Nicotine treatment counteracts perinatal asphyxia-induced changes in the mesostriatal/limbic dopamine systems and in motor behaviour in the four-week-old male rat

Chen, Y; Ögren, Sven Ove; Bjelke, Börje; Bolme, Per; Eneroth, P.; Gross, Johann; Loidl, Fabián; Herrera‐Marschitz, Mario; Andersson, Kurt

doi:10.1016/0306-4522(95)00118-3

Cited by 59 publications

(34 citation statements)

References 39 publications

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“…to the one used in the current study, rat neonates are able to survive up to 20-22 min of added anoxia, without artificial resuscitation (Loidl et al 1994;Boksa et al 1995;Chen et al 1995Chen et al , 1997. However, guinea pigs survived only 2 min of birth anoxia due to the relative maturity of guinea pig CNS at birth.…”

Section: Discussionmentioning

confidence: 68%

“…Using a rat model of global hypoxia during Caesarean section (C-section) birth, several laboratories have demonstrated that dopaminergic systems are sensitive to mild birth alterations (Bjelke et al 1991;Loidl et al 1994;Chen et al 1995Chen et al , 1997 Brake et al 1997a,b; Boksa 1997, 1998;Vaillancourt and Boksa 1998; Berger et al 2000a). Specifically, as adults, rats born by C-section, either with or without addition of a period of global hypoxia, show increased nucleus accumbens dopamine (DA) release in response to repeated stress (Brake et al 1997b) Vaillancourt et al 1999), similar to the reported increased incidence of mild respiratory distress in humans born by C-section (Hales et al 1993).…”

Section: Schizophrenia Is Associated With Increased Birth Complicatiomentioning

confidence: 99%

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Birth Insult Alters Dopamine-Mediated Behavior in a Precocial Species, the Guinea Pig Implications for Schizophrenia

Vaillancourt

Boksa

2000

Neuropsychopharmacology

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Schizophrenia is associated with increased birth complications, suggesting that birth complications might alter CNS dopaminergic activity later in life. In rats, Caesarean section (C-section) birth can produce long term changes in dopaminergic biochemistry and behavior. However rat brain is somewhat immature compared to human brain at birth. The current study tested if mild birth complications also alter dopamine-mediated function in a species with a more mature CNS at birth, the guinea pig. As adults, guinea pigs born by C-section showed increased amphetamine-induced locomotion and disruption of prepulse inhibition (PPI) of acoustic startle, compared to vaginally born controls. Guinea pigs born by C-section withThere is considerable evidence that enhanced mesolimbic dopaminergic activity plays an important role in some of the symptomatology of schizophrenia (e.g., Laruelle et al. 1996Laruelle et al. , 1999Breier et al. 1997; AbiDargham et al. 1998; see reviews by Seeman 1992; Lieberman et al. 1997). In addition, a large number of epidemiological studies have demonstrated that perinatal complications, often involving fetal or neonatal hypoxia, are associated with increased risk for the development of schizophrenia (e.g., Geddes and Lawrie 1995;Jones et al. 1998;Dalman et al. 1999;Hultman et al. 1999;Zornberg et al. 2000; see review by McNeil 1995).Animal modelling provides the opportunity to directly test if a birth complication, such as hypoxia, can cause long term changes in dopaminergic function. Using a rat model of global hypoxia during Caesarean section (C-section) birth, several laboratories have demonstrated that dopaminergic systems are sensitive to mild birth alterations (Bjelke et al. 1991;Loidl et al. 1994;Chen et al. 1995Chen et al. , 1997 Brake et al. 1997a,b; Boksa 1997, 1998;Vaillancourt and Boksa 1998; Berger et al. 2000a). Specifically, as adults, rats born by C-section, either with or without addition of a period of global hypoxia, show increased nucleus accumbens dopamine (DA) release in response to repeated stress (Brake et al. 1997b) Vaillancourt et al. 1999), similar to the reported increased incidence of mild respiratory distress in humans born by C-section (Hales et al. 1993).In relation to the possible clinical relevance of these results, rat brain is generally believed to be somewhat less mature at birth than is the brain of the human newborn. It has been suggested that, at approximately postnatal day 10, the brain of the rat is at the stage of rapid growth, accelerated synaptogenesis, myelinization, and astrocyte proliferation characteristic of the human newborn at term (see review by Romijn et al. 1991). Thus, the model of birth insult in the rat may relate more to premature than to term human brain. To circumvent this limitation, we initiated the current studies to test if mild birth complications also alter DA mediated function in a species with a more mature CNS at birth. The guinea pig is a precocial species, that is, capable of a high degree of independent activity at birth....

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Section: Discussionmentioning

confidence: 68%

Section: Schizophrenia Is Associated With Increased Birth Complicatiomentioning

confidence: 99%

Birth Insult Alters Dopamine-Mediated Behavior in a Precocial Species, the Guinea Pig Implications for Schizophrenia

Vaillancourt

Boksa

2000

Neuropsychopharmacology

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“…As a whole, the more significant effect of asphyxia is on spontaneous motricity. To date, the majority of data using this same perinatal asphyxia model concern the influence on motor behavior and on neurotransmitter systems related with overall activity, focusing on striatal dopaminergic system (14,18,40). It is worth noting that qualitative alterations in spontaneous motricity have been also described in severely asphyxiated human infants (either preterm or term), and they are correlated with the severity of later neurologic outcome and with presence of brain lesions (11).…”

Section: Discussionmentioning

confidence: 99%

Increased Brain Levels of F2-Isoprostane Are an Early Marker of Behavioral Sequels in a Rat Model of Global Perinatal Asphyxia

et al. 2004

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Perinatal asphyxia is a major cause of immediate and postponed brain damage in the newborn. It may be responsible for several delayed neurologic disorders and, in this respect, early markers of brain injury would be relevant for therapeutic intervention as well as for identification of infants at high risk for developmental disabilities. Biochemical measurements (brain F 2 -isoprostane levels) and behavioral tests (ultrasonic vocalization pattern on postnatal days (pnd) 5, 8, and 11, spontaneous motor behaviors on pnd 7 and 12, and homing response on pnd 10) were performed in a rat model of global perinatal asphyxia in the immature neonate. Caesarean section was performed in rats and the pups, still in uterus horns, were placed into a water bath at 37°C for either 10 or 20 min. Caesarean delivered pups were used as controls. Pups experiencing severe (20 min), in contrast to those undergoing the 10 min, asphyctic insult presented with detectable abnormalities including early (two hours after the insult) increase in brain F 2 -isoprostane (a direct marker of oxidative injury) without detectable changes in PGE 2 , COX-2 and iNOS levels, and delayed physical (reduced weight gain on pnd 5 and thereafter) and behavioral disturbances (alterations in ultrasound emission on pnd 11 and spontaneous motricity levels mainly). These findings suggest that increased brain F 2 -isoprostane levels shortly after the asphyctic insult are predictive of delayed behavioral disturbances in the newborn rat. The present 20-min asphyxia model might serve for the assessment of preventive and curative strategies to treat neurologic/behavioral disturbances associated with perinatal asphyxia. Perinatal asphyxia is a major cause of neonatal mortality and irreversible damage to the brain. Severe asphyxia may induce major deficits (cerebral palsy, dystonia, epilepsy) shortly after birth (1), while mild/moderate asphyxia episodes may result in cognitive/attentional disorders later on in development. A critical concept emerging from recent research is that of a "therapeutic window." namely a narrow period of time between the insult and the occurrence of CNS injury, during which adoption of neuroprotective strategies could be effective (2, 3). A primary aim for clinical research is to identify as early as possible reliable indexes of brain injury in the asphyctic newborns to apply potential therapeutic interventions at the optimal time and to identify those infants at high risk for developmental delays and disabilities (4).To date the major advances in the early prediction of hypoxic-ischemic insult have been attained by means of EEG and

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“…Given these findings in schizophrenia, several studies have used a rat model of global anoxia during Caesarean section (C-section) birth to directly test if birth hypoxia alters later dopaminergic function and its responsiveness to stress (Bjelke et al 1991;Loidl et al 1994;Brake et al 1997a,b;Chen et al 1995Chen et al , 1997aElKhodor andBoksa 1997, 1998;Vaillancourt and Boksa 1998). These studies demonstrated that repeated stressinduced DA release from nucleus accumbens (NAcc) and amphetamine-induced behavioral responses are enhanced in adult rats that had been born by C-section, either with or without addition of 15 min of global anoxia, compared to vaginally born controls (Brake et al 1997b;El-Khodor and Boksa 1998).…”

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confidence: 99%

Caesarean Section Birth Produces Long Term Changes in Dopamine D1 Receptors and in Stress-induced Regulation of D3 and D4 Receptors in the Rat Brain

El-Khodor

Boksa

2001

Neuropsychopharmacology

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Nicotine treatment counteracts perinatal asphyxia-induced changes in the mesostriatal/limbic dopamine systems and in motor behaviour in the four-week-old male rat

Cited by 59 publications

References 39 publications

Birth Insult Alters Dopamine-Mediated Behavior in a Precocial Species, the Guinea Pig Implications for Schizophrenia

Birth Insult Alters Dopamine-Mediated Behavior in a Precocial Species, the Guinea Pig Implications for Schizophrenia

Increased Brain Levels of F2-Isoprostane Are an Early Marker of Behavioral Sequels in a Rat Model of Global Perinatal Asphyxia

Caesarean Section Birth Produces Long Term Changes in Dopamine D1 Receptors and in Stress-induced Regulation of D3 and D4 Receptors in the Rat Brain

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