Alumina Cream-Induced Focal Motor Epilepsy in Cats IV. Thickness and Cellularity of Layers in the Perilesional Motor Cortex

Feria‐Velasco, Alfredo; Olivares, Norma; Rivas, Fernando Roldan; Velasco, Marcos; Velasco, Francisco

doi:10.1001/archneur.1980.00500540065008

Cited by 12 publications

(2 citation statements)

References 23 publications

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“…Aluminium hydroxide gel/alumina cream is used to produce animal models of epilepsy, which corresponds to an abnormal synchronization of electrical neuronal activity that can be manifested as an alteration in mental state, tonic or clonic movements, convulsions, and various other psychic symptoms. These temporary abnormal electrophysiological phenomena are also signs of intoxication by aluminium and reflect an imbalance between excitatory and inhibitory brain circuits [261]. Using this model, it has been shown that aluminium provokes a widespread, severe specific reduction of GABA [159], the major inhibitory neurotransmitter in adult mammalian brain, and loss of GABAergic neurons in the absence of significant cytoskeleton alterations [262][263][264].…”

Section: Synaptic Strengthmentioning

confidence: 99%

Does neurotransmission impairment accompany aluminium neurotoxicity?

Gonçalves

Silva

2007

Journal of Inorganic Biochemistry

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Section: Synaptic Strengthmentioning

confidence: 99%

Does neurotransmission impairment accompany aluminium neurotoxicity?

Gonçalves

Silva

2007

Journal of Inorganic Biochemistry

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“…However, we have not found a correlation between lesion size and latency or duration of the GWS (Brailowsky el al., 1988). The role of gliosis and perilesional fibrosis in the origin of epileptic discharges has been questioned (Feria-Velasco et al. 1980).…”

Section: Discussionmentioning

confidence: 99%

Electroencephalographic Study of the GAB A‐Withdrawal Syndrome in Rats

et al. 1990

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The spatial and temporal EEG features of the epileptogenic syndrome induced by cessation of chronic intracortical GABA infusion in normal rats are described. In the initial stages, the paroxysmal discharges (PDs) induced by withdrawal from unilateral GABA application may appear either unilaterally or bilaterally, although with greater amplitude on the infused side. PDs are transitorily accompanied by behavioral signs of distal myoclonus of the body territory corresponding to the infused area (contralateral hindlimb). Later, the paroxysmal activity becomes more localized, circumscribed to the cannula-infused site and with ipsilateral propagation to anterior cortical areas. The amplitude of PDs decreases progressively while their frequency increases, reaching its maximal value at about 4 h after the first PDs have appeared. In the final stages of the syndrome, which may last several days, clinical manifestations are absent and PDs are activated by slow-wave sleep and reduced during REM sleep and waking. Chronic intracortical applications of taurine failed to induce any electroclinical changes on withdrawal and were unable to inhibit the focus elicited by GABA withdrawal, whereas reinstatement of GABA infusion into the epileptogenic area was effective in blocking the paroxysmal activity. Intracortical infusion of baclofen induced the appearance of an epileptogenic focus that waned on withdrawal. The GABA-withdrawal syndrome appears to be a new model of focal status epilepticus; it may be useful as an experimental model of human partial epilepsy to investigate the role of GABAergic neurotransmission.

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