Low doses of urethane effectively inhibit spinal seizures evoked by sudden cooling of toad isolated spinal cord

Piña‐Crespo, Juan C.; Daló, Nelson L.

doi:10.1016/0024-3205(92)90022-h

Cited by 8 publications

(4 citation statements)

References 20 publications

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“…By reducing excitation via glutamate receptor antagonism and enhancing inhibition via potentiation of GABA receptors, urethane-like inhalational anesthetics may reduce excitatory drive on neuronal firing and networks. This action of urethane appears to be model independent as urethane reduces epileptiform activity in rats that experience SE induced by DFP in the current study and blocks the development of amygdala kindled seizures in rodents ( Cain et al, 1989, 1992 ) as well as spinal seizures evoked by sudden cooling in a toad isolated spinal cord preparation ( Piña-Crespo and Daló, 1992 ). Felbamate, which is structurally and functionally similar to urethane, is a very effective anticonvulsant in partial epilepsies.…”

Section: Discussionmentioning

confidence: 67%

“…The widely used veterinary anesthetic urethane (ethyl carbamate) can produce a subanesthetic state of drowsiness or a long-lasting deep level of anesthesia without affecting autonomic and cardiovascular systems ( Soma, 1983 ; Maggi and Meli, 1986 ). Urethane reduces epileptiform activity and blocks the development of amygdala kindled seizures in rodents ( Cain et al, 1989 , 1992 ) as well as spinal seizures evoked by sudden cooling in a toad isolated spinal cord preparation ( Piña-Crespo and Daló, 1992 ). The molecular mechanisms underpinning the anesthetic effects of urethane involve both inhibition of excitatory neurotransmitter receptors and potentiation of inhibitory transmitter receptors ( Hara and Harris, 2002 ).…”

Section: Introductionmentioning

confidence: 99%

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Beneficial Outcome of Urethane Treatment Following Status Epilepticus in a Rat Organophosphorus Toxicity Model

Rojas

Wang

Glover

et al. 2018

eNeuro

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Section: Discussionmentioning

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Beneficial Outcome of Urethane Treatment Following Status Epilepticus in a Rat Organophosphorus Toxicity Model

Rojas

Wang

Glover

et al. 2018

eNeuro

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“…Thus, the urethane dose used in this study (1 mg/ml) is approximately equivalent to doses used as an anesthetic in the rat and it is possible that some of the effects observed here may also be relevant to urethane's anesthetic action. In addition to the reduction of serotonergic and noradrenergic transmission noted here, urethane may also block excitatory amino acid transmission (Dalo and Larson, 1990;Pina-Crespo and Dalo, 1992), and it hyperpolarizes neurons, possibly by increasing potassium conductance (Nicoll and Madison, 1982).…”

Section: Discussionmentioning

confidence: 93%

Urethane reduces contraction to 5-hydroxytryptamine (5-HT) and enhances the action of the 5-HT antagonist ketanserin on the rat thoracic aortic ring

Dringenberg

Vanderwolf

Hamilton

1995

J. Neural Transmission

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The general anesthetic urethane (ethyl carbamate) is widely used in electrophysiological in vivo experiments. However, its pharmacological effects are poorly understood. Here, the effects of urethane on in vitro contractile responses of the rat thoracic aortic ring preparation were investigated. Bath application of 5-HT produced a concentration-dependent contractile response (EC50 = 4.3 x 10(-6) M). Urethane (11.2 mM = 1 mg/ml) shifted the concentration-response curve (CRC) for 5-HT to the right (EC50 = 1.7 x 10(-5) M) and decreased the maximal contraction by 30.8%. The CRC for NA (EC50 = 7.2 X 10(-9)M) was also shifted to the right by urethane (EC50 = 1.4 X 10(-8)M), but the shift of the 5-HT-CRC was twice that of the NA-CRC (3.95 vs. 1.95). The CRC to KCl was shifted rightwards only slightly by urethane (ratio 1.27) and the maximal contraction to KCl was not affected. The CRC to replacement of CaCl2 (0.1-10 mM) to KCl-depolarized vessels in a Ca(2+)-free Krebs solution was unaffected by urethane. Ketanserin (10(-9)M) antagonized the contraction to 5-HT, and a combination of ketanserin and urethane was markedly more effective than either drug alone, decreasing the maximal contraction by 58%. Antagonism of NA contraction by prazosin (5 X 10(-8)M) was not increased by addition of urethane. The urethane dose used here approximates blood and brain concentrations required to produce anesthetic effects in mammals. It is possible that reductions in 5-HT transmission and, to a lesser extent, in NA transmission, but not blockade of Ca2+ or K+ channels, may contribute to the anesthetic effect of urethane. In addition, the action of the selective 5-HT2 antagonist ketanserin is clearly altered by urethane. These findings are important to consider when urethane is used for in vivo neurophysiological investigations, particularly when 5-HT mechanisms are involved.

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“…None of the animals that were placed into the cold room showed the typical convulsion observed using a rapid cooling technique, but we had seen excitation in about 70% of them that was well prevented by pretreatment with urethane. Urethane blocks induction of seizure when the isolated spinal cord is rapidly cooled (Piña‐Crespo & Daló 1992).…”

Section: Discussionmentioning

confidence: 99%

Motor impairment and neuronal damage following hypothermia in tropical amphibians

Daló

Bracho

Piña‐Crespo

2006

Int J Experimental Path

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Although the induction of mild to moderate cerebral hypothermia in mammals can have neuroprotective activity, some deleterious effects have been described when inducing deep hypothermia during cooling of the brain. In the spinal cord, rapid deep cooling can induce seizure activity accompanied by release of the excitatory neurotransmitters, glutamate and aspartate. We used cold-sensitive tropical amphibians as a model to determine (a) the critical temperature inside the central nervous system necessary to induce seizures during rapid cooling; (b) the survival rate during slow deep cooling of the whole animal; and (c) whether deep cooling can cause neuronal cell damage. Seizures induced by deep rapid (or=30 min) deep cooling of the whole animal (12 h at 2-3 degrees C), around 70% of animals died. Spinal reflexes were enhanced when temperatures within the spinal cord reached between 9.0 degrees C and 11.6 degrees C. A fivefold increase in blood glucose level was observed during slow deep cooling. Recovery after slow deep cooling was accompanied by motor impairment and the main histological findings were condensation of the cytoplasm and nuclear pyknosis. Severe neuronal cell damage was characterized by swelling, vacuolated cytoplasm with distended neuronal bodies. These results indicate that deep cooling can easily induce neuronal cell damage in the central nervous system of cold-sensitive animals. They also warn us to the potential sequels associated with the use of deep brain cooling as a neuroprotective strategy.

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Low doses of urethane effectively inhibit spinal seizures evoked by sudden cooling of toad isolated spinal cord

Cited by 8 publications

References 20 publications

Beneficial Outcome of Urethane Treatment Following Status Epilepticus in a Rat Organophosphorus Toxicity Model

Beneficial Outcome of Urethane Treatment Following Status Epilepticus in a Rat Organophosphorus Toxicity Model

Urethane reduces contraction to 5-hydroxytryptamine (5-HT) and enhances the action of the 5-HT antagonist ketanserin on the rat thoracic aortic ring

Motor impairment and neuronal damage following hypothermia in tropical amphibians

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