Abstract:
:Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease that affects upper and lower motor neurons and leads to death a few years after symptom onset. Despite its high morbidity and mortality, its underlying pathogenic mechanisms still remain poorly understood. Although there is increasing evidence for significant changes in the structure and function of synapses on motor neurons, there is a need for a systematic investigation of the role of each synapse subtype in the course of the disease. Here, we focus on large cholinergic synapses on motor neurons, known as C boutons, and investigate their role during ALS progression. We implement a genetic strategy for inactivation of the cholinergic output of C boutons in the SOD1G93A transgenic mouse model of ALS. We demonstrate that although C bouton cholinergic inactivation does not alter mouse survival, it exerts a beneficial effect on motor performance in the rotarod motor task, as evidenced by an increased latency to fall in SOD1G93A mice lacking C bouton cholinergic output. Our results suggest that C bouton cholinergic transmission exerts a negative effect on motor neuron function in ALS, possibly via aberrant excitation, and render C boutons a potential target for future pharmacological intervention.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Konsolaki E,Koropouli E,Tsape E,Pothakos K,Zagoraiou Ldoi
10.1016/j.neuroscience.2020.07.047subject
Has Abstractpub_date
2020-12-01 00:00:00pages
71-80eissn
0306-4522issn
1873-7544pii
S0306-4522(20)30490-5journal_volume
450pub_type
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