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PubMed2002

Selective serotonin reuptake inhibitors decrease impulsive behavior as measured by an adjusting delay procedure in the pigeon.

The inability to delay gratification (reinforcement or reward) is one index of impulsive behavior. In order to measure the willingness of pigeons to delay reinforcement, an adjustable delay schedule was developed that allowed daily approximations of an indifference point between immediate brief access to reinforcer and delayed, longer access to reinforcer. Acute administration of the anxiolytic alprazolam (5 mg/kg) decreased the length of delay tolerated before a larger reinforcement. Likewise, acute administration of the anxiolytic chlordiazepoxide (10 mg/kg) produced a similar, although not significant, effect. Neither acute nor five daily injections of 8-OH-DPAT, a 5-HT(1A) agonist, or WAY100635, a 5-HT(1A) antagonist, affected the length of the delay period. Chronic (17 day), but not acute injections of the selective serotonin reuptake inhibitors (SSRIs) fluoxetine (10 mg/kg), citalopram (10 mg/kg) and paroxetine (3 mg/kg) increased the delay period. When given in addition to 1 mg/kg of 8-OH-DPAT, but not 1 mg/kg WAY100635, the effect of fluoxetine was accelerated in that the increase in delay was observed earlier in the treatment. These data support the use of SSRIs to decrease impulsive behavior. Addition of a 5-HT(1A) agonist, but not a 5-HT(1A) antagonist, to the SSRI may hasten the therapeutic activity of the SSRI in treating impulsivity.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1993

Tryptophanemia and tyrosinemia in adolescents with impulsive behavior.

Tryptophan (TRP) and tyrosine (TYR), respectively the circulating precursors of the central serotonergic (5-HT) and catecholamine systems, were measured in eight adolescents with impulsive behavior regardless of the exact type of disorder. The 6 week study period included weekly blood sampling and clinical evaluation. The ratios of TRP and TYR to large neutral amino acids (LNAA), which indicate the availability for the synthesis of neurotransmitters, were calculated. Comparison of results with eight hospitalized controls of the same age (12.5 to 18 years) revealed lower total TRP levels in four adolescent patients, a lower TRP/LNAA ratio in three adolescents, and a lower free TRP concentration in six adolescents with discretely enhanced albuminemia. A slight increase in TYR and the TYR/LNAA ratio was noted in nearly all of the adolescent patients. Despite the heterogeneity of individual biological results, the impulsive behavior subjects in this study seemed to present abnormalities in neurotransmitter precursors.

Adolescent↗
PubMed2000

Effects of dopaminergic drugs on delayed reward as a measure of impulsive behavior in rats.

RATIONALE: Impulsive individuals exhibit an exaggerated preference for immediate rewards over delayed but larger rewards, perhaps because they value the delayed rewards less. Dopamine (DA) has been postulated to mediate the incentive value of rewards, thus it may also mediate the exaggerated preference for immediate rewards in impulsive individuals. In this paper, we investigate the effects of DA agonists and antagonists on the value of delayed versus immediate rewards. OBJECTIVES: The study had three main objectives: (1) to determine the effects of D1 and D2 type DA antagonists on the value of delayed rewards, (2) to determine the effect of the indirect DA agonist d-amphetamine on the value of delayed rewards, (3) to determine the sensitivity of the adjusting amount (AdjAmt) procedure to acute one-day changes in delay to reward, amount of reward, deprivation level and starting amount. METHODS: In the AdjAmt procedure, rats choose between an adjusting amount of water given immediately (adjusting alternative) and a constant 150 microliters water delayed by 4 s (standard alternative). The immediate amount of water is adjusted across trials until the rat chooses both alternatives with equal frequency (indifference point). The final adjusted amount is an indicator of the subjective value of the standard alternative. RESULTS: The D1/D2 antagonist flupenthixol (25, 50, and 100 micrograms/kg) and the D2 antagonist raclopride (40, 80, and 120 micrograms/kg), decreased the indifference points, whereas the D1 antagonist SCH 23390 (5, 10, and 20 micrograms/kg) did not affect the indifference point. All three DA antagonists slowed responding. The indirect DA agonist amphetamine (0.5, and 1.0 mg/kg) had effects opposite to those of the DA antagonists, it decreased choice latency, increased the number of trials completed and increased the indifference point. Decreasing the water deprivation level (6, 24, and 48 h) had no effect on the indifference points but slowed responding. Increasing the delay to reward (2, 4, and 8 s) and decreasing the amount of water available for choosing the standard alternative (300, 150, 75 microliters) decreased the indifference point. CONCLUSIONS: The results indicate that amphetamine increased the value of delayed rewards (decreased impulsivity) and that D2 but not D1 receptor antagonists decreased the value of delayed rewards (increased impulsivity). The procedure was sensitive to acute 1-day changes in delay and magnitude of reward.

Amphetamine↗
PubMed2001

Ethanol consumption and behavioral impulsivity are increased in protein kinase Cgamma null mutant mice.

Etiological factors influencing the development of alcoholism are complex and, at a minimum, include an interaction between polygenic factors and personality and biological traits. Human and animal studies suggest that some genes may regulate both the traits associated with alcohol abuse, such as decreased sensitivity or anxiety, and vulnerability to alcoholism. The identification of these genes could elucidate neurochemical pathways that are important in the development of alcohol abuse. Results from the present study indicate that the gene encoding the neuronal-specific gamma subtype of protein kinase C (PKCgamma) influences both ethanol consumption and behavioral impulsivity, a personality characteristic associated with Type II alcoholics, in a pleiotropic manner. Mice lacking PKCgamma consume more ethanol in a two-bottle choice paradigm and also demonstrate increased behavioral impulsivity in an appetitive-signaled nosepoke task when compared with wild-type littermate control mice. Therefore, PKCgamma may be an important mechanism within the cell that mediates one or more neurochemical pathways relevant to an increased predisposition to alcoholism.

Administration, Oral↗
PubMed2003

Altered profiles of spontaneous novelty seeking, impulsive behavior, and response to D-amphetamine in rats perinatally exposed to bisphenol A.

Bisphenol A (BPA) is an environmental estrogen with potentially averse effects on public health. We studied the long-term effects of perinatal exposure to BPA on later behavior in adult rats of both sexes. BPA or vehicle was administered orally to mother rats from mating to pups' weaning, at a concentration (0.040 mg/kg) within the range of human exposure. The offspring of both sexes were tested at adolescence (postnatal days 35-45) for novelty preference (experiment 1). After a 3-day familiarization to one side of a two-chamber apparatus, on day 4 rats were allowed to freely explore the whole apparatus. BPA-exposed females spent significantly less time than did controls in exploration of the novel side (i.e., increased neophobia), whereas no effect was found in the male group. At adulthood, the same animals were food deprived and tested for profiles of impulsive behavior (experiment 2), in operant chambers provided with two nose-poking holes (delivering either five or one food pellet). After the establishment of a baseline preference for the large reinforcer, a delay was introduced before the delivery of the five food pellets, which was progressively increased each day (10, 20, 30, 45, 60, 80, 100 sec). As expected, all animals exhibited a progressive shift toward the immediate but smaller reinforcer. A reduced level of impulsive behavior (i.e., a shift to the right in the intolerance-delay curve) was evidenced in BPA-treated rats. The frequency of inadequate responding (during the length of the delay) also provided a measure of restless behavior. Interestingly, the profile of BPA-treated males was feminized, strongly resembling that of control females. Animals were then tested (experiment 3) for the response to an amphetamine challenge (1 mg/kg, subcutaneously). The drug-induced increment activity was significantly less marked in BPA-treated male rats compared with controls. These findings provide clear indirect evidence of long-term alterations in brain monoaminergic function after perinatal BPA exposure. This may be a cause for concern for public health, confirming that exposure to a weak environmental estrogen in the period of sexual differentiation of the brain can influence adult behavior.

Administration, Oral↗
PubMed1998

Lead, attention, and impulsive behavior: changes in a fixed-ratio waiting-for-reward paradigm.

Similar to the effects observed in children diagnosed with attention deficit hyperactivity disorder (ADHD), experimental animals exposed to lead (Pb) exhibit behaviors attributed to "impulsivity" and "inability to inhibit inappropriate responding." Such behaviors have led some to suggest that Pb exposure is associated with attention deficit. Based on the hypothesis that attention deficits are related to an ineffectiveness of delayed reinforcement, this study examined the effects of chronic postweaning Pb exposure on an FR waiting-for-reward paradigm. Rats were exposed chronically from weaning to 0, 50, or 150 ppm Pb acetate in water and following 40 days of exposure, trained on a fixed-ratio (FR) wait behavioral baseline. A total of 50 lever press responses (FR 50) produced food delivery. After earning an FR pellet, "free" pellets could be obtained by waiting; emission of another lever press reinitiated the FR requirement. "Free" pellets were delivered at increasing intervals (2 s, 4 s, 6 s, etc.). Pb exposure increased response rates on the FR schedule and decreased the mean longest waiting time, but also resulted in a higher number of responses per reinforcer than exhibited by controls. These Pb-induced differences are consistent with an inability to manage delays of reinforcement.

Animals↗
PubMed2006

1H MRS-detectable metabolic brain changes and reduced impulsive behavior in adult rats exposed to methylphenidate during adolescence.

Administration of methylphenidate (MPH, Ritalin) to children affected by attention deficit hyperactivity disorder (ADHD) is an elective therapy, which however raises concerns for public health, due to possible persistent neuro-behavioral alterations. We investigated potential long-term consequences at adulthood of MPH exposure during adolescence, by means of behavioral and brain MRS assessment in drug-free state. Wistar adolescent rats (30- to 44-day-old) were treated with MPH (0 or 2 mg/kg once/day for 14 days) and then left undisturbed until adulthood. Levels of impulsive behavior were assessed in the intolerance-to-delay task: Food-restricted rats were tested in operant chambers with two nose-poking holes, delivering one food pellet immediately, or five pellets after a delay whose length was increased over days. MPH-exposed animals showed a less marked shifting profile from the large/late to the small/soon reward, suggesting reduced basal levels of impulsivity, compared to controls. In vivo MRI-guided 1H MRS examinations at 4.7 T in anaesthetised animals revealed long-term biochemical changes in the dorsal striatum (STR), nucleus accumbens (NAcc), and prefrontal cortex (PFC) of MPH-exposed rats. Notably, total creatine and taurine, metabolites respectively involved in bioenergetics and synaptic efficiency, were up-regulated in the STR and conversely down-regulated in the NAcc of MPH-exposed rats. A strong correlation was evident between non-phosphorylated creatine in the STR and behavioral impulsivity. Moreover, unaltered total creatine and increased phospho-creatine/creatine ratio were detected in the PFC, suggesting improved cortical energetic performance. Because of this enduring rearrangement in the forebrain function, MPH-exposed animals may be more efficient when faced with delay of reinforcement. In summary, MPH exposure during adolescence produced enduring MRS-detectable biochemical modifications in brain reward-related circuits, which may account for increased self-control capacity of adult rats.

Animals↗
PubMed1998

Algorithms for pharmacological treatment of personality dimensions: symptom-specific treatments for cognitive-perceptual, affective, and impulsive-behavioral dysregulation.

A pharmacological approach to treating patients with personality disorders (PD) is based on evidence that some dimensions of personality are mediated by variations in neurotransmitter physiology and are responsive to medication effects. Target symptoms for pharmacotherapy in the PD patient are derived from expressions of cognitive-perceptual, affective, and impulsive-behavioral dysregulation of central neurotransmitter functions. Pharmacotherapy is directed at state symptoms during periods of acute decompensation and at trait vulnerabilities, which represent the diathesis to future episodes. A basic assumption of this approach is that neurotransmitter biology transcends Axis I and Axis II definitions and that closely related symptoms may share a common pathophysiology, independent of categorical definition. A common pathophysiology implies the possibility of shared responsiveness to medication. Using a dimensional definition of symptom domains, the author has developed treatment algorithms for cognitive-perceptual symptoms, affective dysregulation, and impulsive-behavioral dyscontrol in personality disorder patients.

Affective Symptoms↗
PubMed1999

Effects of methamphetamine on the adjusting amount procedure, a model of impulsive behavior in rats.

RATIONALE: Moderate doses of d-amphetamine (given both acutely and chronically) have been shown to decrease impulsivity in children with attention deficit hyperactivity disorder (ADHD) and to improve attention and learning in normal adults. In contrast, chronic doses of methamphetamine (METH) in drug abusers have been associated with increased impulsivity, and impairments in learning and attention. OBJECTIVES: We report the effects of METH on an animal model of impulsive behavior. METHODS: Rats were tested using the adjusting amount (AdjAmt) procedure in which the animals choose between a delayed fixed (large) amount of water and an immediate adjusting (small) amount of water. In the acute METH study, rats were given a single dose of 0.5, 1.0, 2.0, and 4.0 mg/kg METH or saline 30 min before testing. In the chronic METH study, we determined the effects of the 4.0 mg/kg dose of METH injected chronically 1 h after behavioral testing for 14 days. Thus the rats were tested using the AdjAmt procedure 22 h after injections of METH or saline. RESULTS: After 0.5, 1.0 and 2.0 mg/kg METH, the rats valued the delayed large rewards more than after saline, indicating that the METH decreased impulsiveness. At the 4.0 mg/kg dose, the rats failed to respond. Rats treated repeatedly with the post-session large behaviorally disruptive dose of METH valued the delayed large rewards less than the saline-treated rats, indicating that this dosing regimen of METH increased impulsiveness. CONCLUSIONS: In these experiments, the rats became less impulsive after acute non-disruptive doses of pre-session METH, whereas they became more impulsive after receiving repeated post-session injections of a dose that was behaviorally disruptive when administered acutely.

Animals↗
PubMed2005

Prostaglandin E receptor EP1 controls impulsive behavior under stress.

Animals under stress take adaptive actions that may lead to various types of behavioral disinhibition. Such behavioral disinhibition, when expressed excessively and impulsively, can result in harm in individuals and cause a problem in our society. We now show that, under social or environmental stress, mice deficient in prostaglandin E receptor subtype EP1 (Ptger1(-/-)) manifest behavioral disinhibition, including impulsive aggression with defective social interaction, impaired cliff avoidance, and an exaggerated acoustic startle response. This phenotype was reproduced in wild-type mice by administration of an EP1-selective antagonist, whereas administration of an EP1-selective agonist suppressed electric-shock-induced impulsive aggression. Dopamine turnover in the frontal cortex and striatum was increased in Ptger1(-/-) mice, and administration of dopaminergic antagonists corrected their behavioral phenotype. These results suggest that prostaglandin E(2) acts through EP1 to control impulsive behavior under stress, a finding potentially exploitable for development of drugs that attenuate impulsive behavior in humans.

Animals↗
PubMed2000

Gonadectomy enhances shock-induced behavioral inhibition in adult male rats: implications for impulsive behavior.

The effects of gonadectomy on shock-induced behavioral inhibition in a modified Vogel's drinking conflict model and on diazepam-induced disinhibition and sedation were investigated in adult male rats. Gonadectomy enhanced shock-induced behavioral inhibition when determined 9, 21, 45, and 65 days, but not 3 days, after operation, without affecting shock sensitivity or drinking motivation. Testosterone-substitution for 21 days following gonadectomy prevented this enhanced inhibition without significantly affecting the behavior in sham-operated rats. Diazepam produced behavioral disinhibition both in sham-operated and gonadectomized rats. However, after the highest dose (16 mg/kg, IP) the disinhibited behavior decreased only in sham-operated animals, most likely due to sedation. Moreover, whereas there was no difference in basal rotarod-performance between controls and gonadectomized rats, the latter animals were less sensitive to diazepam-induced disruption of rotarod walking ability. Sham-operated or gonadectomized animals did not differ with respect to serum diazepam levels at the postinjection times used in the behavioral tests. Taken together, gonadectomized rats were less sensitive towards diazepam-induced sedation, possibly due to a subsensitivity at or beyond GABA(A)/benzodiazepine receptors. Furthermore, the finding that lack of testosterone enhanced shock-induced inhibition could be interpreted to reflect increased impulse control and may involve an altered activation of GABA(A)/benzodiazepine receptors.

Animals↗
PubMed1988

Suicidal behavior, impulsiveness and serotonin.

The authors review the accumulating evidence from preclinical, clinical and postmortem studies suggesting that abnormality in serotonin systems may be associated with both attempts at suicide and aggression towards others and inanimate objects. Although these behaviors are multidetermined they often involve poor impulse control, which may reflect low central serotonin turnover. The need for further studies of possible peripheral biological markers for suicidal and impulsive behavior is discussed.

Female↗
PubMed2001

Electrophysiological assessment of impulsive behavior in healthy subjects.

The different concepts of impulsivity cover a wide range of divergent behaviors. In clinical terms, aspects of impulsivity are both an important feature in several psychiatric conditions related to a low central serotonergic neurotransmission like aggressive behavior and suicidality, and a core symptom of frontal lobe syndromes of various etiologies. Assessment of the different forms of impulsivity so far relies on clinical observations and self-rating questionnaires. Measurements of a distinct brain function associated with impulsive behavior are not available yet, however, electrophysiological parameters of cognitive response control elicited with the execution (Go-condition) and the inhibition (NoGo-condition) of a prepared motor response within the Continuous Performance Test (CPT) might be suitable candidates. By means of a spatial analysis method the centers of gravity (centroids) of the brain electrical fields evoked with Go- and NoGo-responses can be localized and quantified. In the present study, the Go- and NoGo-centroids and the impulsivity score in Eysenck's I(7)-scale were determined in 22 healthy subjects (10 women, 12 men, mean age 42.0+/-10.1 years). Impulsivity was correlated with both, a more anterior location of the Go- (r=0.58, P<0.01) and the NoGo-centroid (r=0.53, P=0.01). These results indicate, that in healthy subjects the amount of I(7)-impulsivity is associated with differences in the prefrontal brain activation pattern during cognitive response control. However, a replication study with a larger sample and an investigation of psychiatric patients with pathological levels of impulsivity are necessary to qualify these topographical ERP-parameters of cognitive response control as valid measures of the brain electrical basis of impulsive behavior.

Adult↗
PubMed1997

Low central nervous system serotonergic activity is traitlike and correlates with impulsive behavior. A nonhuman primate model investigating genetic and environmental influences on neurotransmission.

We have used nonhuman primates to examine developmental and behavioral correlates of CNS serotonergic activity, as measured by concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). These studies show that interindividual differences in CNS serotonin turnover rate exhibit traitlike qualities and are stable across time and settings, with interindividual differences in CSF 5-HIAA concentrations showing positive correlations across repeated sampling. Primates with low CNS serotonergic activity exhibit behaviors indicative of impaired impulse control, unrestrained aggression, social isolation, and low social dominance. Maternal and paternal genetic influences play major roles in producing low CNS serotonin functioning, beginning early in life. These genetic influences on serotonin functioning are further influenced by early rearing experiences, particularly parental deprivation.

Animals↗
PubMed1992

Self-destructive and impulsive behavior in the patient with a borderline personality disorder: rethinking hospital treatment and management.

This article reconsiders current approaches to the inpatient treatment and management of the patient with a borderline personality disorder. It is suggested that current approaches tend to be reactive rather than proactive. An alternative model based on a behavioral therapy program for chronic parasuicidal borderline women, is suggested. The approach reframes self-destructive behavior as a habitual response to overwhelming affect. By targeting core problems such as self-destructive and impulsive behaviors, nurses can help patients begin to consider alternative behavioral responses to intense stress.

Adaptation, Psychological↗
PubMed2000

Impulsivity and AMPA receptors: aniracetam ameliorates impulsive behavior induced by a blockade of AMPA receptors in rats.

The study aimed to ascertain the involvement of central AMPA receptors in impulsive behaviors of aged rats and to examine the effects of aniracetam. Premature response in the two-lever choice reaction task was assessed as an index of impulsivity. Intracerebroventricular injection of 2, 3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), an AMPA receptor antagonist, dose-dependently (10.1-1009 ng/rat) increased only premature response without altering responding speed and choice accuracy 30 min after the injection. Aniracetam (30 mg/kg p.o.), a positive allosteric modulator of AMPA receptors, or AMPA (55.9 ng/rat, co-injected with NBQX) completely restored the NBQX-induced increase in impulsivity. These results indicate that AMPA receptors are tonically involved in the regulation of impulsivity.

Animals↗
PubMed1990

Platelet imipramine binding in children and adolescents with impulsive behavior.

The serotonergic system has been implicated in the regulation of impulsive aggressive behavior either toward oneself or others. Imipramine binding sites were measured in the platelets of 23 impulsive aggressive children. Subjects ratings of total behavior, externalizing behavior, hostility, and aggression, as measured by the Child Behavior Checklist, were inversely correlated with the platelet imipramine binding. These findings are consistent with previous studies that suggest that decreased serotonergic activity is associated with impulsive aggressive behavior.

Adolescent↗