Creation of hyperactive determinant dispatch stations in the caudate nucleus in experimental neuropathological syndromes caused by tetanus toxin

Крыжановский, Г. Н.; Aliev, M. N.

doi:10.1007/bf00797542

Cited by 5 publications

(2 citation statements)

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“…None of these approaches provides a completely satisfactory model for chronic focal epilepsy, however, which requires induction of spontaneous recurrent seizures (SRS) that persist indefinitely. Tetanus toxin has long been known to produce behavioral effects and seizures when applied to the CNS (Brooks and Asanuma, 1962;Carrea and Lanari, 1962;Kryzhanovsky and Aliev, 1976;McGeer et al, 1980), and strong evidence shows that it produces these effects by blocking inhibitory (and to a lesser extent excitatory) transmission presynaptically Mellanby and Green, 1981;Wellhoner, 1982;Bergey et al, 1983). A promising but largely unexploited alternative to these ap-proaches is the tetanus toxin model.…”

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“…A promising but largely unexploited alternative to these ap-proaches is the tetanus toxin model. Tetanus toxin has long been known to produce behavioral effects and seizures when applied to the CNS (Brooks and Asanuma, 1962;Carrea and Lanari, 1962; Kryzhanovsky and Aliev, 1976;McGeer et al, 1980), and strong evidence shows that it produces these effects by blocking inhibitory (and to a lesser extent excitatory) transmission presynaptically Mellanby and Green, 1981;Wellhoner, 1982;Bergey et al, 1983). However, Mellanby et al (Mellanby et al, 1977;Mellanby and George, 1979;Hawkins and Mellanby, 1987) were first to explore its use in producing an animal model for focal epilepsy; they demonstrated and extensively documented in-rats a semichronic*, focal epileptiform jection of tetanus toxin in the hippocampus.…”

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Chronic Semichronic Limbic Epilepsy Produced by Microinjection of Tetanus Toxin in Cat Hippocampus

Darcey

Williamson

1992

Epilepsia

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We describe an animal preparation in which a semichronic or chronic limbic epileptiform syndrome can be produced reliably by unilateral microinjection of tetanus toxin in cat ventral hippocampus. Injections were given at 1-week intervals until abnormal EEG activity was observed. After two to five injections, the animals abruptly began to exhibit intermittent spikes and subclinical discharges that soon gave way to spontaneous and recurrent behavioral seizures which gradually increased in frequency, duration, and severity in the next 12-48 h. Anticonvulsant therapy (phenobarbital, PB) was required within the first 3 days of the syndrome, since life-threatening generalized tonic-clonic seizures (GTCS) and status epilepticus would develop if the animal were left untreated. If severe seizures were prevented by antiepileptic drugs (AEDs) there was complete remission of the syndrome and repeat injection was necessary to reinitiate seizures. Animals that experienced severe seizures or that were reinjected after remission developed a chronic seizure syndrome and could be maintained with AEDs for long times (greater than 1 year) without significant debilitation. Although early spikes and subclinical discharges were typically focal to ipsilateral limbic sites, initial seizures appeared explosively in the form of a high-amplitude, high-frequency discharge, which often had an apparently bilateral limbic onset. On the other hand, chronic seizures had much more gradual onset and spread, often consisting of periodic sharp waves or low-amplitude sinusoidal discharge that was more clearly focal to ipsilateral limbic sites. Throughout the syndrome, ictal behavioral manifestations were highly stereotyped and very comparable to those described by other investigators in studies of clinical and experimental limbic epilepsy. All animals exhibited signs of independent contralateral involvement during the syndrome, ranging from independent contralateral spikes to subclinical discharges with a clear contralateral onset. None of the animals exhibited structural lesions on histologic examination at the level of light microscopy.

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confidence: 99%

Chronic Semichronic Limbic Epilepsy Produced by Microinjection of Tetanus Toxin in Cat Hippocampus

Darcey

Williamson

1992

Epilepsia

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Electrical excitability of motoneurones in early local tetanus

Wiegand

1979

Naunyn-Schmiedeberg's Arch. Pharmacol.

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1. After injection of tetanus toxin into the gastrocnemius muscle of the cat non-synaptic excitability of motoneurones was studied in early local tetanus. Antidromic stimulation of motoneurones was performed onthe toxin-treated side and on the control side of the same cat. 2. The mean resting membrane potential of the motoneurones on the toxin-treated side did not differ from that on the control side. 3. Similarly, no differences were found as to the amplitude of the action potential and its rate of rise as well as to the size and time course of the after-hyperpolarization. 4. The mean input resistance of the motoneurones of the toxintreated side did not differ from that of the motoneurones of the control side. 5. Tetanus toxin did not change the mean refractory period and latency of antidromic responses. 6. It is concluded that the action of tetanus toxin the spinal cord cannot be explained by an action of the toxin on the electrically excitable membrane elements of the motoneurones.

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Tetanus toxin and botulinum A toxin inhibit release and uptake of various transmitters, as studied with particulate preparations from rat brain and spinal cord

Bigalke¹,

Heller²,

Bizzini

et al. 1981

Naunyn-Schmiedeberg's Arch. Pharmacol.

125

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Creation of hyperactive determinant dispatch stations in the caudate nucleus in experimental neuropathological syndromes caused by tetanus toxin

Cited by 5 publications

References 1 publication

Chronic Semichronic Limbic Epilepsy Produced by Microinjection of Tetanus Toxin in Cat Hippocampus

Chronic Semichronic Limbic Epilepsy Produced by Microinjection of Tetanus Toxin in Cat Hippocampus

Electrical excitability of motoneurones in early local tetanus

Tetanus toxin and botulinum A toxin inhibit release and uptake of various transmitters, as studied with particulate preparations from rat brain and spinal cord

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