Stress during pregnancy: effect on catecholamines in discrete brain regions of offspring as adults

Moyer, John A.; Herrenkohl, Lorraine Roth; Jacobowitz, David M.

doi:10.1016/0006-8993(78)90446-8

Cited by 81 publications

(23 citation statements)

References 16 publications

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“…Environmental stressful events during critical periods of development produce enduring neuroendocrinological and neurodevelopmental changes that could influence drug reward responsivity and propensity to addiction (Fride and Weinstock 1989;Henry et al 1994;Moyer et al 1978). Prenatal stress has been found to have long-term effects on the activity of the DA system and on DA-related behaviors (Fride and Weinstock 1989;Moyer et al 1978).…”

Section: Developmental Factors and Rewardmentioning

confidence: 99%

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Drug Addiction, Dysregulation of Reward, and Allostasis

Koob

Moal

2001

Neuropsychopharmacology

2,564

1,962

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This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drugtaking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to BACKGROUNDDrug addiction is a chronically relapsing disorder that is defined by two major characteristics: a compulsion to take the drug with a narrowing of the behavioral repertoire toward excessive drug intake, and a loss of control in limiting intake (American Psychiatric Association 1994; World Health Organization 1992). An important challenge for neurobiological research is to understand the neuroadaptive differences between controlled drug use and loss of control, and by extension, the molecular, cellular and system processes that lead to addiction (Koob and Le Moal 1997).Animal models are critical for understanding the neuropharmacological mechanisms involved in the development of addiction. While there are no complete animal models of addiction, animal models do exist for many elements of the syndrome. These elements can be derived from symptoms or diagnostic criteria for addiction or conceptual frameworks such as different sources of reinforcement (American Psychiatric Association 1994; World Health Organization 1992). Linking neu- 24 , NO . 2 ropharmacological events to animal models can occur at multiple levels of analysis -molecular, cellular and system -and it will only be the integration of these changes across dimensions of analysis that will allow a full understanding of the neurobiology of drug addiction.Advances in neuroscience research are rapidly unr...

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Section: Developmental Factors and Rewardmentioning

confidence: 99%

“…Prenatal stress has been found to have long-term effects on the activity of the DA system and on DA-related behaviors (Fride and Weinstock 1989;Moyer et al 1978). Moreover, there is evidence that prenatal stress increases and prolongs corticosterone secretion in response to stress (Henry et al 1994).…”

Section: Developmental Factors and Rewardmentioning

confidence: 99%

Drug Addiction, Dysregulation of Reward, and Allostasis

Koob

Moal

2001

Neuropsychopharmacology

2,564

1,962

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“…Compared with unstressed controls, prenatally stressed rats showed changes in serotonergic and catecholaminergic systems (Herrenkohl, Ribary , Schlumpf, & Lichtensteiger, 1988;Moyer, Herrenkohl, & Jacobowitz, 1978;Peters, 1986b) as well as in the number of benzodiazepine and opiate receptors (Fride, Dan, Gavish, & Weinstock, 1985;tnsel, Kinsley, Mann, & Bridges, 1990). Further, changes in corticosterone plasma levels induced by stressors are larger in prenatally stressed rats when compared with unstressed controls (Peters, 1982;Fride, Dan, Feldon, Halevy, & Weinstock, 1986;Takahashi, Kalin, Barksdale, & vanden Burgt, 1988).…”

Section: Introductionmentioning

confidence: 97%

Prenatal stress effects on exploratory activity and stress‐induced analgesia in rats

Szuran¹,

Zimmerman²,

Pliška³

et al. 1991

Developmental Psychobiology

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Pregnant rats were exposed three times daily to immobilization stress during gestational Days 15-19. The behavior of their offspring was compared with the behavior of offspring from unstressed control mothers. Although the stress procedure decreased the weight gain of mothers during pregnancy, it slightly but significantly increased the weight of their offspring at birth and at weaning. On postnatal Day 10, prenatally stressed pups returned to their home cage more quickly than did prenatally unstressed control pups during a nest odor discrimination task, but no differences between groups in the number of correct responses were found. On postnatal Days 70-72, prenatally stressed offspring showed increased exploratory activity in a complex tunnel maze compared with control offspring. On postnatal Day 80, analgesia induced by stress (swimming for 3 min in cold water) was determined (tail flick latency). The degree of stress-induced analgesia was smaller in prenatally stressed rats than in control rats. These data suggest that the effects of prenatal stress on behavior are most clearly discernable when such animals are confronted with a novel or stressful situation.

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“…The relationship between prenatal anxi ety on the part of the mother and neonatal development and behavior has been more fully explored in animal models, particularly rodents [7], Effects that have been observed in the offspring of experimentally stressed pregnant females include feminization of males [8,9], and reduced fertility and fecun dity [10]: other observations more closely approximate those from the human studies, namely, growth retardation [11] and behav ioral changes including greater emotionality and decreased learning ability in infancy [5]. The stressors that appear to cause emotional upset in animals encompass a vast range of socioenvironmental factors [cf.…”

mentioning

confidence: 99%

Prenatal Psychological Stress, Dermatoglyphic Asymmetry and Pregnancy Outcome in the Pigtailed Macaque (<i>Macaca nemestrina</i>)

Newell‐Morris

Fahrenbruch

Sackett³

1989

Neonatology

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The relationships between maternal psychosocial stress during pregnancy and asymmetry in dermal ridge count, gestation length, birth weight percentile and survival were examined in 68 pigtailed macaque offspring. Twenty-five pregnant females were stressed daily by capture from 30 through 130 days postconception; 43 control unstressed females were housed under conditions of minimal disturbance. The difference between total intercore dermal ridge counts between right and left hands of the offspring was used as a measure of the perturbed development that theoretically occurs in the presence of a prenatal stressor. Dermatoglyphic asymmetry was significantly higher in the stressed offspring than in the unstressed group (mean asymmetry = 7.3 ± 2.8 and 5.4 ± 2.5, respectively; t = 2.85, p < 0.01). Although maternal stress alone was not related to differential gestation length, birth weight, or survival, high asymmetry (8–13 residual dermal ridges) was significantly associated with increased perinatal mortality.

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Stress during pregnancy: effect on catecholamines in discrete brain regions of offspring as adults

Cited by 81 publications

References 16 publications

Drug Addiction, Dysregulation of Reward, and Allostasis

Drug Addiction, Dysregulation of Reward, and Allostasis

Prenatal stress effects on exploratory activity and stress‐induced analgesia in rats

Prenatal Psychological Stress, Dermatoglyphic Asymmetry and Pregnancy Outcome in the Pigtailed Macaque (<i>Macaca nemestrina</i>)

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