Behavioral Measures Of Anxiety Research Articles

Anxiogenic and stress-inducing effects of peripherally administered acetaldehyde in mice: Similarities with the disulfiram–ethanol reaction

Peripheral accumulation of acetaldehyde, the first metabolite of ethanol, produces autonomic responses in humans called “flushing”. The aversive characteristics of flushing observed in some populations with an isoform of aldehyde dehydrogenase (ALDH2) less active, are the basis for treating alcoholics with disulfiram, an ALDH inhibitor. Although ethanol and centrally formed acetaldehyde have anxiolytic effects, peripheral accumulation of acetaldehyde may be aversive in part because it is anxiogenic. ObjectivesWe investigated the effect of direct administration of acetaldehyde on behavioral measures of anxiety and on hormonal markers of stress in mice. The impact of disulfiram on the anxiolytic actions of ethanol was evaluated. Acetate (a metabolite of acetaldehyde) was also studied. MethodsCD1 male mice received acetaldehyde (0, 25, 50, 75 or 100mg/kg) at different time intervals and were assessed in the elevated plus maze and in the dark–light box. Corticosterone release after acetaldehyde administration was also assessed. Additional experiments evaluated the impact of disulfiram on the anxiolytic effect of ethanol (0 or 1mg/kg), and the effect of acetate on the plus maze. ResultsDirect administration of acetaldehyde (100mg/kg) had an anxiogenic effect at 1, 11 or 26min after IP administration. Acetaldehyde was ten times more potent than ethanol at inducing corticosterone release. Disulfiram did not affect behavior on its own, but blocked the anxiolytic effect of ethanol at doses of 30 and 60mg/kg, and had an anxiogenic effect at the highest dose (90mg/kg) when co-administered with ethanol. Acetate did not affect any of the anxiety parameters. ConclusionsPeripheral administration or accumulation of acetaldehyde produces anxiogenic effects and induces endocrine stress responses. This effect is not mediated by its metabolite acetate.

Single Units in the Medial Prefrontal Cortex with Anxiety-Related Firing Patterns Are Preferentially Influenced by Ventral Hippocampal Activity

The medial prefrontal cortex (mPFC) and ventral hippocampus (vHPC) functionally interact during innate anxiety tasks. To explore the consequences of this interaction, we examined task-related firing of single units from the mPFC of mice exploring standard and modified versions of the elevated plus maze (EPM), an innate anxiety paradigm. Hippocampal local field potentials (LFPs) were simultaneously monitored. The population of mPFC units distinguished between safe and aversive locations within the maze, regardless of the nature of the anxiogenic stimulus. Strikingly, mPFC units with stronger task-related activity were more strongly coupled to theta-frequency activity in the vHPC LFP. Lastly, task-related activity was inversely correlated with behavioral measures of anxiety. These results clarify the role of the vHPC-mPFC circuit in innate anxiety and underscore how specific inputs may be involved in the generation of behaviorally relevant neural activity within the mPFC.

DEVELOPMENTAL PROGRAMMING BY GLUCOCORTICOIDS: MODIFICATION OF POST-METAMORPHIC BEHAVIOR AND NEURAL GENE EXPRESSION AFTER EARLY-LIFE EXPOSURE TO CORTICOSTERONE IN THE FROG XENOPUS LAEVIS

Event Abstract Back to Event DEVELOPMENTAL PROGRAMMING BY GLUCOCORTICOIDS: MODIFICATION OF POST-METAMORPHIC BEHAVIOR AND NEURAL GENE EXPRESSION AFTER EARLY-LIFE EXPOSURE TO CORTICOSTERONE IN THE FROG XENOPUS LAEVIS Christina Silliman1*, Smita Mathews1, Rose Slupski1 and Robert J. Denver1 1 University of Michigan, United States Exposure to stressors early in life can have profound effects on later life phenotypic expression. The effects of stressors may be mediated by glucocorticoids acting to ‘program’ gene expression, leading to long term, stable changes in physiology and behavior. We established an experimental paradigm using the frog Xenopus laevis to investigate long term phenotypic consequences of early life exposure to elevated glucocorticoids. We treated early prometamorphic tadpoles with corticosterone (CORT; 100 nM) or vehicle (ethanol; 0.00025%) for 5 days by addition to the aquarium water, and then reared animals to 2 months post-metamorphosis. This dose of CORT elevated whole body CORT content within the physiological range, which mimicked changes in endogenous CORT following ecologically relevant stressors. CORT-treated animals were smaller than vehicle-treated controls at metamorphosis, but showed catch-up growth, reaching similar body size to controls by 2 months post-metamorphosis. Behavioral assays conducted on juvenile frogs showed that CORT-treated animals displayed significantly greater anxiogenic-like behavior than controls (quantified as time spent escaping from a negative stimulus vs. time at rest). Immunohistochemical analysis showed that early life CORT exposure decreased glucocorticoid receptor immunoreactivity (ir) in the anterior preoptic area, medial pallium and anterior pituitary. By contrast, CORT exposure increased corticotropin-releasing factor-ir in the medial amygdala and bed nucleus of the stria terminalis. Microarray analysis conducted on RNA extracted from the preoptic area/hypothalamus of juvenile frogs identified 47 genes that were differentially expressed between control and CORT-treated animals; 18 upregulated and 28 downregulated. Our findings show distinct physiological and behavioral changes following early life exposure to elevated CORT, and our molecular analyses support that these changes may reflect altered neural gene expression. Acknowledgements Supported by NSF grant IOS 0922583 to RJD References Blaser, R. E., L. Chadwick, et al. "Behavioral measures of anxiety in zebrafish (Danio rerio)." Behav Brain Res 208(1): 56-62. Hu, F., E. J. Crespi, et al. (2008). "Programming neuroendocrine stress axis activity by exposure to glucocorticoids during postembryonic development of the frog, Xenopus laevis." Endocrinology 149(11): 5470-81. Takahashi, L. K., N. H. Kalin, et al. (1989). "Corticotropin-Releasing Factor Modulates Defensive-Withdrawal and Exploratory-Behavior in Rats." Behavioral Neuroscience 103(3): 648-654. White, D. A., M. Kalinichev, et al. (2007). "Locomotor response to novelty as a predictor of reactivity to aversive stimuli in the rat." Brain Research 1149: 141-148. Keywords: Corticosterone, developmental programming, early-life stress, Xenopus laevis Conference: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology, Ann Arbor, United States, 13 Jul - 16 Jul, 2011. Presentation Type: Poster Topic: Stress hormones Citation: Silliman C, Mathews S, Slupski R and Denver RJ (2011). DEVELOPMENTAL PROGRAMMING BY GLUCOCORTICOIDS: MODIFICATION OF POST-METAMORPHIC BEHAVIOR AND NEURAL GENE EXPRESSION AFTER EARLY-LIFE EXPOSURE TO CORTICOSTERONE IN THE FROG XENOPUS LAEVIS. Front. Endocrinol. Conference Abstract: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology. doi: 10.3389/conf.fendo.2011.04.00047 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 15 Jul 2011; Published Online: 09 Aug 2011. * Correspondence: Ms. Christina Silliman, University of Michigan, Ann Arbor, United States, chansi@umich.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Christina Silliman Smita Mathews Rose Slupski Robert J Denver Google Christina Silliman Smita Mathews Rose Slupski Robert J Denver Google Scholar Christina Silliman Smita Mathews Rose Slupski Robert J Denver PubMed Christina Silliman Smita Mathews Rose Slupski Robert J Denver Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Synchronized Activity between the Ventral Hippocampus and the Medial Prefrontal Cortex during Anxiety

The ventral hippocampus, unlike its dorsal counterpart, is required for anxiety-like behavior. The means by which it acts are unknown. We hypothesized that the hippocampus synchronizes with downstream targets that influence anxiety, such as the medial prefrontal cortex (mPFC). To test this hypothesis, we recorded mPFC and hippocampal activity in mice exposed to two anxiogenic arenas. Theta-frequency activity in the mPFC and ventral, but not dorsal, hippocampus was highly correlated at baseline, and this correlation increased in both anxiogenic environments. Increases in mPFC theta power predicted avoidance of the aversive compartments of each arena and were larger in serotonin 1A receptor knockout mice, a genetic model of increased anxiety-like behavior. These results suggest a role for theta-frequency synchronization between the ventral hippocampus and the mPFC in anxiety. They are consistent with the notion that such synchronization is a general mechanism by which the hippocampus communicates with downstream structures of behavioral relevance.

Behavioral measures of anxiety in zebrafish (Danio rerio)

While zebrafish may be a useful behavioral model of human anxiety, it is not obvious which behaviors are accurate measures of anxiety in zebrafish. Beginning with the premise that the most fundamental indicator of fear is avoidance, the goal of the current study was to determine which behaviors are systematically observed in the presence of an avoided stimulus. In a dark/bright preference task, adult zebrafish preferred a black chamber and avoided a white chamber. Then, subjects were confined to each chamber, and their behaviors recorded. A principal component analysis was used to determine which behaviors clustered with the tendency to avoid white. Additionally, the behaviors of High-avoidant and Low-avoidant animals were compared using analysis of variance. Results indicate that confinement to white systematically elicited freezing in animals with a strong dark preference, but not in animals with little preference. Turn rate (erratic movement) was weakly related to avoidance, while thigmotaxis and locomotor activity were poor predictors. Freezing is therefore suggested to be a viable measure of white-induced anxiety, while interpretation of the other behaviors is more ambiguous and will require further investigation.

Interoceptive Sensitivity Modulates Anxiety During Public Speaking

This study explored the relationship between interoceptive sensitivity and the experience of public-speaking anxiety. We compared participants with high and low interoceptive sensitivity concerning self-report and behavioral measures of anxiety and concerning physiological variables before, during, and after a public-speaking task. Participants with high interoceptive sensitivity reported significantly less state anxiety before and after performing a public speech as well as less habitual public-speaking anxiety. No significant differences in behavioral or physiological measures were observed. We assume that individuals with high interoceptive sensitivity, to whom physiological signals are more easily accessible, experience less uncertainty during public speaking and can thus adjust their emotional processes more adequately. This finding appears in line with Damasio’s somatic marker hypothesis, which suggests that reasoning, decision-making, and social behavior are optimized by body-related signals in complex situations.

Effect of medication and psychotherapy on heart rate variability in panic disorder

Panic disorder (PD) patients have been shown to have reduced heart rate variability (HRV). Low HRV has been associated with elevated risk for cardiovascular disease. Our aim was to investigate the effects of treatment on heart rate (HR) in patients with PD through a hyperventilation challenge. We studied 54 participants, 43 with Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) PD and 11 controls. Subjects lay supine with their heads in a plastic canopy chamber, resting for 15 min and then breathing at a rate of 30 breaths per minute for 10 min. HRV was sampled for spectral analysis. Clinical and behavioral measures of anxiety were assessed. Treatment was chosen by patients: either 12 weeks of CBT alone or CBT with sertraline. All patients showed significant decrease on clinical measures from baseline and 31 were treatment responders, 8 dropped out of the study before completion of the 12-week treatment phase and 4 were deemed nonresponders after 12 weeks of treatment. Although both treatments led to significant clinical improvement, only CBT alone demonstrated a significant reduction in HR and increase in HRV. Our study replicated the finding that increased HR and decreased HRV occur in PD patients. Given the evidence of cardiac risk related to HRV, CBT appears to have additional benefits beyond symptom reduction. The mechanisms of this difference between CBT and sertraline are unclear and require further study.

The CRF1 receptor antagonist R121919 attenuates the neuroendocrine and behavioral effects of precipitated lorazepam withdrawal

Corticotropin-releasing factor (CRF) is the primary physiologic regulator of the hypothalamic-pituitary-adrenal (HPA) axis and serves to globally coordinate the mammalian stress response. Hyperactivity of central nervous system CRF neurotransmission, acting primarily via the CRF(1) receptor, has been strongly implicated in the pathophysiology of depression and anxiety. Furthermore, there is evidence of enhanced CRF transcription, release, and neuronal activity after the administration of and withdrawal from several drugs of abuse, including cannabis, cocaine, ethanol, and morphine. Treatment with CRF antagonists has been demonstrated to reduce the severity of certain drug withdrawal symptoms, implicating a specific role for activation of CRF neurons in mediating the anxiogenic and stress-like reactions observed after abrupt drug discontinuation. To extend these findings, we investigated whether pretreatment with the selective CRF(1) receptor antagonist R121919 decreases the behavioral and neuroendocrine activation observed after the precipitation of benzodiazepine (BZ) withdrawal in BZ-dependent rats. Pretreatment with R121919 attenuated the subsequent HPA axis activation, behavioral measures of anxiety, and expression of the CRF gene in the paraventricular nucleus of the hypothalamus, as measured by CRF heteronuclear RNA, which occurs after flumazenil-precipitation of withdrawal from the BZ, lorazepam. These results indicate that the activation of CRF neuronal systems may be a common neurobiological mechanism in withdrawal from drugs of abuse and moreover, that the CRF(1) receptor subtype plays a major role in mediating the effects of CRF on neuroendocrine and behavioral responses during BZ withdrawal. Therefore, CRF(1) receptor antagonists may be of therapeutic utility in the treatment of drug withdrawal syndromes.

Localized injections of midazolam into the amygdala and hippocampus induce differential changes in anxiolytic-like motor activity in mice

Various strains of mice display a reliable increase in motor activity in response to benzodiazepines given at low to moderate doses. This hyperactivity has been described as both an anxiolytic-associated increase in exploratory activity and a nonspecific stimulant effect controlled by central neural mechanisms separate from those involved in the anxiolytic-like effects. The purpose of the current study was to investigate the neural circuitry underlying the hyperactivity effects of benzodiazepines in mice. Specifically, we examined the relationship between anxiety and motor activity after bilateral intra-amygdala or intra-hippocampal microinjections of the nonselective full benzodiazepine receptor agonist midazolam in C57BL/6 mice. Behavioral measures of anxiety and motor activity in open field were examined in mice given localized injections of 0, 2, 8 or 32 nmol of midazolam directed into the amygdala or hippocampus. Midazolam injected into the amygdala at the low dose produced an anxiolytic-like effect, as reflected by an increase in central open field activity. Higher doses injected into the amygdala produced a motor-depressant action, indicative of a drug-induced sedative effect. Infusions into the hippocampus produced a biphasic effect on motor activity with the two lower doses of midazolam producing a motor-stimulant action and the high dose producing a motor-depressant effect. Hippocampus injections produced no anxiolytic-like effects. The current findings demonstrate that injections of midazolam produced a regional dissociation of the anxiety-related and motor-related parameters and provide evidence that the stimulant and anxiolytic effects of benzodiazepines are independent phenomena regulated by different central mechanisms.

Stress During Gestation Alters Postpartum Maternal Care and the Development of the Offspring in a Rodent Model

Epidemiological studies suggest that environmental adversity can alter parental care and thus influence child development. We addressed the question of whether stressors can directly affect parental behavior using a rodent model of stable, individual differences in maternal behavior. Lactating rat mothers were characterized as high or low in pup-directed licking/grooming (LG) behavior, rebred, and subjected to 7 days of intermittent stress or control conditions during gestation. Female rats were mated a third time without any subsequent intervention. Maternal behavior, oxytocin receptor (OTR) binding, and offspring behavior were examined. Stress reduced OTR levels and pup LG of high LG mothers to levels comparable with those of low LG mothers. The adult offspring of the gestational stress/high LG mothers resembled those of low LG mothers on behavioral measures of anxiety and maternal behavior, as well as OTR levels. The results of the third mating revealed an enduring effect of gestational stress on both mother and offspring maternal LG. These findings suggest that stress can directly alter maternal care through the neuroendocrine systems that normally regulate this behavior. Thus, the effects of environmental adversity can be transmitted across generations through a nongenomic mechanism involving maternal care.

Single or multiple reproductive experiences attenuate neurobehavioral stress and fear responses in the female rat

The female brain is a dynamic structure, which expresses its plasticity most readily following reproductive experience (RE). In Experiment 1, we generated nulliparous (NP), primiparous (PP), and multiparous (MP) females (none, one, and two litters, respectively). Two weeks following the weaning of the first/second six-pup litters, the age-matched MP and PP and the non-pup-exposed NP animals were subjected to a 60-min restraint stress paradigm (enclosure in a Plexiglas restraint tube). The brains were removed and processed for c-fos immunoreactivity ( c-fos-IR) in CA3 region of the hippocampus (HI) and in basolateral amygdala (BLA). MP and PP females had very similar numbers of c-fos-IR neurons in both HI and BLA, whereas both were lower than NPs. In a second experiment, the same groups were generated, together with primigravid (PG; first pregnancy) and multigravid (MG; second pregnancy) females, tested in late pregnancy. The animals were exposed to a 30-min trial in an open field and were killed, and the brains were again examined for c-fos-IR. The parous and gravid animals displayed less reactivity to the stress of the open field (i.e., reductions in behavioral measures of anxiety) and significantly less c-fos expression in both CA3 and BLA. The gravid animals displayed significantly less c-fos expression in CA3 and BLA compared to parous females, although neither group differed as a result of a second RE. The data suggest that reproductive (viz., hormonal) and/or maternal (viz., pup exposure) experience may inure a female and her brain to stress, rendering her less susceptible to the behavioral—or other—disruptions that stress sensitivity can produce. Together, these data suggest that the experiences of motherhood (pregnancy, pup exposure, suckling stimulation, etc.) summate to produce reductions in anxiety and stress responsiveness that start before and last long after pup exposure and care. Such reductions may be adaptive in the face of demands placed upon the parous vs. the NP female.

Increased anxiety and "depressive" symptoms months after MDMA ("ecstasy") in rats: drug-induced hyperthermia does not predict long-term outcomes.

There is some uncertainty whether the acute hyperthermia caused by MDMA (ecstasy) plays a significant role in determining the long-term neurotoxic effects on brain 5-HT systems and associated changes in mood and behaviour. The present study assessed whether long-term behavioural and cognitive changes seen in MDMA-treated rats are affected by hyperthermia at the time of drug administration. Male Wistar rats were treated with MDMA (4x5 mg/kg i.p. over 4 h on 2 consecutive days) or vehicle at either a high ambient temperature (28 degrees C) or a low ambient temperature (16 degrees C). Eight to 18 weeks later, rats were tested in behavioural measures of anxiety (social interaction and emergence tests), a test of cognition (object recognition test) and the forced swim test of depression. At the conclusion of behavioural testing the rats were killed and their brains analysed using HPLC. MDMA treatment caused a clear and consistent hyperthermia at 28 degrees C and hypothermia at 16 degrees C. Months later, rats pre-treated with MDMA at either 16 or 28 degrees C displayed increased anxiety in the social interaction and emergence tests and reduced escape attempts and increased immobility in the forced swim test. MDMA pre-treatment was also associated with poorer memory on the object recognition test, but only in rats given the drug at 28 degrees C. Rats pre-treated with MDMA showed loss of 5-HT in the hippocampus, striatum, amygdala and cortex, regardless of body temperature at the time of dosing. However, 5-HIAA loss in the amygdala and hippocampus was greater in rats pre-treated at 28 degrees C. Dopamine in the striatum was also depleted in rats given MDMA. These results indicate that hyperthermia at the time of dosing with MDMA is not necessary to produce subsequent 5-HT depletion and anxiety in rats. They also extend previous findings of long-term effects of brief exposure to MDMA in rats to include apparent "depressive" symptoms in the forced swim model.

Manipulation of focus of attention and its effects on anxiety in high-anxious individuals and repressors

There were four groups of participants: low-anxious (low anxiety-low defensiveness), repressors (low anxiety-high defensiveness), high-anxious (high anxiety-low defensiveness), and defensive high-anxious (high anxiety-high defensiveness). They were exposed to self-focus and other-focus conditions, and self-report, physiological, and behavioural measures of anxiety were recorded. The focus manipulation (self vs. other) was effective, with all four groups having higher self-reported anxiety in the self-focus condition. It was found that self-focused attention accounted for a significant amount of variation in self-reported anxiety. The findings were discussed within the theoretical framework proposed by Eysenck (1997).

Brain Metabolism of Progesterone, Coping Behaviour and Emotional Reactivity in Male Rats from Two Psychogenetically Selected Lines

Brain metabolites of progesterone such as tetrahydroprogesterone (THP) act on GABAA receptors and have anxiolytic properties. The formation of THP and its 5 alpha-reduced precursor, dihydroprogesterone (DHP) was measured in vitro in various microdissected brain areas obtained from males of two psychogenetically selected rat lines, i.e. the Roman High-(RHA/Verh) and low-(RLA/Verh) Avoidance rats, which are known to differ in emotional reactivity and/or anxiety. The behavioural and neuroendocrine responses of these rats were also measured following exposure to a novel environment in two different test situations. The formation of DHP and THP was found to be significantly higher in the frontal cortex (FCX), and DHP in the bed nucleus of the stria terminalis (BST), of the hypoemotional RHA/Verh rats. In addition, enzymatic activity in the FCX was found to be inversely correlated with behavioural measures of anxiety. These results suggest that individual, possibly genetically-determined differences in brain production of endogenous anxiolytics derived from progesterone may account at least in part for the behavioural differences characterizing these two lines, and provide further evidence that neurosteroids acting on the GABAergic system may play an important role in modulating physiological and/or behavioural responses to environmental stressors.

Complex effects of GABA-ergic agents on anxiety

The paper reviews the role of GABA-ergic mechanisms in anxiety and summarizes the data on complex bimodal effects produced by GABA-ergic agents on receptors and behavioral measures of anxiety. Possible physiological mechanisms of such effects on anxiety have been discussed. The paper reviews some paradoxical anxiotropic effects produced by certain GABA-ergic agents in behavioral tests of anxiety. Currently existing traditional views on GABA-ergic mechanisms that underlie anxiety and anxiety-related states are critically re-considered.

Behavioral measures of anxiety during opiate withdrawal

Heightened anxiety is a major component of the withdrawal syndromes associated with ethanol and sedative hypnotic medications. Because of similarities between the opiate and sedative-hypnotic withdrawal syndromes as well as data implicating heightened noradrenergic tone with opiate withdrawal, we investigated changes in anxiety measures identified by plus-maze and social interaction testing during opiate withdrawal. Because Sprague Dawley rats had very low levels of entry into plus-maze open arms, further studies were conducted using the Long-Evans strain. Long-Evans rats received continuous infusions of morphine sulfate at 44 mg/kg per day delivered by osmotic pump over 7 days while control animals received inert implants. During the first 3 days of withdrawal, the number and time of entries into open and closed arms of a plus-maze was recorded. Both social and aggressive behaviors were scored during pairings of groups of two socially naive animals. Body weight was significantly reduced in morphine-treated animals prior to and during withdrawal. Both the number of entries into open plus-maze arms and the time spent in open areas increased over the 3 days of testing. However, no difference in plus-maze activity was detected between morphine-treated and control subjects. On the third day of withdrawal, social interaction time was greater in pairs of withdrawn and control subjects compared to pairs of two control subjects. In conclusion, behavioral measures of anxiety are not increased during opiate withdrawal.

Does behavioral treatment of social phobia lead to cognitive changes?

Little is known about specific effects of behavioral and cognitive treatment methods. The goal of this study was to examine the effect of a “pure” performance-based exposure treatment (i.e., without cognitive intervention) on the anxiety-related cognitions of subjects with social phobia (public speaking anxiety). Thirty-six such persons were recruited. Pairs of subjects matched by age, sex, and severity of phobia were randomly assigned to either a treatment or waiting-list control group. Eighteen people received a purely behavioral treatment for 8 sessions over a period of 8 weeks; 18 served as the wait-list control group. Before and after treatment, subjective, cognitive, and behavioral measures of anxiety were taken. Results showed that a purely behavioral treatment led to improvement in measures of behavioral, subjective, and cognitive anxiety. This research adds to the literature on cognitive or behavioral treatment of social phobia showing that cognitive restructuring can occur without specific cognitive treatment, and that interventions for phobia are not necessarily mode specific.

Does Behavioral Treatment of Social Phobia Lead to Cognitive Changes?

Examined the effect of a pure performance-based exposure treatment (i.e., without cognitive intervention) on the anxiety-related cognitions of 36 adults (mean age 46.57 yrs) with social phobia (public speaking anxiety). Pairs of Ss matched by age, sex, and severity of phobia were randomly assigned to either a treatment or waiting-list control group. 18 Ss received a purely behavioral treatment for 8 sessions over 8 weeks. Subjective, cognitive, and behavioral measures of anxiety were taken pre- and post-treatment. Results show that a purely behavioral treatment led to improvement in measures of behavioral, subjective, and cognitive anxiety. This research adds to the literature on cognitive or behavioral treatment of social phobia showing that cognitive restructuring can occur without specific cognitive treatment, and that interventions for phobia are not necessarily mode-specific.

Comparison of alcohol-preferring (P) and nonpreferring (NP) rats on tests of anxiety and for the anxiolytic effects of ethanol

Rats of the selectively bred alcohol-preferring P and alcohol-nonpreferring NP lines were evaluated using three different behavioral measures of anxiety. Compared with NP rats, P rats (1) showed greater footshock-induced suppression of operant responding in an approach-avoidance conflict test; (2) spent less time in the open arms of an elevated plus maze; and (3) took longer in a passive avoidance test to step down from a platform to a grid floor where footshock was received 24 hours earlier. These findings indicate a greater degree of anxiety in the P than in the NP line of rats in these situations. Pretreatment with intraperitoneal (IP) ethanol (0.5–1.0 g/kg) injections produced anticonflict or anxiolytic effects in P but not in NP rats. However, the anticonflict effects of ethanol were small relative to those produced by chlordiazepoxide (CDP, 7.5 mg/kg) in both lines. The results demonstrate that selective breeding for divergent oral ethanol preference has produced associated differences between the P and NP lines of rats in behavioral tests of anxiety and in the anxiolytic effects of ethanol.

Social-desirability responding in the assessment of social skill and anxiety.

The present study examines the relationship between social-desirability responding and both self-report and behavioral measures of assertion, conversational skill, and social anxiety. With one exception (Conflict Resolution Inventory-Nonassertion Scale), behavioral and self-report measures of assertion were unrelated to the social-desirability response set. Global but not specific behavioral measures of conversational skill were confounded with social-desirability responding. Self-report (e.g., Social Avoidance and Distress Scale) but not behavioral measures of anxiety were correlated with social-desirability scores. The need to evaluate further the psychometric properties of cognitive-behavioral measures is discussed.