Zinc Transporter 3 (ZnT3) in the Enteric Nervous System of the Porcine Ileum in Physiological Conditions and during Experimental Inflammation

Abstract

Zinc transporter 3 (ZnT3) is a member of the solute-linked carrier 30 (SLC 30) zinc transporter family. It is closely linked to the nervous system, where it takes part in the transport of zinc ions from the cytoplasm to the synaptic vesicles. ZnT3 has also been observed in the enteric nervous system (ENS), but its reactions in response to pathological factors remain unknown. This study, based on the triple immunofluorescence technique, describes changes in ZnT3-like immunoreactive (ZnT3-LI) enteric neurons in the porcine ileum, caused by chemically-induced inflammation. The inflammatory process led to a clear increase in the percentage of neurons immunoreactive to ZnT3 in all “kinds” of intramural enteric plexuses, i.e., myenteric (MP), outer submucous (OSP) and inner submucous (ISP) plexuses. Moreover, a wide range of other active substances was noted in ZnT3-LI neurons under physiological and pathological conditions, and changes in neurochemical characterisation of ZnT3+ cells in response to inflammation depended on the “kind” of enteric plexus. The obtained results show that ZnT3 is present in the ENS in a relatively numerous and diversified neuronal population, not only in physiological conditions, but also during inflammation. The reasons for the observed changes are not clear; they may be connected with the functions of zinc ions and their homeostasis disturbances in pathological processes. On the other hand, they may be due to adaptive and/or neuroprotective processes within the pathologically altered gastrointestinal tract.

Influence of Acrylamide Administration on the Neurochemical Characteristics of Enteric Nervous System (ENS) Neurons in the Porcine Duodenum

“…This is congruent with the phenomenon of neural plasticity, described by many authors as an adaptation in ENS neurons to disturbances of homeostasis and pathological factors manifested by the change of neurochemical features of neurons, overexpression of certain genes, or a reduction in the expression of others [32]. The plasticity of ENS neurons has been confirmed in studies demonstrating the effect of pathological gut conditions, intoxications, and other experimental treatments in numerous animal models and humans [13,15,18,19,21,25,33].…”

“…The reaction of the ENS to pathological factors expressed as a change in the chemical coding of intramural neurons may be the first subclinical symptom of GI tract disorders. Previous reports revealed that gastrointestinal disturbances accompanying metabolic diseases, and naturally and experimentally induced inflammatory conditions and toxins, such as mycotoxins or bisphenol A, led to changes in the expression of neuroactive substances in ENS neurons within the intestines [15][16][17][18][19]. These changes are evidence of the high plasticity of the nervous system and may help recognize neuropeptides involved in protection of neurons from damage.…”

Bisphenol A Causes Liver Damage and Selectively Alters the Neurochemical Coding of Intrahepatic Parasympathetic Nerves in Juvenile Porcine Models under Physiological Conditions

“…VAChT is an enzyme important for the proper neural functioning of the PSNS (parasympathetic nervous system). The PSNS is the most commonly used part of the autonomic nervous system (ANS), and is often known as the “rest and digest” portion of the ANS [ 37 , 38 ]. The PSNS is characterized by its use of acetylcholine as the main neurotransmitter for cellular communication.…”

“…The PSNS is characterized by its use of acetylcholine as the main neurotransmitter for cellular communication. Tissues associated with the PSNS are characterized as having many acetylcholine receptors [ 18 , 37 , 38 ]. The results of this study found no significant changes in the VAChT + nerve fibers.…”

Immunohistochemical characteristics of porcine intrahepatic nerves under physiological conditions and after Bisphenol A administration

“…After at least 2 weeks, the fragments of liver were frozen at -23°C and cut into 10 μm-thick sections using a microtome (Microm, HM 525, Walldorf, Germany). The sections were subjected to a routine single-labelling immunofluorescence technique according to the method described previously by Gonkowski and Wojtkiewicz [17,18,35,59]. A condensed description of the method is as follows: 45 min of drying; incubation with a blocking solution, which included 10% normal goat serum, 0.1% bovine serum albumin, 0.01% NaN3, Triton ×-100 and thimerozal in phosphate buffered saline (PBS) for 1 h; overnight incubation with a polyclonal "primary" antibody directed towards SP, GAL, PACAP, CGRP, or CART; incubation (for 1 h) with species-specific antisera conjugated to fluorescein isothiocyanate (FITC) or biotin, which was visualised by a streptavidin-CY3 complex (the specification of primary and secondary antibodies used in the present study is shown in Table 1).…”