scholarly journals Long-term observation of incremental response and antibodies to voltage-gated calcium channels in patients with Lambert–Eaton myasthenic syndrome: two case reports

2015 ◽  
Vol 9 (1) ◽  
Author(s):  
Ilka Schneider ◽  
Malte E Kornhuber ◽  
Frank Hanisch
2021 ◽  
Vol 11 (8) ◽  
pp. 1035
Author(s):  
Maria Pia Giannoccaro ◽  
Patrizia Avoni ◽  
Rocco Liguori

The neuromuscular junction (NMJ) is the target of a variety of immune-mediated disorders, usually classified as presynaptic and postsynaptic, according to the site of the antigenic target and consequently of the neuromuscular transmission alteration. Although less common than the classical autoimmune postsynaptic myasthenia gravis, presynaptic disorders are important to recognize due to the frequent association with cancer. Lambert Eaton myasthenic syndrome is due to a presynaptic failure to release acetylcholine, caused by antibodies to the presynaptic voltage-gated calcium channels. Acquired neuromyotonia is a condition characterized by nerve hyperexcitability often due to the presence of antibodies against proteins associated with voltage-gated potassium channels. This review will focus on the recent developments in the autoimmune presynaptic disorders of the NMJ.


1993 ◽  
Vol 3 (5-6) ◽  
pp. 451-454 ◽  
Author(s):  
Pascale David ◽  
Nicole Martin-Moutot ◽  
Christian Leveque ◽  
Oussama El Far ◽  
Masami Takahashi ◽  
...  

2005 ◽  
Vol 93 (5) ◽  
pp. 3012-3015 ◽  
Author(s):  
Yu Fu ◽  
Patricia Shinnick-Gallagher

Synaptic plasticity in the amygdala is thought to underlie aversive or rewarding learning and emotional memories. In this study, different mechanisms were found to underlie synaptic plasticity in lateral (LA) and basolateral (BLA) amygdala pathways to the primary output nucleus of the amygdala, the central amygdala (CeA). Specifically, 1) long-term potentiation (LTP) at the BLA-CeA synapses was independent of inhibition and mediated through N-methyl-d-aspartate receptors (NMDARs) and L-type voltage-gated calcium channels (VGCCs), and 2) LTP in the LA-CeA pathway was gated by inhibition and mediated through VGCCs but not NMDARs.


2002 ◽  
Vol 25 (5) ◽  
pp. 715-724 ◽  
Author(s):  
Ashwin Pinto ◽  
Kazuo Iwasa ◽  
Claire Newland ◽  
John Newsom-Davis ◽  
Bethan Lang

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