Epileptogenic action of caffeine during anoxia in the neonatal rat hippocampus

Dzhala, Volodymyr; Desfreres, Luc; Melyan, Zare; Ben-Ari, Yehezkel; Khazipov, Roustem

doi:10.1002/1531-8249(199907)46:1<95::aid-ana14>3.0.co;2-1

Cited by 31 publications

(25 citation statements)

References 58 publications

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“…This developmental effect of caffeine may involve the blockade of A 2A Rs because caffeineinduced modifications could be reproduced with a selective A 2A R antagonist, although we cannot rule out contributions of the other targets of caffeine, for example, A 1 receptors, as shown during parturition (48). Caffeine treatment did not have a major influence on food and water intake or on the day/night rhythm of female mice.…”

Section: Discussionmentioning

confidence: 99%

Adenosine Receptor Antagonists Including Caffeine Alter Fetal Brain Development in Mice

et al. 2013

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pregnancy.longitudinal prospective human studies will be needed to evaluate the consequences of caffeine consumption during effects of adenosine receptor antagonists including caffeine on brain development in humans. Retrospective and neuronal types as well as impaired memory on certain types of memory tests. This study raises questions about the that adult offspring of pregnant mice treated with adenosine receptor antagonists had reduced numbers of certain antagonists were more susceptible to seizures when exposed to a seizure-inducing agent. They further demonstrated into target regions. They then showed that 1-week-old offspring of pregnant mice treated with adenosine receptor delayed the migration of specific populations of neurons during brain maturation, resulting in their delayed insertion They found that caffeine or an adenosine receptor antagonist that specifically blocks type 2A adenosine receptors added caffeine to the drinking water of female mice throughout pregnancy and lactation. Monique Esclapez, 1,2 † Christophe Bernard 1,2 * † Consumption of certain substances during pregnancy can interfere with brain development, leading to deleterious long-term neurological and cognitive impairments in offspring. To test whether modulators of adenosine receptors affect neural development, we exposed mouse dams to a subtype-selective adenosine type 2A receptor (A 2A R) antagonist or to caffeine, a naturally occurring adenosine receptor antagonist, during pregnancy and lactation. We observed delayed migration and insertion of g-aminobutyric acid (GABA) neurons into the hippocampal circuitry during the first postnatal week in offspring of dams treated with the A 2A R antagonist or caffeine. This was associated with increased neuronal network excitability and increased susceptibility to seizures in response to a seizure-inducing agent. Adult offspring of mouse dams exposed to A 2A R antagonists during pregnancy and lactation displayed loss of hippocampal GABA neurons and some cognitive deficits. These results demonstrate that exposure to A 2A R antagonists including caffeine during pregnancy and lactation in rodents may have adverse effects on the neural development of their offspring.

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Section: Discussionmentioning

confidence: 99%

Adenosine Receptor Antagonists Including Caffeine Alter Fetal Brain Development in Mice

et al. 2013

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“…We next examined whether DL-BHB affects GDPs, which are dependent on depolarizing actions of GABA and are very sensitive to alterations of neuronal excitability and to insufficient energy supply Dzhala et al, 1999;Allène et al, 2008). As shown in Figure 4, GDPs occurred synchronously with extracellular field potentials and were readily identified in wholecell recordings by their characteristic shape and kinetics.…”

Section: Dl-bhb Does Not Alter Gdpsmentioning

confidence: 99%

Depolarizing Actions of GABA in Immature Neurons Depend Neither on Ketone Bodies Nor on Pyruvate

Tyzio¹,

Allène²,

Nardou³

et al. 2011

J. Neurosci.

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“…Thus, in the postnatal rat hippocampus, there is a bell-shaped age dependence of susceptibility to various epileptogenic agents and conditions including kainic acid (8,317,620), electrical stimulation (464), hypoxia (288), GABA A antagonists (233,323,599), fever (32,277,546), GABA B receptor antagonists (427), adenosine A1 antagonists (171), and high potassium (172,282,325). The developmental changes in GABAergic function (50,53) could explain the higher incidence of seizures of immature neurons in addition to other candidate mechanisms (for reviews, see Refs.…”

Section: A Gaba and The High Incidence Of Seizures Of The Immature Bmentioning

confidence: 99%

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

Ben-Ari

Gaı̈arsa

Tyzio

et al. 2007

Physiological Reviews

1,136

1,123

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Developing networks follow common rules to shift from silent cells to coactive networks that operate via thousands of synapses. This review deals with some of these rules and in particular those concerning the crucial role of the neurotransmitter γ-aminobuytric acid (GABA), which operates primarily via chloride-permeable GABAAreceptor channels. In all developing animal species and brain structures investigated, neurons have a higher intracellular chloride concentration at an early stage leading to an efflux of chloride and excitatory actions of GABA in immature neurons. This triggers sodium spikes, activates voltage-gated calcium channels, and acts in synergy with NMDA channels by removing the voltage-dependent magnesium block. GABA signaling is also established before glutamatergic transmission, suggesting that GABA is the principal excitatory transmitter during early development. In fact, even before synapse formation, GABA signaling can modulate the cell cycle and migration. The consequence of these rules is that developing networks generate primitive patterns of network activity, notably the giant depolarizing potentials (GDPs), largely through the excitatory actions of GABA and its synergistic interactions with glutamate signaling. These early types of network activity are likely required for neurons to fire together and thus to “wire together” so that functional units within cortical networks are formed. In addition, depolarizing GABA has a strong impact on synaptic plasticity and pathological insults, notably seizures of the immature brain. In conclusion, it is suggested that an evolutionary preserved role for excitatory GABA in immature cells provides an important mechanism in the formation of synapses and activity in neuronal networks.

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Epileptogenic action of caffeine during anoxia in the neonatal rat hippocampus

Cited by 31 publications

References 58 publications

Adenosine Receptor Antagonists Including Caffeine Alter Fetal Brain Development in Mice

Adenosine Receptor Antagonists Including Caffeine Alter Fetal Brain Development in Mice

Depolarizing Actions of GABA in Immature Neurons Depend Neither on Ketone Bodies Nor on Pyruvate

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

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