Publications by authors named "S Hallermann"

Article Synopsis
  • Autoantibodies against LGI1 are linked to autoimmune encephalitis, impacting the limbic system and causing seizures and memory issues.
  • The study focused on how these autoantibodies influence synaptic structure and function, revealing effects on neurotransmitter release.
  • Results showed that LGI1 autoantibodies enhanced neurotransmission by increasing release probability but did not affect presynaptic calcium channels; however, they reduced certain potassium channel densities.
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Article Synopsis
  • Latrodectism, caused by widow spider bites, leads to severe pain and various health complications, posing a significant global health issue, particularly in developing countries.
  • Current treatments include equine serum-derived antivenoms, which have potential risks like allergic reactions, batch variability, and controversial efficacy since latrodectism is seldom fatal.
  • Research has developed fully human antibodies that effectively neutralize alpha-latrotoxin from widow spiders, demonstrating potential for safer, more targeted therapies and diagnostics in the future.
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Understanding the function of the human brain requires determining basic properties of synaptic transmission in human neurons. One of the most fundamental parameters controlling neurotransmitter release is the presynaptic action potential, but its amplitude and duration remain controversial. Presynaptic action potentials have so far been measured with high temporal resolution only in a limited number of vertebrate but not in human neurons.

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One striking clinical hallmark in patients with autoantibodies to leucine-rich glioma inactivated 1 (LGI1) is the very frequent focal seizure semiologies, including faciobrachial dystonic seizures (FBDS), in addition to the amnesia. Polyclonal serum IgGs have successfully modelled the cognitive changes in vivo but not seizures. Hence, it remains unclear whether LGI1-autoantibodies are sufficient to cause seizures.

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Pre- and postsynaptic forms of long-term potentiation (LTP) are candidate synaptic mechanisms underlying learning and memory. At layer 5 pyramidal neurons, LTP increases the initial synaptic strength but also short-term depression during high-frequency transmission. This classical form of presynaptic LTP has been referred to as redistribution of synaptic efficacy.

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