2009
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Abstract: Certain antiepileptic drugs (AEDs) that are commonly used to treat seizures in children also affect cognition, and these effects can persist into adulthood, long after drug withdrawal. Widespread enhancement of apoptosis may be one mechanism underlying these lasting cognitive changes. Whether AEDs affect other processes in brain development during early postnatal life has not, however, been systematically analyzed. Here we determined whether chronic administration of common AEDs during early life alters cell p… Show more

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“…Stefovska et al (Stefovska et al, 2008) reported a decrease in neurogenesis in the subgranular zone after 3 doses of phenobarbital in the neonatal rat. Chen et al (Chen et al, 2009) corroborated these decreases in hippocampal neurogenesis after chronic administration to neonatal rats, and also reported a conservation of the relative proportions of newborn neuronal and glial cell types. It is possible that these are model-dependent differences: the experiments cited previously were performed in naïve rodents, while our ischemia model has already demonstrated suppressed neurogenesis in the DG after the stroke event (Kadam et al, 2008; Kadam et al, 2009a).…”
Section: Discussionmentioning
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“…Stefovska et al (Stefovska et al, 2008) reported a decrease in neurogenesis in the subgranular zone after 3 doses of phenobarbital in the neonatal rat. Chen et al (Chen et al, 2009) corroborated these decreases in hippocampal neurogenesis after chronic administration to neonatal rats, and also reported a conservation of the relative proportions of newborn neuronal and glial cell types. It is possible that these are model-dependent differences: the experiments cited previously were performed in naïve rodents, while our ischemia model has already demonstrated suppressed neurogenesis in the DG after the stroke event (Kadam et al, 2008; Kadam et al, 2009a).…”
Section: Discussionmentioning
“…Other groups have also shown that brief exposure (P7–P8) to higher doses of phenobarbital (75 mg/kg) led to decreased neuronal number in the thalamus, striatum, frontal cortex, and hippocampus of rodents [171,210,224]. In addition, phenobarbital exposure from P7–P34 leads to a decrease in hippocampal progenitor cell proliferation, decreased expression of a marker of immature cells, and decreased survival of postnatally generated neurons in the adolescent animal [225,226], suggesting that drug exposure affects postnatal neurogenesis in the hippocampus. Rats exposed to phenobarbital during the first three weeks of life also have impaired development of olfactory bulb (∼25% reduction in medial olfactory bulb volume), with the greatest reductions in neuronal number in the external layers (mitral and glomerular neurons) and significant but more modest effects on the granule cell layer [227].…”
Section: Animal (Rodent) Postnatal Exposurementioning
“…Type-2 progenitors in adult hippocampus express GABA A receptors that can be activated by synaptic stimuli and stimulate differentiation (Deisseroth and Malenka, 2005; Wang et al, 2005). Antiepileptic drugs, such as the barbiturate phenobarbital, which also act on the GABAergic system by binding to GABA A receptors (Rudolph et al, 1999), decrease neurogenesis by about 60% in the DG (Chen et al, 2009) and have cognitive effects that persist after drug cessation (Chen et al, 2009). Alcohol, which, like BZDs, modulates GABA A receptors to induce sedation (Laukkanen et al, 2013), decreases DG neurogenesis by up to 50% in adult rats after long-term exposure (Jang et al, 2002; Nixon and Crews, 2002; Rice et al, 2004).…”
Section: Discussionmentioning
“…Increased GABA activation via GABA A receptor agonists, such as BZD, appears to cause neuronal apoptosis in the developing brain of rodents (Chen et al, 2009). We found that mature granule neuron were fewer in subjects co-treated with BZD compared with subjects treated with antidepressant alone, and in BZD co-treated MD were comparable to untreated MD.…”
Section: Discussionmentioning