Effective electrical head-only stunning produces a seizure-like state followed by a period of analgesia seen in animals allowed to recover. Passing of a 1·0 A current (50 Hz, 500 V) for less than 0·2 s, through the head of a sheep does not produce a seizure-like state as evidenced by recorded electroencephalogram. Corresponding to this lack of seizure-like state, the release of the neurotransmitters glutamate and aspartate, in the brain, occurs to levels associated with arousal rather than seizure. At a duration of 0·2 s, the same stun parameters as above produce a seizure-like state and the release of glutamate and aspartate rises dramatically. The length of the seizure-like state, and the levels of release of glutamate, aspartate and a third neurotransmitter gamma amino-4-butyric acid (GABA), increased with stun duration until 4·0 s duration, where a peak in these parameters was seen. Stun durations of 2·0, 4·0, 8·0 and 12·0 s all produce similar effects. At a duration of 20 s, however, the length of the seizure-like state and the release of neurotransmitters is less than at shorter stun durations. For welfare purposes a head-only electrical stun, of 1·0 A, at a duration as low as 0·2 s produces unconsciousness and analgesia to subsequent slaughter procedures. However, maximum welfare benefits appear attainable at durations between 2·0 and 20·0 s.
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http://dx.doi.org/10.1016/0309-1740(94)00043-7 | DOI Listing |
Neuropharmacology
March 2025
Department of Neurology, Columbia University Irving Medical Center, 710 West 168th Street, New York, NY, 10032-3784, USA. Electronic address:
Tumor associated epilepsy is a common and debilitating co-morbidity of brain tumors, for which inadequate treatments are available. Additionally, animal models suggest a potential link between seizures and tumor progression. Our group has previously described a mouse model of diffusely infiltrating glioma and associated chronic epilepsy.
View Article and Find Full Text PDFEpilepsia
December 2024
Shanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science and Institutes of Brain Science, Fudan University, Shanghai, China.
Objective: The piriform cortex (PC) plays a critical role in ictogenesis, where an excitation/inhibition imbalance contributes to epilepsy etiology. However, the epileptic dynamics of the gamma-aminobutyric acid (GABA) system and the precise role of GABAergic neurons within the PC in epilepsy remain unclear.
Methods: We combined Ca and GABA sensors to investigate the dynamics of Gad2-expressing neurons and GABA levels, and selectively manipulated GABAergic neurons in the PC through chemogenetic inhibition and caspase3-mediated apoptosis targeting Gad2 interneurons.
Nat Neurosci
December 2024
Department of Neurological Surgery, University of California, San Francisco, San Francisco, CA, USA.
Seizures are made up of the coordinated activity of networks of neurons, suggesting that control of neurons in the pathologic circuits of epilepsy could allow for control of the disease. Optogenetics has been effective at stopping seizure-like activity in non-human disease models by increasing inhibitory tone or decreasing excitation, although this effect has not been shown in human brain tissue. Many of the genetic means for achieving channelrhodopsin expression in non-human models are not possible in humans, and vector-mediated methods are susceptible to species-specific tropism that may affect translational potential.
View Article and Find Full Text PDFCureus
October 2024
Medicine, NYC Health + Hospitals, New York, USA.
Cell Metab
January 2025
Division of Glial Disease and Therapeutics, Center for Translational Neuromedicine, Department of Neurosurgery, University of Rochester Medical Center, Rochester, NY 14642, USA; Division of Glial Disease and Therapeutics, Center for Translational Neuromedicine, University of Copenhagen, 2200 Copenhagen, Denmark; Center for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Copenhagen N, Denmark. Electronic address:
The brain's ability to rapidly transition between sleep, quiet wakefulness, and states of high vigilance is remarkable. Cerebral norepinephrine (NE) plays a key role in promoting wakefulness, but how does the brain avoid neuronal hyperexcitability upon arousal? Here, we show that NE exposure results in the generation of free fatty acids (FFAs) within the plasma membrane from both astrocytes and neurons. In turn, FFAs dampen excitability by differentially modulating the activity of astrocytic and neuronal Na, K, ATPase.
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