Cholinesterases in Tripartite Neuromuscular Synapse.

The neuromuscular junction (NMJ) is a tripartite synapse in which not only presynaptic and post-synaptic cells participate in synaptic transmission, but also terminal Schwann cells (TSC). Acetylcholine (ACh) is the neurotransmitter that mediates the signal between the motor neuron and the muscle but also between the motor neuron and TSC. ACh action is terminated by acetylcholinesterase (AChE), anchored by collagen Q (ColQ) in the basal lamina of NMJs.

Influence of the Activation of NMDA Receptors on the Resting Membrane Potential of the Postsynaptic Cell at the Neuromuscular Junction.

Impaired function or insufficient expression of glutamate N-methyl-D-aspartate (NMDA) receptors underlies a number of brain pathologies; these receptors are, therefore, regarded as a pharmacological target for many neuroactive drugs. It was shown that in the CNS, this type of glutamate receptors participate in the processes of neuronal excitation, synaptic plasticity [1, 2], and excitotoxicity in neurodegenerative diseases and are also involved in the pathogenesis of epilepsy and seizures. However, until recently, the presence and activity of NMDA receptors beyond the CNS had never been considered.

Data demonstrating the Finnish wood pellet industry and future perspectives.

This article contains data related to the research article entitled "A survey analysis of the wood pellet industry in Finland: Future perspectives" (S. Proskurina, E. Alakangas, J.

Regulation of acetylcholinesterase activity by nitric oxide in rat neuromuscular junction via N-methyl-D-aspartate receptor activation.

Acetylcholinesterase (AChE) is an enzyme that hydrolyses the neurotransmitter acetylcholine, thereby limiting spillover and duration of action. This study demonstrates the existence of an endogenous mechanism for the regulation of synaptic AChE activity. At the rat extensor digitorum longus neuromuscular junction, activation of N-methyl-d-aspartate (NMDA) receptors by combined application of glutamate and glycine led to enhancement of nitric oxide (NO) production, resulting in partial AChE inhibition.