Morphological comparison of small nerve fibres in gastric mucosa in non-diabetic and Type 2 diabetic subjects.

AIM: To determine changes in small nerve fibres in gastric mucosa in patients with Type 2 diabetes by morphological observation. METHODS: In twenty-five non-diabetic and 21 Type 2 diabetic participants, gastric mucosal biopsy under endoscopy was performed. Innervation in gastric mucosa was detected using immunohistochemical staining. Anti-protein gene product (PGP) 9.5 positive nerves underwent morphological observation and quantitative analysis. RESULTS: Small nerve fibres in gastric mucosa were shortened in the diabetic subjects. The ratio of gastric mucosal protrusions maintaining nerve fibres between gastric pits to total observed protrusions was lower in patients with Type 2 diabetes compared with the non-diabetic subjects (ratio of innervated protrusion/total protrusion: 0.49 +/- 0.12 vs. 0.89 +/- 0.06, P < 0.05). CONCLUSIONS: This study sets the scene for further research to investigate the relationship between gastric mucosal nerves and autonomic neuropathy or diabetic peripheral neuropathy.

Volatile anesthetic isoflurane inhibits LTP induction of hippocampal CA1 neurons through α4ß2 nAChR subtype-mediated mechanisms.

BACKGROUND AND PURPOSE: Volatile anesthetic isoflurane contributes to postoperative cognitive dysfunction and inhibition of long-term potentiation (LTP), a synaptic model of learning and memory, but the mechanisms are uncertain. Central neuronal α4ß2 subtype nicotinic acetylcholine receptors (nAChRs) are involved in the induction of LTP in the hippocampus. Isoflurane inhibits α4ß2 nAChRs at concentrations lower than those used for anesthesia. Therefore, we hypothesized that isoflurane-inhibited LTP induction of hippocampal CA1 neurons via α4ß2 nAChRs subtype inhibition. METHODS: Transverse hippocampal slices (400µm thick) were obtained from male rats (6-8 weeks old). Population spikes were evoked using extracellular electrodes by electrical stimulation of the Schaffer collateral-commissural pathway of rat hippocampal slices. LTP was induced using high frequency stimulation (HFS; 100Hz, 1s). Clinically relevant concentrations (0.125-0.5mM) of isoflurane with or without nicotine (nAChRs agonist), mecamylamine (nAChRs antagonist), 3-[2(S)-2-azetidinylmethoxy] pyridine (A85380) and epibatidine (α4ß2 nAChRs agonist), dihydro ß erythroidine (DHßE) (α4ß2 nAChRs antagonist) were added to the perfusion solution 20min before HFS to test their effects on LTP by HFS respectively. RESULTS: A brief HFS induced stable LTP in rat hippocampal slices, but LTP was significantly inhibited in the presence of isoflurane at concentrations of 0.125-0.5mM. The inhibitive effect of isoflurane on LTP was not only reversible and could be prevented by nAChRs agonist nicotine and α4ß2 nAChRs agonist A85380 and epibatidine, but also mimicked and potentiated by nAChRs antagonist mecamylamine and α4ß2 nAChRs antagonist DHßE. CONCLUSIONS: Inhibition of α4ß2 nAChRs subtype of hippocampus participates in isoflurane-mediated LTP inhibition.