Maternal Caffeine Ingestion Increases the Tyrosine Level in Neonatal Rat Cerebrum

Tanaka, Harumi; Nakazawa, Kazuharu

doi:10.1159/000243173

Cited by 10 publications

(3 citation statements)

References 15 publications

(23 reference statements)

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“…In addition, rats treated with 15 mg/kg/day caffeine during the neonatal period exhibited reduced expression of TH in the carotid body (Bairam et al 2009), which may be related with respiratory system dysfunction (Montandon et al 2008). Exposure to caffeine (0.4 g/L in drinking water) during pregnancy/lactation also increases TH levels in the cerebellum of neonatal rats (Tanaka and Nakazawa 1990). Our results, together with data in the literature, suggest that caffeine treatment could have an important impact on local neural circuitry in the developing retinal tissue.…”

Section: Caffeine Alters the Neurochemistry Of The Chicken Embryo Retinasupporting

confidence: 69%

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Caffeine exposure alters adenosine system and neurochemical markers during retinal development

Brito

Pereira-Figueiredo

Socodato

et al. 2016

Journal of Neurochemistry

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Evidence points to beneficial properties of caffeine in the adult central nervous system, but teratogenic effects have also been reported. Caffeine exerts most of its effects by antagonizing adenosine receptors, especially A 1 and A 2A subtypes. In this study, we evaluated the role of caffeine on the expression of components of the adenosinergic system in the developing avian retina and the impact of caffeine exposure upon specific markers for classical neurotransmitter systems. Caffeine exposure (5-30 mg/kg by in ovo injection) to 14-day-old chick embryos increased the expression of A 1 receptors and concomitantly decreased A 2A adenosine receptors expression after 48 h. Accordingly, caffeine (30 mg/kg) increased receptors from 18 and 24 h. Kinetic assays of [ 3 H]-S-(4-nitrobenzyl)-6-thioinosine binding to the equilibrative adenosine transporter ENT1 revealed an increase in B max with no changes in K d , an effect accompanied by an increase in adenosine uptake. Immunohistochemical analysis showed a decrease in retinal content of tyrosine hydroxylase, calbindin and choline acetyltransferase, but not Brn3a, after 48 h of caffeine injection. Furthermore, retinas exposed to caffeine had increased levels of phosphorylated extracellular signalregulated kinase and cAMP-response element binding protein.Overall, we show an in vivo regulation of the adenosine system, extracellular signal-regulated kinase and cAMPresponse element binding protein function and protein expression of specific neurotransmitter systems by caffeine in the developing retina.

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Section: Caffeine Alters the Neurochemistry Of The Chicken Embryo Retinasupporting

confidence: 69%

“…). Exposure to caffeine (0.4 g/L in drinking water) during pregnancy/lactation also increases TH levels in the cerebellum of neonatal rats (Tanaka and Nakazawa ). Our results, together with data in the literature, suggest that caffeine treatment could have an important impact on local neural circuitry in the developing retinal tissue.…”

Section: Discussionmentioning

confidence: 99%

Caffeine exposure alters adenosine system and neurochemical markers during retinal development

Brito

Pereira-Figueiredo

Socodato

et al. 2016

Journal of Neurochemistry

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“…By what mechanism might early caffeine exposure increase the probability of inhibited behavior? Caffeine exposure has various effects on the developing fetus, such as increased arousal (Devoe, Murray, Youssif, & Arnaud, 1993), decreased brain weight (Palm et al, 1978;Groisser, Rosso, & Winick, 1982;Tanaka & Nakazawa, 1990;Tanaka, Nakazawa, Arima, & Iwaski, 1984;Yazdani, Hartman, Miller, Temples, & Nakamoto, 1988;Yazdani, Joseph, Grant, Hartman, & Nakamoto, 1990), increased deposition of zinc in various brain regions (Nakamoto et al, 1991), increased cerebral tyrosine (Tanaka & Nakazawa, 1990), and .inhibition of myelin synthesis (Fuller & Wiggins, 1981;Yazdani et al, 1988), but it is difficult to predict how these mechanisms would affect behavior. A more direct link to BI is the finding that caffeine consumption increases the concentration of norepinephrine in maternal serum (Kirkinen, Jouppila, Koivula, Vuori, & Pukka, 1983).…”

Section: Linking Prenatal Caffeine Exposure and Behavioral Inhibitionmentioning

confidence: 99%

Can Prenatal Caffeine Exposure Affect Behavioral Inhibition?

Reznick

1999

Review of General Psychology

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Given the widespread use of caffeine and its potential nonoptimal effects during pregnancy, it is remarkable and distressing that almost nothing is known about the long-term effects of prenatal caffeine exposure in humans. Research on nonhumans reveals that prenatal caffeine exposure is associated with an enduring tendency toward a profile of fearfulness, hypoactivity, and exaggerated stress in uncertain situations. A similar pattern of behavioral inhibition has been observed in humans and has been attributed to various causes such as inborn temperament or environmental influences. The author's conjecture is that prenatal caffeine exposure could be an additional factor contributing to the tendency toward behavioral inhibition. One mechanism for this effect is that caffeine causes an upregulation of adenosine receptors, thus creating a vulnerability to adenosine-induced inhibition of neuronal firing and neurotransmitter release. Caffeine (1,3,7-trimethylxanthine, found in coffee) and the related methylxanthines theophylline (1,3-dimethylxanthine, found in tea) and theobromine (3,7-dimethylxanthine, found in cocoa products) are consumed daily by more than 80% of the world's population (R. M. Gilbert, 1984), and world coffee consumption is increasing (D'Amicis & Viani, 1993). Caffeine is also present in soft drinks and prescription and nonprescription medicines, making caffeine the most widely used of all psychoactive drugs (Nehlig, Daval, & Debry, 1992). The average per capita intake of caffeine in the United States is 200 mg daily, which is the average dosage obtained in two cups of coffee, two or three cups of tea, three or four cola drinks, or six to eight analgesics-pain relievers (e.g., Anacin; J. C.

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Epileptogenic action of caffeine during anoxia in the neonatal rat hippocampus

et al. 1999

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Excessive maternal caffeine consumption can lead to fetal and neonatal pathology, but the underlying mechanisms have not been determined. Here, we report that low doses of caffeine generate seizures when applied in conjunction with brief anoxic episodes in the hippocampus of neonatal rats in vitro. In control conditions, brief (4–6 minutes) anoxic episodes reversibly depressed evoked synaptic responses and blocked the physiological pattern of network activity. In the presence of caffeine (50 μM), similar anoxic episodes generated ictal (29%) or interictal (33%) epileptiform activities often followed during reoxygenation by recurrent spontaneous seizure activity that persisted for several hours. These effects are likely mediated by a blockade of adenosine receptors by caffeine because (1) in control conditions, caffeine antagonized the inhibitory effect of selective A1 receptor agonist N6‐cyclopentyladenosine on excitatory synaptic responses, and (2) epileptogenic effects of caffeine were reproduced by selective A1 receptor antagonist 8‐cyclopentyl‐1,3‐dipropylxanthine and theophylline. Our findings suggest that endogenous adenosine released during anoxia acting via A1 receptors prevents seizures in the neonatal hippocampus and that the antagonism of these receptors by caffeine leads to epileptogenesis. This study suggests concerns about the safety of caffeine in the fetus and newborn. Ann Neurol 1999;46:95–102

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Maternal Caffeine Ingestion Increases the Tyrosine Level in Neonatal Rat Cerebrum

Cited by 10 publications

References 15 publications

Caffeine exposure alters adenosine system and neurochemical markers during retinal development

Caffeine exposure alters adenosine system and neurochemical markers during retinal development

Can Prenatal Caffeine Exposure Affect Behavioral Inhibition?

Epileptogenic action of caffeine during anoxia in the neonatal rat hippocampus

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