Bias in beliefs about the self is associated with depressive but not anxious mood.

BACKGROUND: Biases in beliefs about the self are associated with psychopathology and depressive and anxious mood, but it is not clear if both negative and positive beliefs are associated with depression or anxiety. We examined these relationships in people who present with a wide range of depressive and anxious mood across diagnostic categories. METHODS: We probed positive and negative beliefs about the self with a task in which 74 female participants with either affective disorder (depression and/or anxiety), borderline personality disorder or no psychiatric history indicated the degree to which 60 self-related words was "like them" or "not like them". Depressive and anxious mood were assessed with the Beck Depression Inventory-II and the Beck Anxiety Inventory. RESULTS: The participants with no psychiatric history (n=25) reported a positive bias in their beliefs about the self, the participants with affective disorder (n=23) reported no bias, and the participants with BPD (n=26) reported a negative bias. Two hierarchical multiple regressions demonstrated that the positive and negative beliefs contributed additively to the ratings of depression (corrected for anxiety), but did not contribute to the ratings of anxiety (corrected for depression). LIMITATIONS: Despite the apparent small sample size, the regression analyses indicated adequate sampling. Anxiety is a much more heterogeneous condition than is depression, so it may be difficult to find relevant self-descriptors. Only measures of endorsement were used. CONCLUSIONS: Biases in beliefs about the self are associated with depressed, but not anxious mood, across diagnostic categories.

Changes in the relationship between self-reference and emotional valence as a function of dysphoria.

The self-positivity bias is found to be an aspect of normal cognitive function. Changes in this bias are usually associated with changes in emotional states, such as dysphoria or depression. The aim of the present study was to clarify the role of emotional valence within self-referential processing. By asking non-dysphoric and dysphoric individuals to rate separately the emotional and self-referential content of a set of 240 words, it was possible to identify the differences in the relationship between self-reference and emotional valence, which are associated with dysphoria. The results support the existence of the self-positivity bias in non-dysphoric individuals. More interestingly, dysphoric individuals were able to accurately identify the emotional content of the word stimuli. They failed, however, to associate this emotional valence with self-reference. These findings are discussed in terms of attributional self-biases and their consequences for cognition.

Seeing yourself in a positive light: brain correlates of the self-positivity bias.

Individuals are found to have better recall for self-referent information than other types of information. However, attribution research has shown that self-reference is highly correlated with emotional valence. The present study attempted to identify and separate the processing of self-reference and emotional valence using ERPs. Participants performed a two-choice task, judging the self-referential content of positive and negative words. Reaction times revealed an interaction between self-reference and emotional valence. Faster responses occurred after self-positive and non-self negative words as compared to self-negative and non-self-positive words. A similar interaction was identified in ERP waveforms in the time range of the N400 component at fronto-central electrode sites, with larger N400 amplitudes for words outwith the self-positivity bias. Thus, the size of the N400 may indicate the extent to which information is discrepant with the individual's self-concept.

A model of personality change after traumatic brain injury and the development of the Brain Injury Personality Scales.

OBJECTIVE: The aims of this study were to develop models of personality change after traumatic brain injury (TBI) based on information provided by the TBI survivor and a significant other (SO), and to compare the models generated from the two different sources of information. METHODS: Individuals with and without TBI and an SO were interviewed separately about their current personality. The SOs were also interviewed about the personality of the TBI survivor before the injury. A subset of TBI survivors and their SOs were interviewed twice to assess test-retest reliability. Items which were not associated with personality change after TBI, which could not be measured reliably or which did not contribute to the model, were excluded. RESULTS: Of the 123 original items, 29 items from the interview with the survivor and 31 items from the interview with the SO were retained to form the Brain Injury Personality Scales. Separate factor analyses of ratings from each interview (survivor and SO) resulted in seven first order factors. The second order factor analyses for each interview resulted in four factors. Concordance between the information obtained from the two interviews was low. CONCLUSIONS: The information obtained from the interviews with the TBI survivors and the SOs produced two models with a similar structure: three superordinate factors of personality items (affective regulation, behavioural regulation and engagement) and one superordinate factor of items relevant to mental state (restlessness and range of thought). Despite the similarity in structure, the content of the information obtained from the two interviews was different.

Performance on tests of frontal lobe function reflect general intellectual ability.

Recent studies have indicated that performance on tests of frontal lobe function are highly associated with general intellectual ability (g). Some authors have even claimed that the available evidence does not support a more specific account of frontal lobe function than to provide a general intellectual function for the performance of goal directed tasks. We examined the relationship between performance on the WAIS-R (as a measure of g) and performance on standard tests of frontal lobe function in 123 healthy individuals. Our results demonstrate that in healthy individuals (i) performance on the most popular tests of frontal lobe function shares significant variance, and (ii) a large proportion of that shared variance is highly associated with performance on the Wechsler Adult Intelligence Scales-Revised (WAIS-R), so that the tests are similar to the extent that they measure g. Performance on the Modified Card Sorting Test (MCST), however, is not related to g. The results support the claim that many tests of frontal lobe function measure primarily a non-specific intellectual function but also indicate that some tests, like the MCST, may be assessing more specific cognitive operations.

Performance on the Modified Card Sorting Test by normal, healthy individuals: relationship to general intellectual ability and demographic variables.

OBJECTIVES: The aim of this study was to obtain normative data for the Modified Card Sorting Test (MCST), and to examine the relationship between performance on this task, general intellectual ability and demographic variables. DESIGN: A sample of 146 healthy individuals was tested with a demographic distribution (age, sex, socioeconomic class) similar to that of the British population. METHODS: The MCST and the Wechsler Adult Intelligence Scales--Revised were administered to 146 people aged between 16 and 75 years. RESULTS: Most people (56.6%) completed six categories, and many people made perseverative errors. Approximately 8% of the participants made over 50% perseverative errors. Performance on the MCST varied with age, years of education and general intellectual ability. Individuals with a Full Scale Intelligence Quotient (FSIQ) below 100 showed much more variability in performance than individuals with an FSIQ over 100. Detailed percentile norms for the performance on different indices of the test are presented. CONCLUSIONS: The performance of individuals on the MCST is more closely associated with general intellectual ability than with demographic variables.

Frontal lobe impairment in schizophrenia: relationship to intellectual functioning.

Schizophrenic subjects (N = 48) and individually matched healthy controls were administered the Verbal Scale of the Wechsler Adult Intelligence Scale (VIQ) and a test of verbal fluency. The verbal fluency and VIQ scores of the schizophrenic subjects were significantly lower than the scores of the control subjects. An additional sample of healthy subjects (N = 144) was used to generate a regression equation for the prediction of verbal fluency scores from Verbal IQ and age. The verbal fluency scores obtained by the schizophrenic subjects were significantly lower than the scores predicted from the regression equation, whereas a significant difference was not obtained in the matched controls. These results provide further evidence of frontal lobe dysfunction in schizophrenia.

Brain tumors in children and adolescents--III. Effects of radiation and hormone status on intelligence and on working, associative and serial-order memory.

The effects on intelligence and memory of two post-surgical conditions (radiation treatment, hormone deficiency and supplementation) were explored in 46 children and adolescents with tumors in a variety of brain sites. Verbal intelligence, but not non-verbal intelligence, varied positively with age at radiation treatment. Memory for word meanings was unrelated to either radiation history or to hormone status. Severe deficits in serial position memory occurred with impaired hormone function and an older age at tumor onset. Severe deficits in working memory were associated with a history of radiation and a principal tumor site that involved thalamic/epithalamic brain regions. Radiation treatment and hormone status affect later cognitive function in children and adolescents with brain tumors. Although the greater vulnerability of the verbal intelligence of the younger radiated child and the serial order memory of the child with later tumor onset and hormone disturbances remain to be explained, and although the form of the relationship between radiation and tumor site is not fully understood, the data highlight the need to consider the cognitive consequences of pediatric brain tumors according to a set of markers that include maturational rate, hormone status, radiation history, and principal site of the tumor.

Bovine neurophysin-II stimulates prolactin release without involvement of dopaminergic prolactin-release inhibiting factor receptor in the estradiol-primed male rat.

Neurophysins have been considered to be physiologically inert carrier proteins for the neurohypophysial hormones, oxytocin and vasopressin. We have observed that bovine neurophysin-II indirectly stimulates prolactin release in estradiol-primed male rats. The release of prolactin is regulated by a dual hypothalamic control system, the prolactin-release-inhibiting factor and the prolactin-releasing factor. We have tried to clarify whether neurophysin-II is acting through stimulation of prolactin-releasing factor by eliminating the possibility of dopaminergic prolactin release-inhibiting factor release. Male rats were primed with estradiol and functional dopaminergic prolactin release-inhibiting factor receptors were completely blocked by pretreatment with a large dose of pimozide (3 mg/kg), a dopaminergic receptor blocking agent. The neurophysin-II stimulated prolactin release in the rats which did not have any functional dopaminergic prolactin release-inhibiting factor receptors suggesting that neurophysin-II likely initiates a chain of events which eventually stimulates prolactin-releasing factor release since the possibility of involvement of the dopaminergic prolactin release-inhibiting factor system is eliminated. Opioids are known to be one of a chain of events which transmit external stress into a stimulation of prolactin release. Naloxone, a mu-receptor antagonist, was injected 20 min before neurophysin-II administration into rats which were primed with estradiol and pretreated with pimozide (3 mg/kg), but the naloxone administration did not block the prolactin release stimulated by neurophysin-II injection. This result indicates that opioids are not one of the chain of events between initiation of stimulation by neurophysin-II and prolactin release.

Regulation of pituitary alpha-subunit, beta-luteinizing hormone and prolactin messenger ribonucleic acid by gonadotropin-releasing hormone and estradiol in hypogonadal mice.

We have investigated the effects of three different GnRH injection regimens and the effects of estradiol benzoate (EB) on expression of the common alpha-subunit, beta-LH, and PRL genes in male and female hpg mice. GnRH was injected once daily (100 ng), every 2 h (100 ng) or every 30 min (25 ng), and EB (10 micrograms) was injected once daily. The effects of continuous exposure to the superactive agonist D-Trp6-GnRH released from microcapsules were also studied. Northern blot analysis showed that administration of GnRH increased alpha-subunit mRNA levels 2- to 10-fold in male and female hpg but not normal mice and had no significant effect on beta-LH or beta-TSH mRNA levels. The greatest increase in alpha-mRNA occurred when 100 ng GnRH were injected every 2 h and could be detected within 6 h of the first GnRH injection. More frequent injections (25 ng every 30 min) were less effective in increasing alpha-mRNA, as was prolonged exposure to the D-Trp6-GnRH superagonist. The increase in alpha-mRNA was associated with an increase in pituitary FSH content of similar magnitude. Continuous exposure of the pituitary gland to D-Trp6-GnRH (approximately 1500 ng/day) resulted in a smaller (2-fold) increase in alpha-mRNA and pituitary FSH content, suggesting that desensitization had occurred. EB had little effect on beta-LH mRNA and did not alter alpha-mRNA levels or affect the increase in alpha-mRNA caused by GnRH. Injection of GnRH every 2 h increased pituitary PRL mRNA levels in female but not male hpg mice, probably due to an indirect effect resulting from increased estrogen secretion. We conclude that GnRH administration to hpg mice significantly increases alpha-subunit but not beta-LH mRNA levels and that maximal effects occur with 100 ng GnRH injections every 2 h. Although EB does have direct effects upon pituitary gonadotropin content in hpg mice, the absence of significant changes in alpha- and beta-LH mRNA suggests that these effects may be largely posttranscriptional.

Morphine can stimulate prolactin release independent of a dopaminergic mechanism.

Prolactin release is controlled by prolactin-release inhibiting factor (PIF), possibly dopamine, and an unidentified putative hypothalamic prolactin-releasing factor (PRF). Morphine and related opioids may indirectly stimulate prolactin release by inhibiting PIF release and (or) by stimulating putative PRF release. In the present study, we have completely blocked the dopaminergic receptors in normal male rats by pretreatment with a large dose of pimozide (3 mg/kg) to demonstrate if putative PRF has a role in morphine-induced prolactin release. Morphine sulfate (10 mg/kg) was still able to stimulate prolactin release in the rat without any functional dopaminergic PIF receptors. When naloxone (3 mg/kg) was injected 20 min before the morphine in the pimozide-treated rat, plasma prolactin concentration was not affected by morphine indicating that the stimulatory effect of this opioid on prolactin release in the pimozide-pretreated rat was mediated by mu-receptors. We can conclude that morphine can stimulate prolactin release through a mechanism apparently independent of dopaminergic receptors, one possible route being through a putative PRF.

Bovine 'neurophysin II' stimulates growth hormone release in the estradiol-primed male rat.

Basal plasma concentrations of growth hormone (GH) were monitored in both normal and estradiol-primed male rats by the collection of sequential blood samples from freely moving rats, via chronic intraatrial cannulae. Blood was sampled every 2 min for a period of 80 min and plasma GH levels determined by radioimmunoassay. The normal male rats displayed a pulsatile release of GH, while the estradiol-primed male rats exhibited a relatively steady level of plasma GH concentration. The rats exposed to high levels of estradiol (1.59 +/- 0.42 nmol/l plasma) also had a higher mean value of basal GH concentration. An injection of 100 micrograms/kg of bovine neurophysin II did not alter GH release in the normal male rats. However, it did significantly elevate GH levels in the estradiol-primed animals to a mean peak level approximately six times the mean basal level. The administration of 100 micrograms/kg of bovine neurophysin I to estradiol-primed male rats did not produce any change in plasma GH levels and thus eliminates the possibility of the nonspecific stimulation of neurophysin II on GH release.

Current status of the rat prolactin releasing factor.

The release of prolactin is governed by both inhibiting and releasing factors. Basal plasma concentration of prolactin is controlled mainly through inhibition by a prolactin release-inhibiting factor (PIF), while acute stimulation of prolactin release is believed to be caused by a prolactin-releasing factor (PRF). It is the general consensus that PIF is dopamine. The PRF plays an important role in stimulation of prolactin release, and there are promising putative PRFs.

Pulsatile release of immunoreactive luteinizing hormone (irLH) in hypophysectomized male rats.

The concentration of plasma luteinizing hormone (LH) was monitored every minute by radioimmunoassay in male rats that were either hypophysectomized, or castrated and hypophysectomized. Castrated rats showed a pulsatile fluctuation of plasma immunoreactive LH (irLH) concentration with an elevated basal level, confirming previous work. The hypophysectomized and castrated hypophysectomized rats also showed pulsatile changes in plasma irLH concentration. This unexpected result indicates that ectopic irLH is not only actively released after hypophysectomy, but is released in pulses. The pulse interval was approximately 20 minutes for all 3 groups. The slope of the rate of decline of plasma irLH in the castrated rats is parallel to a theoretical disappearance rate of 5 min, while these slopes in the hypophysectomized and castrated hypophysectomized rats correspond to a 1 to 2-min disappearance rate. The difference in these slopes implies that the two irLH molecules may not be identical.

Bovine neurophysin II has prolactin-releasing activity in the estradiol-primed male rat.

In the course of the search for the prolactin-releasing factor (PRF), we noticed that the posterior pituitary contained strong PRF activity and subsequently traced this activity to that of bovine neurophysin-II (NP-II). NP-II prepared in our lab was judged to be a homogeneous preparation according to Sephadex G-75 gel filtration, DEAE ion exchange chromatography and polyacrylamide gel electrophoresis. While neurophysin-I (NP-I) injections of 100 micrograms/kg and 1,000 micrograms/kg elevated plasma prolactin in estradiol-primed male rats to 30% and 50% over the control value, respectively, NP-II doses of 100, 1,000 micrograms/kg increased plasma prolactin concentration in estradiol-primed male rats to 130% and 170% over the control value, respectively. The lowest dose of NP-II needed to increase plasma prolactin concentration was 10 micrograms/kg. Since neurophysin does not stimulate prolactin release from the ectopic pituitary under the kidney capsule nor from lactotrophs in a primary monolayer culture system, neurophysin is believed to act indirectly on the pituitary, presumably through a neurotransmitter and/or hypothalamic releasing (or inhibiting) factor. We propose that NP-II may be one element in the complex chain of the prolactin-releasing mechanism.

Surgery depresses pulsatile growth hormone release in rats for up to 2 days.

In order to study the pulsatile release of rat growth hormone in a stress-free environment, many investigators obtain sequential blood samples from individual rats bearing an indwelling, right atrial cannula. There has been little systematic study of the stressful effects of the cannulation procedure on the pulsatile release of rat growth hormone. We examined the acute and chronic effects of right atrial cannulation on growth hormone release in male rats by monitoring plasma growth hormone concentration at every 2 min. Right atrial cannulation was performed under ether anaesthesia. Blood was collected from the rats for a 2 h period (11.00-13.00 h), either immediately following, or 2, 3 or 7 days following the surgery. When blood was collected 7 days after surgery, growth hormone was released in large bursts. The amplitude of these bursts however, did not differ significantly from the bursts of growth hormone in rats cannulated 3 days prior to blood collection. On the other hand, the bursts of hormone release in rats cannulated immediately or 2 days before blood collection were significantly smaller in amplitude than those in rats cannulated 3 days before collection, but were not significantly different from each other. In many of the rats cannulated immediately before or 2 days before blood collection, pulsatile growth hormone release was completely suppressed. The results of the study suggest that blood sampling from right atrial cannulae to measure the plasma concentration of rat growth hormone should not be carried out until at least 3 days after the cannulation procedure.

Gamma-aminobutyric acid is not likely a physiological prolactin-inhibiting factor.

Basal plasma prolactin concentration is controlled by tonic inhibition. The major prolactin-inhibiting factor (PIF) is believed to be dopamine. Factors other than dopamine have also been suggested as possible physiological PIF. One of the major candidates for the nondopaminergic PIF is considered to be gamma-aminobutyric acid (GABA). We have carefully examined the possible physiological role of GABA by monitoring, at every 2 min, the circulating prolactin concentration after GABA administration, in conscious freely moving rats. GABA (0.1 or 1 g/kg) had no significant direct effect on plasma prolactin in rats in which the dopaminergic receptors were completely blocked by pimozide, nor in hypophysectomized rats in which a pituitary had been grafted under the kidney capsule and was therefore removed from any hypothalamic influence. The effects of bicuculline, a GABA-receptor-blocking agent, was examined in order to find out whether a tonic inhibition is exerted by GABA after elimination of tonic dopaminergic inhibition on prolactin secretion. The pimozide-treated rat in which the dopaminergic tone is completely eliminated did not show any prominent elevation of plasma prolactin concentration after bicuculline (300 micrograms/kg) administration. However, GABA did have an inhibitory effect in a primary pituitary cell monolayer culture system. Therefore, we conclude that GABA does not play a significant role as a physiological PIF and that the inhibitory effect of GABA in vitro is of a pharmacological nature.