Genetic and metabolic studies have been done on a large kindred in which several males are affected by a syndrome of borderline mental retardation and abnormal behavior. The types of behavior that occurred include impulsive aggression, arson, attempted rape, and exhibitionism. Analysis of 24-hour urine samples indicated markedly disturbed monoamine metabolism. This syndrome was associated with a complete and selective deficiency of enzymatic activity of monoamine oxidase A (MAOA). In each of five affected males, a point mutation was identified in the eighth exon of the MAOA structural gene, which changes a glutamine to a termination codon. Thus, isolated complete MAOA deficiency in this family is associated with a recognizable behavioral phenotype that includes disturbed regulation of impulsive aggression.

https://science.sciencemag.org/content/sci/262/5133/578.full.pdf

Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A

• Dysfunction of the central serotonergic system has been variously associated with depression and with suicidal and/or impulsive aggressive behavior. To evaluate central serotonergic function in relation to these variables, prolactin responses to a singledose challenge with fenfluramine hydrochloride (60 mg orally), a serotonin releasing/uptake-inhibiting agent, were examined in 45 male patients with clearly defined major affective (n = 25) and/or personality disorder (n 20) and in 18 normal male control patients. Prolactin responses to fenfluramine among all patients were reduced compared with responses of controls. Reduced prolactin responses to fenfluramine were correlated with history of suicide attempt in all patients but with clinician and selfreported ratings of impulsive aggression in patients with personality disorder only; there was no correlation with depression. These results suggest that reduced central serotonergic function is present in a subgroup of patients with major affective and/or personality disorder and is associated with history of suicide attempt in patients with either disorder, but with impulsive aggression in patients with personality disorder only.

Serotonergic Studies in Patients with Affective and Personality Disorders: Correlates with Suicidal and Impulsive Aggressive Behavior

Animal research suggests that central serotonergic neurons are involved in behavioral suppression, particularly anxiety-related inhibition. The hypothesis linking decreased serotonin transmission to reduced anxiety as the mechanism in the anxiolytic activity of benzodiazepines conflicts with most clinical observations. Serotonin antagonists show no marked capacity to alleviate anxiety. On the other hand, clinical signs of reduced serotonergic transmission (low 5-HIAA levels in the cerebrospinal fluid) are frequently associated with aggressiveness, suicide attempts, and increased anxiety. The target article attempts to reconcile such human and animal findings by investigating whether anxiety reduction or increased impulsivity is more Likely to account for animal behavioral changes associated with decreased serotonergic transmission. The effects of manipulating central serotonin in experimental anxiety paradigms in animals (punishment, extinction, novelty) are reviewed and compared with the effects of antianxiety drugs. Anxiety seems neither necessary nor sufficient to induce control by serotonergic neurons on behavior. Further evidence suggests that behavioral effects of anxiolytics thought to be mediated by decreases in anxiety are not caused by the ability of these drugs to reduce serotonin transmission. Blockade of serotonin transmission, especially at the level of the substantia nigra, results in a shift of behavior toward facilitation of responding. This behavioral shift is particularly marked when there is competition between acting and restraining response tendencies and when obstacles prevent the immediate attainment of an anticipated reward. It is proposed that serotonergic neurons are involved not only in behavioral arousal but also in enabling the organism to arrange or tolerate delay before acting. Decreases in serotonin transmission seem to be associated with the increased performance of behaviors that are usually suppressed, though not necessarily because of the alleviation of anxiety, which might contribute to the suppression.

Reconciling the role of central serotonin neurons in human and animal behavior

In traditional practices of Ayurvedic and Chinese medicine, numerous plants have been used to treat cognitive disorders, including neurodegenerative diseases such as Alzheimer's disease (AD). An ethnopharmacological approach has provided leads to identifying potential new drugs from plant sources, including those for cognitive disorders. Many drugs currently available in Western medicine were originally isolated from plants, or are derived from templates of compounds isolated from plants. Some anticholinesterase (anti-ChE) alkaloids isolated from plants have been investigated for their potential in the treatment of AD, and are now in clinical use. Galantamine, isolated from several plants including Lycoris radiata Herb., which was used in traditional Chinese medicine (TCM), is licensed in the United Kingdom for the treatment of mild to moderate AD. Various other plant species have shown pharmacological activities relevant to the treatment of cognitive disorders, indicating potential for therapeutic use in disorders such as AD. This article reviews some of the plants and their active constituents that have been used in traditional Ayurvedic medicine and TCM for their reputed cognitive-enhancing or antiageing effects. Plants and their constituents with pharmacological activities that may be relevant for the treatment of cognitive disorders, including enhancement of cholinergic function in the central nervous system (CNS), anti-inflammatory and antioxidant activities, are discussed.

Plants used in Chinese and Indian traditional medicine for improvement of memory and cognitive function.

OBJECTIVE: The authors describe the clinical characteristics of self-injurious behavior, giving special emphasis to self-injurious behavior occurring among individuals with character disorders. DATA COLLECTION: They review data suggesting the involvement of serotonergic, dopaminergic, and opiate neurotransmitter systems in the expression of self-injurious behavior. FINDINGS: Self-injurious behavior occurs among mentally retarded individuals, psychotic patients, prison populations, and individuals with severe character disorders. Although theoretical psychological models of self-injurious behavior are helpful in understanding the patient's experience of self-injury, no generally useful therapeutic approach has yet evolved from these models. Data derived from animal models and treatment studies suggest the involvement of opiatergic and dopaminergic mechanisms in self-injury among the mentally retarded. Serotonergic influences on self-injurious behavior may be present in varying forms of this behavior. The scientific literature on the benefits of pharmacological agents for mentally retarded individuals is beset with a number of problems. Support is emerging, however, for the use of lithium and carbamazepine with self-injuring mentally retarded patients, and some behavioral interventions appear to be successful for mentally retarded individuals. Self-injuring patients with borderline personality disorder may benefit from milieu treatment. CONCLUSIONS: Although no form of treatment has yet been demonstrated to be of general benefit, the literature suggests that therapeutic trials with dopamine antagonists, serotonin reuptake inhibitors, and opiate antagonists may be of value. Language: en

Self-injurious behavior: a review of the behavior and biology of self-mutilation.

Determination of rat brain tissue catecholamines using liquid chromatography with electrochemical detection

The effects of dietary excesses of tryptophan, histidine, tyrosine or choline and of a tryptophan-free diet were examined on shock-induced fighting, muricide and jump-flinch thresholds. Following the tryptophan-free diet, shock-induced fighting and pain sensitivity were specifically increased. The increased incidence of muricide was not specific to the lack of tryptophan in the diet. Groups of rats which were pair fed chow or had 0.15% L-tryptophan added to the tryptophan-free diet increased muricide as well. Brain 5-HT levels were 41% depleted following the tryptophan-free diet and reduced 13% with the 0.15% tryptophan supplement. In addition body weights were reduced in the three groups compared to control. None of the excess diets affected shock-induced fighting, muricide and jump-flinch thresholds. Body weights were decreased in the excess tryptophan, histidine, tyrosine and choline groups. These data indicate that the expression of different forms of aggression appears to be influenced by a tryptophan deficiency in the diet, but not excesses of tryptophan, tyrosine, histidine and choline.

Effects of dietary supplements and a tryptophan-free diet on aggressive behavior in rats.

Using two procedures known to enhance shock-induced defensive fighting (SIF) and mouse-killing--septal lesions and 5,7-DHT lesions--we determined if a 5% tryptophan-loaded diet could reverse the lesion effects. The results indicated that SIF, but not mouse-killing, could be maintained at normal levels following dietary tryptophan loading in both septally lesioned and 5,7-DHT lesioned rats. This behavioral reversal was independent of pain sensitivity, feeding, drinking and body weight levels. Regional brain analysis of monoamines and metabolites indicated that the lesions produced substantial depletions in 5-HT and 5-HIAA with minimal reduction or no change in catecholamines. Dietary tryptophan loading elevated 5-HT and 5-HIAA in unlesioned animals and partially restored 5-HT and 5-HIAA levels in lesioned animals. These patterns of depletion and repletion were confined to the hippocampus following septal lesions and distributed throughout the brain following 5,7-DHT lesions. The results are discussed in terms of a possible hippocampal mediation of the dietary tryptophan reversal in shock-induced defensive fighting following lesioning.

Dietary tryptophan reversal of septal lesion and 5,7-DHT lesion elicited shock-induced fighting.

The effects of a tryptophan-free diet on isolation-induced fighting and predatory cricket killing in mice were examined. The results demonstrated that consumption of a tryptophan-free diet for 18-20 days decreased both the number of fighters and duration of isolation-induced fighting; increased the number of cricket-killing mice and decreased the latencies to attack and the latencies to kill crickets; reduced brain serotonin 27%; increased water intake 38%; and decreased body weight 27% without affecting food intake. To determine if these effects were due specifically to the lack of dietary tryptophan, other groups of mice were fed a 5% tryptophan load in the standard chow; a 0.15% tryptophan supplement in the tryptophan-free diet; or a 3 grams/day restricted chow diet. The lack of tryptophan in the diet produced the marked inhibition in isolation-induced fighting, the reduction in brain serotonin, and the large decrease in body weight. The other non-specific effects appeared to be related to general factors such as dietary need for the cricket killing or diet composition (other than the lack of tryptophan) for the water intake.

Dietary tryptophan modulation and aggressive behavior in mice

The limbic system and aggression in humans.

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