GABA or sodium-bromide-induced plasticity of neurites of mouse neuroblastoma cells in culture

Eins, S.; Spoerri, P.E.; Heyder, E

doi:10.1007/bf00214987

Cited by 35 publications

(17 citation statements)

References 8 publications

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“…Moreover, the finding that the effects of THIP can be blocked by picrotoxin Belhage et al, 1990), a specific blocker of the GABA-operated chloride channel (Olsen,198 I), suggests that changes in the membrane potential via GABA-operated chloride channels may be important. This notion is in accordance with the findings (Job et al, 1980;Eins et al, 1983;Toldi et al, 1986) that bromide, by changing the membrane potential, exerts a neurotrophic effect similar to that produced by GABA. Moreover, recent studies in this laboratory of the effect of bromide on GABA receptor expression on granule cells in culture have shown that bromide is able to induce low-affinity GABA receptors (Belhage et al, 1990).…”

Section: Discussionsupporting

confidence: 93%

Effects of Inhibitors of Protein Synthesis and Intracellular Transport on the γ‐Aminobutyric Acid Agonist‐Induced Functional Differentiation of Cultured Cerebellar Granule Cells

Belhage

Hansen

Meier

et al. 1990

Journal of Neurochemistry

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The effect of inhibitors of protein synthesis (actinomycin D, cycloheximide), proteases (leupeptin), and intracellular transport (colchicine, monensin) on the gamma-aminobutyric acid (GABA) agonist [4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP)]-induced changes in morphological differentiation and GABA receptor expression was investigated in cultured cerebellar granule cells. After 4 days in culture the neurons were exposed to the inhibitors for 6 h in the simultaneous presence of THIP. Subsequently, cultures were either fixed for electron microscopic examination or used for preparation of membranes for [3H]GABA binding assays. In some experiments the functional activity of the newly induced low-affinity GABA receptors was assessed by investigation of the ability of GABA to inhibit neurotransmitter release from the neurons. These experiments were performed to differentiate between an intracellular and a plasma membrane localization of the receptors. In all experiments cultures treated with THIP alone served as controls. The inhibitors of protein synthesis totally abolished the ability of THIP to induce low-affinity GABA receptors. In contrast, the inhibitors of intracellular transport as well as the protease inhibitor did not affect this parameter. However, studies of effects of GABA on transmitter release from monensin-treated cultures showed that transmitter release could not be inhibited by GABA in these cells in spite of the presence of low-affinity GABA receptors in the membrane preparations. This indicates that the low-affinity receptors were not located in the plasma membrane. This is in good agreement with the corresponding morphological findings, that monensin treatment led to an intense vacuolization of the Golgi apparatus, thereby preventing intracellular transport of the newly synthesized GABA receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 93%

Effects of Inhibitors of Protein Synthesis and Intracellular Transport on the γ‐Aminobutyric Acid Agonist‐Induced Functional Differentiation of Cultured Cerebellar Granule Cells

Belhage

Hansen

Meier

et al. 1990

Journal of Neurochemistry

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“…Early studies showed that applications of GABA to cultures of mouse neuroblastoma cells triggered a series of changes including proliferation of coated vesicles and the appearance of electron-dense material aggregated at the inner aspect of the plasma membrane (136,186). The same group showed that GABA treatments affect the growth and development of embryonic chick cortical and retinal neurons in culture, including the length and branching of the neurites (582).…”

Section: E Early Trophic Actions Of Gabamentioning

confidence: 99%

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

Ben-Ari

Gaı̈arsa

Tyzio

et al. 2007

Physiological Reviews

1,140

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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“…The first evidence that GABA may affect neurite outgrowth was provided by Eins et al (1983). Indeed, they demonstrated that differentiated C1300 mouse neuroblastoma cells treated with GABA showed an increase in the length and branching of processes (Eins et al, 1983).…”

Section: In Vitro Studiesmentioning

confidence: 99%

“…Indeed, they demonstrated that differentiated C1300 mouse neuroblastoma cells treated with GABA showed an increase in the length and branching of processes (Eins et al, 1983). A large amount of in vitro evidence has been provided ever since in several brain areas and diverse species.…”

Section: In Vitro Studiesmentioning

confidence: 99%

GABAergic control of neurite outgrowth and remodeling during development and adult neurogenesis: general rules and differences in diverse systems

Sernagor

Chabrol

Bony

et al. 2010

Front. Cell. Neurosci.

118

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During development, Gamma-aminobutyric acidergic (GABAergic) neurons mature at early stages, long before excitatory neurons. Conversely, GABA reuptake transporters become operative later than glutamate transporters. GABA is therefore not removed efficiently from the extracellular domain and it can exert significant paracrine effects. Hence, GABA-mediated activity is a prominent source of overall neural activity in developing CNS networks, while neurons extend dendrites and axons, and establish synaptic connections. One of the unique features of GABAergic functional plasticity is that in early development, activation of GABAA receptors results in depolarizing (mainly excitatory) responses and Ca2+ influx. Although there is strong evidence from several areas of the CNS that GABA plays a significant role in neurite growth not only during development but also during adult neurogenesis, surprisingly little effort has been made into putting all these observations into a common framework in an attempt to understand the general rules that regulate these basic and evolutionary well-conserved processes. In this review, we discuss the current knowledge in this important field. In order to decipher common, universal features and highlight differences between systems throughout development, we compare findings about dendritic proliferation and remodeling in different areas of the nervous system and species, and we also review recent evidence for a role in axonal elongation. In addition to early developmental aspects, we also consider the GABAergic role in dendritic growth during adult neurogenesis, extending our discussion to the roles played by GABA during dendritic proliferation in early developing networks versus adult, well established networks.

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GABA or sodium-bromide-induced plasticity of neurites of mouse neuroblastoma cells in culture

Cited by 35 publications

References 8 publications

Effects of Inhibitors of Protein Synthesis and Intracellular Transport on the γ‐Aminobutyric Acid Agonist‐Induced Functional Differentiation of Cultured Cerebellar Granule Cells

Effects of Inhibitors of Protein Synthesis and Intracellular Transport on the γ‐Aminobutyric Acid Agonist‐Induced Functional Differentiation of Cultured Cerebellar Granule Cells

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

GABAergic control of neurite outgrowth and remodeling during development and adult neurogenesis: general rules and differences in diverse systems

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