Morphological correlates of altered neuronal activity in organotypic cerebellar cultures chronically exposed to anti-GABA agents

Seil, Fredrick J.; Drake-Baumann, Rosemarie; Leiman, Arnold L.; Herndon, Robert M.; Tiekotter, Kenneth L.

doi:10.1016/0165-3806(94)90219-4

Cited by 35 publications

(23 citation statements)

References 34 publications

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“…A transient loss of inhibitory terminals could explain the transient loss of paired pulse inhibition (37). The sprouting of the axon of GABAergic neurons has been reported in another preparation (38); in the hippocampus, it could occur in parallel with the well-documented recovery of excitatory terminals via the sprouting of excitatory axons in TLE (31,3947).…”

Section: Loss Of Interneurons In Tlementioning

confidence: 99%

What is GABAergic Inhibition? How Is it Modified in Epilepsy?

et al. 2000

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Summary: A deficit of γ‐aminobutyric acid‐ergic (GABAergic) inhibition is hypothesized to underlie most forms of epilepsy. Although apparently a straightforward and logical hypothesis to test, the search for a deficit of GABAergic inhibition in epileptic tissue has revealed itself to be as difficult as the quest for the Holy Grail. The investigator faces many obstacles, including the multiplicity of GABAergic inhibitory pathways and the multiplicity of variables that characterize the potency of inhibition within each inhibitory pathway. Perhaps more importantly, there seems to be no consensual definition of GABAergic inhibition. The first goal of this review is to try to clarify the notion of GABAergic inhibition. The second goal is to summarize our current knowledge of the various alterations that occur in the GABAergic pathways in temporal lobe epilepsy. Two important features will emerge: (a) according to the variable used to measure GABAergic inhibition, it may appear increased, decreased, or unchanged; and (b) these modifications are brain area‐ and inhibitory pathway‐specific. The possible functional consequences of these alterations are discussed.

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Section: Loss Of Interneurons In Tlementioning

confidence: 99%

What is GABAergic Inhibition? How Is it Modified in Epilepsy?

et al. 2000

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“…Anatomic (Sloper et al, 1980; Ribak et al, 1982; Houser et al, 1986; De Lanerolle et al, 1989; Marco et al, 1996; Rosen et al, 1998; Spreafico et al, 1998; DeFelipe, 1999; Andre et al, 2001) and/or electrophysiologic data (Franck & Schwartzkroin, 1984; Ashwood & Wheal, 1986; Franck et al, 1988; Neumann-Haefelin et al, 1995; Williamson et al, 1999; Zhu & Roper, 2000; Sayin et al, 2003) document decreases in numbers of interneurons and/or postsynaptic inhibition in epileptogenic hippocampus and neocortex. However, other data emphasize the preservation of GABAergic neurons after various types of injury, and the potential for sprouting new inhibitory connections (Nieoullon & Dusticier, 1981; Goldowitz et al, 1982; Westenbroek et al, 1988; Babb et al, 1989a,b; Davenport et al, 1990; Seil et al, 1994; Magloczky & Freund, 2005). Both enhanced inhibitory input (e.g., Gulyas & Freund, 1996; Tamas et al, 1998; Bacci et al, 2003) and decreased excitatory drive onto interneurons (Sloviter, 1991; Lothman et al, 1996; Doherty & Dingledine, 2001) have been proposed as potential epileptogenic mechanisms, (but see Bernard et al, 1998; Jacobs & Prince, 2005).…”

Section: Methodsmentioning

confidence: 99%

Clinical neurophysiology with special reference to the electroencephalogram

Avanzini¹

2009

Epilepsia

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Summary In the nineteenth and early twentieth centuries, many important discoveries in nervous system structure and function involved the electrical properties of nerve tissue. The application of these advances, as well as those in electronic amplification and recording, led to the discovery of the human electroencephalogram (EEG) by Hans Berger, a German psychiatrist. Originally received with skepticism, the EEG became a subject of intense interest, and after World War II, became a leading clinical and experimental tool in neurology. Today, it remains important especially in the study and treatment of epilepsy. Though the EEG has also given rise to more sophisticated applications, these remain based on Berger’s initial work, one of the great discoveries of medical history.

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“…This concentration of PTX, in the absence of antibodies to neurotrophins, resulted in a 50% increase in the number of Purkinje cell axosomatic synapses after 15 DIV, compared to an over 100% increase when the concentration was 2 × 10 -4 M (Seil et al, 1994). When antibodies to BDNF and NT-4 were included in the nutrient medium along with PTX, the number of Purkinje cell axosomatic synapses was similar to that in untreated control cultures, indicating that the effect of increased neuronal activity on inhibitory synaptogenesis had been mitigated (Seil and Drake-Baumann, 2000).…”

Section: Neurotrophins and Activity-dependent Plasticitymentioning

confidence: 98%

“…As the organotypic cerebellar culture model presented a system in which GABAergic inhibition played a key role, and as structural and functional relationships in such cultures were well defined both during development and after maturation, we thought that it was an ideal system in which to explore further the effects of enhanced neuronal activity on cortical development. We continuously exposed cerebellar cultures from explantation separately to two anti-GABA agents, PTX and bicuculline (Seil et al, 1994). PTX is thought to work by uncoupling the GABA A receptor site from the chloride channel, thus preventing the latter from opening, while bicuculline competitively blocks the GABA A receptor.…”

Section: A Different Form Of Neuroplasticitymentioning

confidence: 99%

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The changeable nervous system: Studies on neuroplasticity in cerebellar cultures

Seil

2014

Neuroscience & Biobehavioral Reviews

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Circuit reorganization after injury was studied in a cerebellar culture model. When cerebellar cultures derived from newborn mice were exposed at explantation to a preparation of cytosine arabinoside that destroyed granule cells and oligodendrocytes and compromised astrocytes, Purkinje cells surviving in greater than usual numbers were unensheathed by astrocytic processes and received twice the control number of inhibitory axosomatic synapses. Purkinje cell axon collaterals sprouted and many of their terminals formed heterotypical synapses with other Purkinje cell dendritic spines. The resulting circuit reorganization preserved inhibition in the cerebellar cortex. Following this reorganization, replacement of the missing granule cells and glia was followed by a restitution of the normal circuitry. Most of these developmental and reconstructive changes were not dependent on neuronal activity, the major exception being inhibitory synaptogenesis. The full complement of inhibitory synapses did not develop in the absence of neuronal activity, which could be mitigated by application of exogenous TrkB receptor ligands. Inhibitory synaptogenesis could also be promoted by activity-induced release of endogenous TrkB receptor ligands or by antibody activation of the TrkB receptor.

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Morphological correlates of altered neuronal activity in organotypic cerebellar cultures chronically exposed to anti-GABA agents

Cited by 35 publications

References 34 publications

What is GABAergic Inhibition? How Is it Modified in Epilepsy?

What is GABAergic Inhibition? How Is it Modified in Epilepsy?

Clinical neurophysiology with special reference to the electroencephalogram

The changeable nervous system: Studies on neuroplasticity in cerebellar cultures

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