Immunoreactivity of neuron-specific enolase (NSE) in human pancreas in health and type 1 diabetes mellitus.

The role of neuron-specific enolase (glycolytic enzyme; marker of nerve fibers and Langerhans islet in human pancreas) in the development of type 1 diabetes mellitus was studied in autopsy specimens from 6 adult patients. Autopsied specimens of the pancreas from 7 subjects without carbohydrate metabolism disorders served as the control. Autopsied specimens of the pancreas from a child with the clinical diagnosis of type 1 diabetes mellitus, a child without carbohydrate metabolism disorders, and from 7 human fetuses of 15-40 weeks gestation were also studied. In control specimens, the neuron-specific enolase was detected in the pancreatic nerve fibers and Langerhans islets. Studies of pancreatic tissue specimens from adult patients with type 1 diabetes mellitus showed no immunopositive reaction to neuron-specific enolase in insulin-negative specimens. A possible mechanism of type 1 diabetes mellitus development is suggested.

Possible involvement of lactate in neuroglial interaction through nicotinic cholinergic synapses in the cranial cervical sympathetic ganglion.

Activities of LDH and its H- and M-isoforms in neurons and satellite gliocytes of the cranial cervical sympathetic ganglion in rabbits under normal conditions and during nicotinic cholinergic synapse blockade were evaluated by integral cytophotometry in tissue sections. Normally activity of H-isoform predominates in neurons and M-isoform in satellite gliocytes. Blockade of the cranial cervical sympathetic ganglion significantly decreased LDH activity (H- and M-isoforms) in neurons in direct proportion to the number of blocked nicotinic cholinergic receptors. Activity of M-isoform in satellite gliocytes decreased with increasing the degree of blockade, while activity of H-isoform did not change. The isoenzyme profile of LDH in satellite gliocytes reached the level of intact neurons. Presumably, lactate production in satellite gliocytes is regulated by sympathetic neurons through nicotinic cholinergic synapses.