GABAergic Interneurons Facilitate Mossy Fiber Excitability in the Developing Hippocampus

Nakamura, Michiko; Sekino, Yuko; Manabe, Toshiya

doi:10.1523/jneurosci.4672-06.2007

Cited by 34 publications

(38 citation statements)

References 33 publications

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“…This increased mossy fiber excitability caused by depolarizing action of GABA gradually decreased with development and eventually disappeared at around postnatal day 30. These results suggested that GABA released from interneurons acted on axonal GABA receptors on mossy fibers and contributed at least partially to the activity-and age-dependent facilitation in the hippocampus (472).…”

Section: H Glutamatergic Mossy Fiber Synapses Have An Early Mixed Gamentioning

confidence: 84%

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

Ben-Ari

Gaı̈arsa

Tyzio

et al. 2007

Physiological Reviews

1,143

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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Section: H Glutamatergic Mossy Fiber Synapses Have An Early Mixed Gamentioning

confidence: 84%

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

Ben-Ari

Gaı̈arsa

Tyzio

et al. 2007

Physiological Reviews

1,143

1,123

View full text Add to dashboard Cite

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“…Another mechanism of activity-dependent signal amplification has been reported at hippocampal mossy fiber (376). In immature hippocampus, repetitive stimulation of the mossy fiber pathway not only facilitates synaptic transmission but also facilitates the amplitude of the presynaptic volley, the electrophysiological signature of the presynaptic action potential in the axon recorded extracellularly.…”

Section: B Signal Amplification Along the Axonmentioning

confidence: 99%

Axon Physiology

Debanne

Campanac

Bialowas

et al. 2011

Physiological Reviews

557

492

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Axons are generally considered as reliable transmission cables in which stable propagation occurs once an action potential is generated. Axon dysfunction occupies a central position in many inherited and acquired neurological disorders that affect both peripheral and central neurons. Recent findings suggest that the functional and computational repertoire of the axon is much richer than traditionally thought. Beyond classical axonal propagation, intrinsic voltage-gated ionic currents together with the geometrical properties of the axon determine several complex operations that not only control signal processing in brain circuits but also neuronal timing and synaptic efficacy. Recent evidence for the implication of these forms of axonal computation in the short-term dynamics of neuronal communication is discussed. Finally, we review how neuronal activity regulates both axon morphology and axonal function on a long-term time scale during development and adulthood.

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“…All experiments were performed with neurosphere cultures that were passaged Ͻ15 times. Additionally, cultures were exposed to methanol at 320 md/dl for 5 d. Because the GABA type-A (GABA A ) receptor mediates many of ethanol's actions (Ma et al, 2001;Kalluri and Ticku, 2002;Abe et al, 2004), and functional GABA A receptors are present in fetal VZ neuroepithelial cells (Owens et al, 1999;Maric et al, 2001), we also used the GABA A antagonist picrotoxin (at 100 M) (Nakamura et al, 2007), to block the effects of ethanol in some experiments. In control experiments, neurosphere cultures were exposed to picrotoxin by itself (at 100 M) for 5 d to mimic the duration of ethanol exposure.…”

Section: Neurosphere Cultures and Alcohol Treatmentmentioning

confidence: 99%

Competing Interactions between Micro-RNAs Determine Neural Progenitor Survival and Proliferation after Ethanol Exposure: Evidence from anEx VivoModel of the Fetal Cerebral Cortical Neuroepithelium

Sathyan¹,

Golden²,

Miranda³

2007

J. Neurosci.

263

280

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The fetal brain is sensitive to a variety of teratogens, including ethanol. We showed previously that ethanol induced mitosis and stem cell maturation, but not death, in fetal cerebral cortex-derived progenitors. We tested the hypothesis that micro-RNAs (miRNAs) could mediate the teratogenic effects of ethanol in a fetal mouse cerebral cortex-derived neurosphere culture model. Ethanol, at a level attained by alcoholics, significantly suppressed the expression of four miRNAs, miR-21, -335, -9, and -153, whereas a lower ethanol concentration, attainable during social drinking, induced miR-335 expression. A GABA A receptor-dependent mechanism mediated miR-21, but not miR-335 suppression, suggesting that divergent mechanisms regulate ethanol-sensitive miRNAs. Antisense-mediated suppression of miR-21 expression resulted in apoptosis, suggesting that miR-21 is an antiapoptotic factor. miR-335 knockdown promoted cell proliferation and prevented death induced by concurrently suppressing miR-21, indicating that miR-335 is a proapoptotic, antimitogenic factor whose actions are antagonistic to miR-21. Computational analyses identified two genes, Jagged-1, a Notch-receptor ligand, and embryonic-lethal abnormal vision, Drosophila-like 2 (ELAVL2), a brain-specific regulator of RNA stability, as presumptive targets of three of four ethanol-sensitive micro-RNAs. Combined knockdown of miR-335, -21, and -153 significantly increased Jagged-1 mRNA. Furthermore, ethanol induced both Jagged-1 and ELAVL2 mRNA. The collective suppression of micro-RNAs is consistent with ethanol induction of cell cycle and neuroepithelial maturation in the absence of apoptosis. These data identify a role for micro-RNAs as epigenetic intermediaries, which permit teratogens to shape complex, divergent developmental processes, and additionally demonstrate that coordinately regulated miRNAs exhibit both functional synergy and antagonism toward each other.

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GABAergic Interneurons Facilitate Mossy Fiber Excitability in the Developing Hippocampus

Cited by 34 publications

References 33 publications

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

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

Axon Physiology

Competing Interactions between Micro-RNAs Determine Neural Progenitor Survival and Proliferation after Ethanol Exposure: Evidence from anEx VivoModel of the Fetal Cerebral Cortical Neuroepithelium

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