GABA: an excitatory transmitter in early postnatal life

Cherubini, Enrico; Gaı̈arsa, Jean-Luc; Ben‐Ari, Yehezkel

doi:10.1016/0166-2236(91)90003-d

Cited by 1,029 publications

(647 citation statements)

References 63 publications

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“…A switch in GABAergic transmission, from depolarization to hyperpolarization, during neuronal development has been demonstrated in many studies (Ben-Ari et al, 1989;Cherubini et al, 1991;Owens et al, 1996) (Fig. 5b, top).…”

Section: Measurement Of Resting [Clmentioning

confidence: 66%

“…It was later established that the shift from depolarizing GABA responses in young animals to hyperpolarizing responses in adult animals correlated with changes of the equilibrium potential of Cl − towards more negative potentials (Cherubini et al, 1991;Owens et al, 1996), with the onset of the expression of Cl − -extruding transporters such as KCC2 (Rivera et al, 1999), and with a decrease in the expression of Cl − -accumulating transporters such as NKCC1 (Yamada et al, 2004). However, the presumed decrease in [Cl − ] i occurring during development has not yet been visualized in brain slices or in vivo.…”

Section: Clomeleon Reports Neuronal [Cl − ] Imentioning

confidence: 99%

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Imaging synaptic inhibition in transgenic mice expressing the chloride indicator, Clomeleon

et al. 2006

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Section: Measurement Of Resting [Clmentioning

confidence: 66%

Section: Clomeleon Reports Neuronal [Cl − ] Imentioning

confidence: 99%

Imaging synaptic inhibition in transgenic mice expressing the chloride indicator, Clomeleon

et al. 2006

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“…Most importantly, they demonstrate that conductive impairment at a very early age may induce re-organization within auditory cortex, where CHL occurring later in development may promote a different mode or temporal sequence of cortical re-organization. These different modes may include potential plastic changes (e.g., Irvine, 2007) or perturbed expression of neurotransmitters or their receptors (e.g., Cherubini et al, 1991;Gao et al, 1999;Kilman et al, 2002;Yu et al, 2006). Regardless of the underlying mechanism, our main observation remains that in response to low frequency sound stimulation, CHL, but not CA, decreases activity in auditory cortex.…”

Section: Developmental Effects Of Unilateral Chlmentioning

confidence: 88%

Consequences of unilateral hearing loss: Cortical adjustment to unilateral deprivation

Hutson¹,

Durham²,

Imig³

et al. 2008

Hearing Research

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The effect of unilateral hearing loss on 2-deoxyglucose (2-DG) uptake in the central auditory system was studied in post-natal day 21 gerbils. Three weeks following a unilateral conductive hearing loss (CHL) or cochlear ablation (CA), animals were injected with 2-DG and exposed to an alternating auditory stimulus (1 and 2 kHz tones). Uptake of 2-DG was measured in the inferior colliculus (IC), medial geniculate (MG), and auditory cortex (fields AI and AAF) of both sides of the brain in experimental animals and in anesthesia-only sham animals (SH). Significant differences in uptake, compared to SH, were found in the IC contralateral to the manipulated ear (CHL or CA) and in AAF contralateral to the CHL ear. We hypothesize that these findings may result from loss of functional inhibition in the IC contralateral to CA, but not CHL. Altered states of inhibition at the IC may affect activity in pathways ascending to auditory cortex, and ultimately activity in auditory cortex itself. Altered levels of activity in auditory cortex may explain some auditory processing deficits experienced by individuals with CHL.

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“…These functions demonstrate that chloride is important in mechanisms of cell volume and pH control. It is now acknowledged that, in contrast to most other biological ions, chloride resting concentration shows significant variation among different mammalian cell types, as well as throughout the lifetime of some cell types (Cherubini et al, 1991;Chipperfield and Harper, 2000). The present review explores the role of chloride in glial function and correlates these concepts with new findings on cloned channels.…”

Section: Introductionmentioning

confidence: 86%

Chloride/anion channels in glial cell membranes

Walz

2002

Glia

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At least seven different chloride/anion currents have now been identified in astrocytes, oligodendrocytes/Schwann cells, and microglia. Only for two of these currents is the corresponding gene known. One of these genes is not encoding for a chloride channel, but for a class of mitochondria-like pores also found in cell membranes. Astrocytes and oligodendrocytes differ in their resting properties: astrocytes accumulate chloride but do not have a significant permeability. Oligodendrocytes have a close to passive distribution and a significant permeability. Under certain circumstances, astrocytes can express a resting chloride conductance. Reactive and neoplastic astrocytes as well as astrocytes with an altered shape exhibit a resting conductance. The function of these channels certainly involves volume regulation. Other possible functions are potassium homeostasis, migration, proliferation (in microglia), and involvement in spreading depression waves. Of greatest interest are two phenomena discovered in situ: The ClC-2 channel is only found in astrocytic endfeet near blood capillaries adjacent to neuronal GABA A receptors. In the supraoptic nucleus of the hypothalamus, there is an osmosensitive astrocytic taurine release. This released taurine interacts with glycine receptors in neighboring neurons, causing inhibition. It is assumed that with the future availability of more in situ, rather than in vitro, studies, an increased number of such complex interactions between glial cells, neurons, and blood vessels will be discovered.

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GABA: an excitatory transmitter in early postnatal life

Cited by 1,029 publications

References 63 publications

Imaging synaptic inhibition in transgenic mice expressing the chloride indicator, Clomeleon

Imaging synaptic inhibition in transgenic mice expressing the chloride indicator, Clomeleon

Consequences of unilateral hearing loss: Cortical adjustment to unilateral deprivation

Chloride/anion channels in glial cell membranes

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