Prenatal cocaine exposure disrupts the development of the serotonergic system

Akbari, Homayoon M.; Kramer, H. Kenneth; Whitaker‐Azmitia, Patricia M.; Spear, Linda P.; Azmitia, Efrain C.

doi:10.1016/0006-8993(92)90450-n

Cited by 138 publications

(55 citation statements)

References 40 publications

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“…This hypothesis has also been supported in animal studies [1,8,15,30,63,67,85,86,92,94]. The prefrontal cortex is one site that is thought to control arousal, attention, and mood, as well as executive functioning (the ability to plan and carry out actions) [17,23].…”

Section: Discussionmentioning

confidence: 77%

The effects of prenatal cocaine use on infant development

Richardson¹,

Goldschmidt²,

Willford³

2008

Neurotoxicology and Teratology

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This study examined the effect of prenatal cocaine use on infant physical, cognitive, and motor development, and temperamental characteristics, controlling for other factors that affect infant development. Women were, on average, 26.8 years old, had 12 years of education, and 46% were African American. During the first trimester, 18% were frequent users of cocaine (≥ 1 line/day). The infants were, on average, 14.6 months old at this follow-up phase. Women who used cocaine during pregnancy rated their infants as more fussy/difficult and unadaptable than did women who did not use cocaine. Cocaine use in the second trimester was associated with significantly lower motor scores on the Bayley Scales of Infant Development (BSID) [9]. There was no effect of prenatal cocaine use on BSID mental performance or on growth. These findings are consistent with other reports in the literature and with the hypothesis that prenatal cocaine exposure affects development through changes in neurotransmitter systems.

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Section: Discussionmentioning

confidence: 77%

The effects of prenatal cocaine use on infant development

Richardson¹,

Goldschmidt²,

Willford³

2008

Neurotoxicology and Teratology

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“…see Ref. [7]) likewise appears to increase into adolescence. Weanling rats exhibit only about 70% of adult levels of the DA transporter in PFC, ACC, and olfactory tubercles [102], while binding to the DA and 5HT transporters reach levels not significantly different from adults by early-mid adolescence (P28-35) [545].…”

Section: Alterations In Prefrontal Cortex and Limbic Brain Regionsmentioning

confidence: 89%

The adolescent brain and age-related behavioral manifestations

Spear

2000

Neuroscience & Biobehavioral Reviews

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4,301

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To successfully negotiate the developmental transition between youth and adulthood, adolescents must maneuver this often stressful period while acquiring skills necessary for independence. Certain behavioral features, including age-related increases in social behavior and risk-taking/novelty-seeking, are common among adolescents of diverse mammalian species and may aid in this process. Reduced positive incentive values from stimuli may lead adolescents to pursue new appetitive reinforcers through drug use and other risk-taking behaviors, with their relative insensitivity to drugs supporting comparatively greater per occasion use. Pubertal increases in gonadal hormones are a hallmark of adolescence, although there is little evidence for a simple association of these hormones with behavioral change during adolescence. Prominent developmental transformations are seen in prefrontal cortex and limbic brain regions of adolescents across a variety of species, alterations that include an apparent shift in the balance between mesocortical and mesolimbic dopamine systems. Developmental changes in these stressor-sensitive regions, which are critical for attributing incentive salience to drugs and other stimuli, likely contribute to the unique characteristics of adolescence. ᭧

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“…169 Several drug treatment studies have shown this negative feedback of 5-HT on development of 5-HTergic neurons. [170][171][172][173][174][175][176][177][178][179][180] Alterations in 5-HTT function 181 and hypothalamic 5-HT levels 182 may be in part responsible for altered HPA axis activity in adult PS offspring. 183 PS may lead to an altered set-point of the HPA axis and 5-HT system, increasing susceptibility to later (depressive) disorders.…”

Section: Stressmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

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Prenatal cocaine exposure disrupts the development of the serotonergic system

Cited by 138 publications

References 40 publications

The effects of prenatal cocaine use on infant development

The effects of prenatal cocaine use on infant development

The adolescent brain and age-related behavioral manifestations

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

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