Membrane Potential of CA3 Hippocampal Pyramidal Cells During Postnatal Development

Tyzio, Roman; Ivanov, Anton; Bernard, Christophe; Holmes, Gregory L.; Ben-Ari, Yehezkel; Khazipov, Roustem

doi:10.1152/jn.00172.2003

Cited by 179 publications

(221 citation statements)

References 35 publications

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“…In isolated hippocampal slice preparations, the resting potential in the cell bodies of immature pyramidal neurons has been reported to be approximately Ϫ85 mV in quiescent cells in which activity has been blocked (Leinekugel et al, 1997;Fricker et al, 1999); without blocking activity, this value decreased to Ϫ77 mV (Tyzio et al, 2003). In this case, is the BDNF secretion that we observe likely to occur in vivo?…”

Section: Discussionmentioning

confidence: 68%

Single-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor

Magby¹,

Bi²,

Chen³

et al. 2006

J. Neurosci.

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Brain-derived neurotrophic factor (BDNF) is a key regulator of hippocampal synaptic plasticity in the developing and adult nervous system. It can be released from pyramidal neuron dendrites in an activity-dependent manner and has therefore been suggested to serve as a signal that provides the retrograde intercellular communication necessary for Hebbian plasticity and hippocampal-dependent learning. Although much has been learned about BDNF function by field stimulation of hippocampal neurons, it is not known whether moderate action potential-independent depolarization of single cells is capable of releasing sufficient BDNF to influence transmission at individual synapses. In this study, we show directly at the single-cell level that such modulation can occur. By using K-252a, anti-BDNF antibody, and interruption of regulated release, we confirm a model in which postsynaptic depolarization elicits calcium-dependent release of BDNF that diffuses retrogradely and enhances presynaptic transmitter release.

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Section: Discussionmentioning

confidence: 68%

Single-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor

Magby¹,

Bi²,

Chen³

et al. 2006

J. Neurosci.

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“…In particular, the polarity of the GABA A R-mediated postsynaptic responses, which depends both on RMP and E Cl Ϫ and on the action potential threshold (AP thresh ), should be investigated in the newborn mice. All three parameters (RMP, E Cl Ϫ , and AP thresh ) need to be investigated in conditions that do not affect their measurement (Tyzio et al, 2003;Rheims et al, 2008). In conclusion, our results suggest that the nVPM-to-nRT inhibitory feedback loop may stand as an important checkpoint to generate spindles in the thalamocortical circuit before active whisking.…”

mentioning

confidence: 81%

Early Development of the Thalamic Inhibitory Feedback Loop in the Primary Somatosensory System of the Newborn Mice

Evrard¹,

Ropert²

2009

J. Neurosci.

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Spontaneous neuronal activity plays an important role during the final development of the brain circuits and the formation of the primary sensory maps. In young rats, spindle bursts have been recorded in the primary somatosensory cortex. They are correlated with spontaneous muscle twitches and occur before active whisking. They bear similarities with the spindles recorded in adult brain that occur during early stages of sleep and rely on a thalamic feedback loop between the glutamatergic nucleus ventroposterior medialis (nVPM) and the GABAergic nucleus reticularis thalami (nRT). However, whether a functional nVPM-nRT loop exists in newborn rodents is unknown. We studied the reciprocal synaptic connections between nVPM and nRT in thalamic acute slices from mice from birth [postnatal day 0 (P0)] until P9. We first demonstrated that nVPM-to-nRT EPSCs could be distinguished from corticothalamic EPSCs by their inhibition by 5-HT attributable to the transient expression of functional presynaptic serotonin 1B receptors. The nVPM-to-nRT EPSCs and nRT-to-nVPMIPSCs were both detected the first day after birth; their amplitude near 2 nS was relatively stable until P5. At P6 -P7, there was a rapid and simultaneous increase of both nVPM-to-nRT EPSCs and nRT-to-nVPM IPSCs that reached 8 and 9 nS, respectively. Our results show that the thalamic synapses implicated in spindle activity are functional shortly after birth, suggesting that they could already generate spindles during the first postnatal week. Our results also suggest an inhibitory action of 5-HT on the spindle bursts of the newborn mice.

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“…, the driving force of chloride ions through the GABA A channel (Tyzio et al, 2003). Therefore, when i GABA A ϭ 0 pA, DF GABA A ϭ ϪV p .…”

Section: Methodsmentioning

confidence: 99%

Dopamine-Deprived Striatal GABAergic Interneurons Burst and Generate Repetitive Gigantic IPSCs in Medium Spiny Neurons

Dehorter¹,

Guigoni²,

Lopez³

et al. 2009

Journal of Neuroscience

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Striatal GABAergic microcircuits modulate cortical responses and movement execution in part by controlling the activity of medium spiny neurons (MSNs). How this is altered by chronic dopamine depletion, such as in Parkinson's disease, is not presently understood. We now report that, in dopamine-depleted slices of the striatum, MSNs generate giant spontaneous postsynaptic GABAergic currents (single or in bursts at 60 Hz) interspersed with silent episodes, rather than the continuous, low-frequency GABAergic drive (5 Hz) observed in control MSNs. This shift was observed in one-half of the MSN population, including both "D 1 -negative" and "D 1 -positive" MSNs. Single GABA and NMDA channel recordings revealed that the resting membrane potential and reversal potential of GABA were similar in control and dopamine-depleted MSNs, and depolarizing, but not excitatory, actions of GABA were observed. Glutamatergic and cholinergic antagonists did not block the GABAergic oscillations, suggesting that they were generated by GABAergic neurons. In support of this, cell-attached recordings revealed that a subpopulation of intrastriatal GABAergic interneurons generated bursts of spikes in dopamine-deprived conditions. This subpopulation included low-threshold spike interneurons but not fast-spiking interneurons, cholinergic interneurons, or MSNs. Therefore, a population of local GABAergic interneurons shifts from tonic to oscillatory mode when dopamine deprived and gives rise to spontaneous repetitive giant GABAergic currents in one-half the MSNs. We suggest that this may in turn alter integration of cortical signals by MSNs.

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Membrane Potential of CA3 Hippocampal Pyramidal Cells During Postnatal Development

Cited by 179 publications

References 35 publications

Single-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor

Single-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor

Early Development of the Thalamic Inhibitory Feedback Loop in the Primary Somatosensory System of the Newborn Mice

Dopamine-Deprived Striatal GABAergic Interneurons Burst and Generate Repetitive Gigantic IPSCs in Medium Spiny Neurons

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