolimbic circuitry mediating behavioral and physiologic arousal. These relations may contribute to a biological mechanism by which genetic variation in cholinergic neurotransmission affects cognition, mood, and autonomic cardiac function.

Adult↗

PubMed2006

Dispositional impulsivity in normal and abnormal samples.

Impulsive behaviors, which can include aggression, substance use and suicide, are common and core features of the DSM Axis II Cluster B personality disorders. The construct of dispositional impulsivity is multidimensional and a number of self-report measures have been created to represent features of this trait (e.g., novelty seeking, behavioral disinhibition, nonplanning). Because these questionnaires are rarely administered together in the same sample, little is known about how they are related to one another. The current study was conducted to examine the structure of dimensional impulsive personality traits in a large normative sample (n=351). Analyses revealed that dispositional impulsivity was represented by three moderately correlated latent factors labeled thrill seeking, nonplanning and disinhibited behavior. Confirmatory factor analyses were also used to examine the extent to which the internal structure of these impulsive personality traits was similar in a sample defined as abnormal (i.e., DSM-III-R Cluster B PD diagnoses; n=70). Results revealed that the structure of these traits was consistent across the two samples in a model that constrained factor loadings and structural covariances (NFI=0.89; CFI=95; RMSEA=0.04). In addition, correlational relationships between the impulsivity factor scores and behavioral and sociodemographic factors (e.g., socioeconomic status, substance use) were consistent across the two samples. These results help to establish a common framework for understanding the multidimensional nature of impulsivity. Results from these analyses also lend support to a large body of work that demonstrates that normal and abnormal personality features are related.

Aggression↗

PubMed2006

Neural basis of individual differences in impulsivity: contributions of corticolimbic circuits for behavioral arousal and control.

The objective of the current study was to analyze the neural correlates of behavioral arousal and inhibitory control as they relate to individual differences in impulsivity via well-established functional MRI amygdala reactivity and prefrontal inhibitory control paradigms in healthy adult subjects. Impulsivity correlated positively with activity of the bilateral ventral amygdala, parahippocampal gyrus, dorsal anterior cingulate gyrus (BA 32), and bilateral caudate. Conversely, impulsivity correlated negatively with activity of the dorsal amygdala and ventral prefrontal cortex (BA 47). Together, these findings suggest that dispositional impulsivity is influenced by the functional interplay of corticolimbic behavioral arousal and control circuits.

Adult↗

PubMed2006

Catechol-O-methyltransferase Val158Met genotype variation is associated with prefrontal-dependent task performance in schizotypal personality disorder patients and comparison groups.

OBJECTIVE: A single-nucleotide polymorphism of the gene coding for catechol-O-methyltransferase (COMT Val(158)Met) is associated with prefrontal-dependent task performance in schizophrenia. We evaluated the relationship of the COMT genotype with diagnostic status and cognitive performance in schizotypal personality disorder. METHODS: Unmedicated outpatients with schizotypal personality disorder (SPD; n = 67) and non-schizotypal personality disorder (NSPD; n = 154) by DSM-III-R, and normal control (NC; n = 60) participants were genotyped at the COMT Val(158)Met locus. Of these, 98 Caucasians (23 SPD, 52 NSPD and 23 NC) performed a brief neurocognitive battery: Wisconsin Card Sorting Test (WCST), Paced Auditory Serial Addition Test (PASAT), California Verbal Learning Test (CVLT), Visuospatial Working Memory (DOT) and Visual Delayed Recall (Wechsler Memory Scale Visual Reproduction, WMS-VR). RESULTS: Allele distribution was not significantly different in the full sample (by chi(2)) for the SPD group compared with either the NC or combined NC/NSPD groups. In analyses of variance of Caucasian individuals, the SPD group performance met or approached significantly worse performance than NC, NSPD or both groups, on the PASAT, CVLT and WMS-VR. In regression analyses of cognitive performance, the COMT genotype was significantly associated with performance on WCST and PASAT, independent of diagnosis, with the Val/Val genotype associated with the worse performance. CONCLUSIONS: (1) Allelic variation in COMT activity is unrelated to the diagnosis of SPD in this sample. (2) Individuals with SPD exhibit multiple deficits in prefrontal and temporal lobe-dependent tasks. (3) The COMT genotype is related to performance on prefrontal cortex-dependent tasks and may contribute to the deficit in prefrontal-dependent memory processes in SPD as it does in schizophrenia.

Adult↗

PubMed2006

Developing an agenda for translational studies of resilience and vulnerability following trauma exposure.

Here we outline a translational research agenda for studies of resilience, defined as the process of adapting well in the face of adversity or trauma. We argue that an individual differences approach to the study of resilience, in which the full range of behavioral and biological responses to stress exposure is examined can be applied across human samples (e.g., people who have developed psychopathology versus those who have not; people who have been exposed to trauma versus those who have not) and even, in some cases, across species. We delineate important psychological resilience-related factors including positive affectivity and optimism, cognitive flexibility, coping, social support, emotion regulation, and mastery. Key brain regions associated with stress-related psychopathology have been identified with animal models of fear (e.g., extinction and fear conditioning; memory reconsolidation) and we describe how these regions can be studied in humans using neuroimaging technology. Finally, we cite recent research identifying neuroendocrine markers of resilience and recovery in humans (e.g., neuropeptide Y [NPY], dehydroepiandrosterone [DHEA]) that can also be measured, in some cases, in other species. That exposure to adversity or trauma does not necessarily lead to impairment and the development of psychopathology in all people is an important observation. Understanding why this is so will provide clues for the development of therapeutic interventions for those people who do develop stress-related psychopathology, or even for the prevention of adverse outcomes.

Brain Chemistry↗

PubMed2005

The metabolic syndrome is associated with reduced central serotonergic responsivity in healthy community volunteers.

CONTEXT: The pathobiology of the metabolic syndrome remains unclear. The central nervous system is likely to be involved via regulation of eating, physical activity, blood pressure, and metabolism. OBJECTIVE: The objective of this study was to test the hypothesis that low central serotonergic activity is associated with the metabolic syndrome. DESIGN, SETTING, PARTICIPANTS: This was a cross-sectional study of 345 healthy community volunteers, aged 30-55 yr, not taking medications for hypertension, lipid disorders, or diabetes. OUTCOME MEASURES: Central serotonergic responsivity was assessed with the iv citalopram challenge test. The serum prolactin area under the curve (AUC) over 150 min was calculated, and all analyses were adjusted for age, sex, plasma citalopram concentration, and baseline prolactin. The metabolic syndrome was defined according to the National Cholesterol Education Program (NCEP) and International Diabetes Federation (IDF) criteria. Insulin resistance was estimated by homeostasis model assessment. RESULTS: Compared with other individuals, persons meeting either NCEP or IDF criteria for the metabolic syndrome had lower mean prolactin responses (P < 0.05 for both). Using logistic regression, a decrease in prolactin AUC of 1 sd (-13.6 ng/ml.h) more than doubled the odds of having the metabolic syndrome (NCEP criteria: odds ratio, 2.38; 95% confidence interval, 1.14-4.97; P = 0.02; IDF criteria: odds ratio, 2.80; 95% confidence interval, 1.48-5.30; P = 0.002). Finally, the prolactin AUC was negatively associated with insulin resistance (beta = -0.03, P = 0.02). CONCLUSIONS: Corroborating previous evidence, the metabolic syndrome was associated with diminished brain serotonergic activity as reflected in a comparative blunting of the prolactin response to a selective serotonergic challenge. This association may have implications for the etiology, prevention, and treatment of the metabolic syndrome.

Adult↗

PubMed2005

The socio-economic status of communities predicts variation in brain serotonergic responsivity.

BACKGROUND: We reported previously that the socio-economic status (SES) of individuals predicts variation in brain serotonergic responsivity, as assessed by neuropharmacological challenge in an adult community sample, and that this association is qualified by allelic variation in the serotonin transporter gene-linked polymorphic region (5-HTTLPR). Here we examine whether serotonergic responsivity covaries similarly with the SES of communities, as indexed by US Census data in the same study sample. METHOD: Community SES was defined by levels of income, economic disadvantage, housing costs, and educational attainment of census tracts in which 249 locally recruited study participants (54% male) resided. Serotonergic responsivity was assessed as the baseline-adjusted, peak plasma prolactin (Prl) concentration following acute administration of the serotonin-releasing agent, fenfluramine; tissue for DNA extraction and 5-HTTLPR genotyping was available on 131 participants. RESULTS: Subjects residing in census tracts of lower SES showed a blunted Prl response to fenfluramine (diminished serotonergic responsivity) relative to individuals living in more affluent neighborhoods. When adjusted for personal income and education, SES at the community level continued to predict fenfluramine-stimulated Prl responses and did so independently of 5-HTTLPR genotype. CONCLUSIONS: Area-level indices of relative social and economic disadvantage covary with individual differences in brain serotonergic responsivity, and this association is, in part, independent of individually defined SES. These findings may be relevant to reported effects of low community SES on the prevalence of psychiatric disorders or behaviors associated with dysregulation of central serotonergic function, such as depression, impulsive aggression, and suicide.

Adult↗

PubMed2005

A convergent-divergent approach to context processing, general intellectual functioning, and the genetic liability to schizophrenia.

Convergent and divergent validity are critically important in developing psychological measures that reveal interpretable deficits in disordered populations. This article reports on 2 studies that evaluated the validity of context processing measures. In Experiment 1, a confirmatory factor analysis of data from 481 healthy adults established the convergent validity of 2 context processing measures and showed that context processing accounted for significant amounts of variance in standard IQ and working memory measures. In Experiment 2, 20 schizophrenia patients, 16 of their healthy siblings, and 28 controls were evaluated using a novel, short context processing measure, the dot pattern expectancy (DPX) task. The DPX was sensitive to specific deficits in schizophrenia patients and their healthy siblings. These findings support the construct validity of context processing measures, suggest context processing is a component of intellectual functioning, and demonstrate that brief context processing measures remain sensitive to psychopathological deficits.

Adult↗

PubMed2004

Randomized trial of the effects of simvastatin on cognitive functioning in hypercholesterolemic adults.

PURPOSE: In our initial study of the potential effects of cholesterol-lowering interventions on cognitive functioning, treatment with lovastatin as compared with placebo caused performance decrements on several neuropsychological tests, whereas scores on other tests were unaffected. The current study was designed to confirm and extend those findings. METHODS: The study comprised 308 hypercholesterolemic adults between 35 and 70 years of age. Employing a randomized double-blind design, we assigned participants to daily treatment with placebo, 10 mg of simvastatin, or 40 mg of simvastatin for 6 months. A neuropsychological test battery was administered to assess cognitive functioning at baseline and at the end of the treatment period. RESULTS: A total of 283 subjects completed the study: 94 subjects on placebo, 96 taking 10 mg of simvastatin, and 93 taking 40 mg of simvastatin. Compared with placebo, decremental effects of simvastatin treatment were found on tests previously observed to be sensitive to statins (P = 0.008; difference in summary z scores = 0.18; 95% confidence interval [CI]: 0.07 to 0.29) and on tests not previously administered (P = 0.04; difference in summary z scores = 0.17; 95% CI: 0.05 to 0.29), but not on tests previously observed to be insensitive to statins (P = 0.84; difference in summary z scores = 0.02; 95% CI: -0.07 to 0.10). For the three tests specifically affected by simvastatin, effects on cognitive performance were small, manifest only as failure to improve during the 6 months of treatment (compared with placebo), and were confounded by baseline differences on one test. CONCLUSION: This study provides partial support for minor decrements in cognitive functioning with statins. Whether such effects have any long-term sequelae or occur with other cholesterol-lowering interventions is not known.

Adult↗

PubMed2004

Serotonergic function in the central nervous system is associated with daily ratings of positive mood.

Serotonin constrains a broad array of animal and human behavior and may also inhibit the expression of mood or affective states among humans. For the most part, this research has focused on the association of central serotonergic function with negative affectivity (i.e., anxiety, depression, hostility), with less attention on the relationship between serotonergic function and positive affect or mood. The current study was conducted to examine the relationship between a measure of central serotonergic activity and daily ratings of positive and negative mood in a nonpatient sample. Two hundred and fifty-four adults, aged 24-60, completed end-of-day ratings of positive and negative mood items over 7 consecutive days. A neuropharmacological challenge was administered to index central serotonergic function, i.e., the maximal prolactin (PRL) response to fenfluramine, a serotonin releasing agent. Hierarchical linear regression analyses indicated that the peak PRL response to fenfluramine was positively associated with positive mood, averaged over 7 days, after controlling for known predictors of the PRL response. This relationship remained significant after controlling for average negative mood, for the presence of a current DSM-III-R diagnosis, and for trait measures of Neuroticism and Extraversion. In contrast, the PRL response to fenfluramine was not associated with average negative mood, although it was inversely correlated with trait negative affectivity (i.e., Neuroticism). These results suggest that deficiencies in serotonergic function may reflect the relative absence of positive mood.

Adult↗

PubMed2004

A comparison of d, l-fenfluramine and citalopram challenges in healthy adults.

Dimensional personality characteristics (e.g. impulsivity) and related behaviors and psychiatric disorders are linked to abnormalities of central nervous system (CNS) serotonergic functioning. Although neuroendocrine [e.g. plasma prolactin (PRL)] responses to the serotonin agonist, fenfluramine, have been used widely to index CNS serotonergic responsivity, safety concerns constrain continued use of fenfluramine. Citalopram, which inhibits serotonin reuptake, may serve as an alternative pre-synaptic neuropharmacologic challenge agent, due to its high selectivity and absence of intrinsic activity at serotonin or other receptor families. Twenty-two healthy adults who had been administered a fenfluramine challenge before May 1996 completed a 5-h oral citalopram challenge 3-6 years later. PRL responsivity to citalopram correlated significantly with PRL response to fenfluramine for baseline-corrected maximal and area-under-the-curve (AUC) indices ( r's > or =0.49, P's< or =0.02). The magnitude of the correlations is notable given the length of time between challenges. The results support the use of citalopram as an alternate neuroendocrine challenge to index CNS serotonergic responsivity.

Adult↗

PubMed2004

Socio-economic status covaries with central nervous system serotonergic responsivity as a function of allelic variation in the serotonin transporter gene-linked polymorphic region.

It was reported recently that exposure to an adverse rearing environment lowers central nervous system (CNS) serotonergic activity in a nonhuman primate (rhesus monkeys), but only among animals having the shorter variant of a functional, biallelic repeat polymorphism in the regulatory region of the serotonin transporter (5-HTT) gene. Because repeat variants of the same core sequence affect transcriptional efficiency of the 5-HTT gene in humans, we examined whether biallelic variation in the 5-HTT gene-linked polymorphic region (5-HTTLPR) acts analogously to modulate a previously described association between socio-economic status (SES) and CNS serotonergic function. The 5-HTTLPR was genotyped in 139 adult men and women (n = 75 and 64) who were administered a standard neuroendocrine challenge to assess central serotonergic responsivity (plasma prolactin (PRL) response to the serotonin releasing agent, fenfluramine). Socio-economic status was estimated from reported income and years of education. Hierarchical linear regression showed serotonergic responsivity to be predicted by the interaction of 5-HTTLPR genotype and SES (p = 0.018). Individuals of lower income and less education had lower peak PRL concentrations following administration of fenfluramine than did subjects ranking higher on these dimensions, but only among persons possessing at least one 5-HTTLPR short allele. Within genotype, SES covaried moderately with the PRL response to fenfluramine among subjects who were homozygous for the short allele (r18 = 0.50, p < 0.03). A similar association was present at lesser magnitude in heterozygotes (r70 = 0.24, p < 0.05) and absent among subjects homozygous for the long allele (r45 = -0.04, n.s.). Findings were comparable for men and women and persisted on re-analysis restricted to persons without current Axis I psychopathology. We conclude that allelic variation at 5-HTTLPR moderates the influence of social position on CNS serotonergic responsivity.

Adult↗

PubMed2004

Low central nervous system serotonergic responsivity is associated with the metabolic syndrome and physical inactivity.

The metabolic syndrome, recognized by the co-occurrence of general or abdominal obesity, hypertension, dyslipidemia, insulin resistance, and dysglycemia, appears to involve disturbances in metabolism, autonomic function, and health-related behaviors. However, physiological processes linking the components of the metabolic syndrome remain obscure. The current study examined associations of central nervous system serotonergic function with each metabolic syndrome risk variable, the metabolic syndrome, and physical activity. The subjects were 270 adult volunteers who participated in a study of cardiovascular disease risk factors and neurobehavioral functioning. Central serotonergic responsivity was indexed as the prolactin (PRL) response evoked by the serotonin-releasing agent, fenfluramine. Across the sample, low PRL response was associated with greater body mass index, higher concentrations of triglycerides, glucose, and insulin, higher systolic and diastolic blood pressure, greater insulin resistance, and less physical activity (P < 0.03-0.001). There also existed an inverse linear relationship between PRL response and the number of metabolic syndrome risk factors individuals possessed (P for trend = 0.002). Finally, a 1 SD decline in PRL response was associated with an odds ratio for the metabolic syndrome of 2.05 (95% confidence interval, 1.10-3.83; P = 0.002) and 5.70 (95% confidence interval, 1.69-19.25; P = 0.005), according to the definitions of the National Cholesterol Education Program and the World Health Organization, respectively. These findings reveal a heretofore unrecognized association between reduced central serotonergic responsivity and the metabolic syndrome.

Adult↗

PubMed2003

Neurobiologic function and temperament in subjects with personality disorders.

BACKGROUND: Personality traits have been hypothesized to involve specific neurotransmitter systems. In order to test this model, the relationship between the responses to serotonergic and noradrenergic probes, central cerebrospinal fluid (CSF) measures of monoamine neurotransmitters and the Tridimensional Personality Questionnaire (TPQ) were evaluated in a cohort of personality disorder subjects. METHODS: A total of 142 patients meeting at least one personality disorder (meeting Diagnostic and Statistical Manual of Mental Disorders, Third Edition-Revised criteria) participated in these studies. The prolactin response to fenfluramine (a measure of serotonin function) was obtained for 110 subjects; growth hormone response to clonidine (a measure of noradrenergic function) was obtained for 77 subjects, while homovanillic acid (HVA) at baseline, an index of dopaminergic function, was available for 103 subjects. Measures of central neurotransmitter function (dopaminergic, serotonergic, and noradrenergic: HVA, 5-hydroxyindolacetic acid, and 3-methoxy-4-hydroxyphenylglycol, respectively) were available for 36 subjects. Separate regression analyses utilizing each of the hypothesized associations, where the TPQ total scores were used as the dependent measures and the biologic indices were the independent measures were conducted. Exploratory correlational analyses between these biologic measures and the four dimensions of the TPQ (and its subscales) were also conducted. (Correlations are reported if they would remain significant at P<.01 level after Bonferroni correction for multiple comparisons across the six neuroendocrine measures). RESULTS: In the regression analyses, there was a trend association between CSF and plasma HVA in predicting novelty-seeking (P<.07). No other significant associations were found in the other three measures. Regarding the individual correlational analyses, the persistence scale of the TPQ was significantly positively correlated with the growth hormone response to clonidine (r=.30, P<.008). The sentimentality subscale (reward dependence) was positively correlated with CSF 5-hydroxyindolacetic acid (r=0.45, P<.001), while the attachment subscale (also reward dependence) was correlated with CSF 3-methoxy-4-hydroxyphenylglycol (r=0.49, P<.002). CONCLUSION: Limited support was provided for a relationship between monoamines, particularly dopamine and novelty-seeking as well as norepinephrine and reward dependence but other hypothesized relationships were not supported by these measures.

Brain↗

PubMed2002

Central nervous system serotonergic responsivity and aggressive disposition in men.

To determine whether normative variability in aggressive behavior correlates negatively with central nervous system (CNS) serotonergic function among men, plasma prolactin (PRL) responses to a standard fenfluramine challenge (administered to assess central serotonergic responsivity) were examined in relation to interview-assessed aggression histories among 118 adult males derived from a nonpatient, community sample. Fenfluramine-induced, peak PRL rises were smaller in subjects whose 'aggression' scores fell above the sample median, compared to their less aggressive counterparts (P<.002). Across subjects, participants' peak PRL responses likewise covaried inversely with aggression history (r(s)=-.32, P<.0005). Additional analyses were conducted on data of 58 subjects who had also been genotyped for a functional polymorphism in the promoter region of the X chromosomal, monoamine oxidase-A (MAO-A) gene. The four variants of this repeat polymorphism were grouped for analysis (alleles '1+4' vs. '2+3') based on prior report of enhanced transcriptional efficiency in MAO-A promoter constructs containing alleles 2 and 3 (repeats of intermediate length). Men in the 2/3 allele group had significantly higher aggression scores (P<.05) and smaller peak PRL responses to fenfluramine (P<.009) than men in the 1/4 allele group. When adjusted by analysis of covariance for concomitant variability in subjects' PRL responses, aggressive disposition no longer varied significantly by genotype. This finding suggests that association of the MAO-A promoter polymorphism with this behavioral phenotype may be mediated, in part, by allele-specific variation in central serotonergic responsivity.

Adult↗

PubMed2002

Short-term suppression of ovarian function and immune measures in healthy women.

Ovarian function was suppressed to postmenopausal levels with a GnRH agonist for four months in healthy, premenopausal women to examine the effect of short-term alterations in sex steroid exposure on immune measures at rest and in response to standardized laboratory stressors. Twenty-two women were assessed at three times: (a) during the early follicular phase of the menstrual cycle; (b) after ovarian function had been suppressed by a GnRH agonist; and (c) either in the early follicular phase after the resumption of regular menstrual cycling (group labeled Cycle), or when women received estradiol transdermally in conjunction with a GnRH agonist (group labeled Patch). A third group of 11 women was assessed at similar time points, but in a different order of pharmacologic intervention to evaluate the effects of ovarian function suppression that were not confounded by habituation to the laboratory stressors (group labeled Hormone Control). Finally, 15 women served as control subjects to control for the effects of time, seasonality and blood collection procedures on immune measures (group labeled Immune Control). Immune measures included circulating cell counts, response to mitogens (PHA and PWM), and NK cytotoxicity. Results revealed no consistent changes in basal or stress-induced immune measures that varied with a period of short-term suppression of ovarian function. Basal and acute stress-induced cell counts showed moderate to high temporal stability over a six to ten month time interval.

Adult↗

PubMed2002

Retest reliability of prolactin response to dl-fenfluramine challenge in adults.

Neuropharmacologic probes to assess central nervous system (CNS) serotonergic responsivity (e.g., dl-fenfluramine) stimulate serotonergic neurotransmission, thereby causing proportional release of pituitary-derived hormones into the circulation. Individual differences in these hormonal responses are thus thought to reflect dimensional variability in central serotonergic activity, which may, in turn, underlie variation in serotonin-related traits of personality (e.g., impulsivity, behavioral inhibition, harm avoidance). However, the long-term temporal stability of neuropharmacologic indices of CNS serotonergic responsivity has not previously been tested in nonpsychiatric patients. dl-Fenfluramine was administered here to 57 adults, aged 24-60 years, on two occasions 6 months apart, to examine the retest reliability of fenfluramine-induced prolactin [PRL] response to fenfluramine. Baseline PRL concentration (i.e., before administration of fenfluramine) was highly stable over the 6 months (r = 0.88). Variability in serotonergic responsivity, adjusted for baseline PRL concentration, age, sex, and drug concentration during the challenge, was moderately reproducible (r = 0.50 for peak DeltaPRL and 0.57 for PRL "area under the curve," p <.0001). These findings are consistent with speculation that variability in indices of central serotonergic function reflects a temporally stable dimension of individual differences.

Adult↗