Effects of inflammation and axotomy on expression of acetylcholine transferase and nitric oxide synthetase within the cocaine- and amphetamine-regulated transcript-immunoreactive neurons of the porcine descending colon.

This study reports changes in expression of acetylcholine transferase (AChT) and nitric oxide synthetase (NOS) in neurons immunoreactive for cocaine- and amphetamine-regulated transcript (CART) peptides during chemically-driven inflammation and axotomy in the porcine descending colon. The co-localization of the neurotransmitters with CART was studied by double immunofluorescence in the myenteric plexus (MP) and outer submucosal plexus (OSP) of the porcine descending colon under physiological and selected pathological conditions. In control animals, neurons expressing CART also expressed AChT in 25.37 ± 0.98% and 26.73 ± 0.96% in the MP and OSP, respectively. Neuronal co-expression of CART with NOS occurred in 90.66 ± 2.13% and 88.09 ± 2.96% in the MP and OSP, respectively. Following axotomy the number of neurons co-expressing CART and AChT decreased to 16.50 ± 3.20% in the MP and increased to 35.49 ± 2.04% in the OSP, while the number of neurons co-expressing CART and NOS increased to 96.66 ± 2.38% in the MP and 97.46 ± 2.22% in the OSP. Experimentally-induced colitis resulted in an increase in the number of neurons co-expressing CART and AChT to 42.40 ± 2.28% in the MP and 63.62 ± 1.83% in the OSP. Similarly, in these animals the number of neurons co-expressing CART and NOS increased to 93.9 ± 2.58% in the MP and 90.43 ± 2.09% in the OSP. Sham-operated controls showed expression levels of 26.22 ± 0.66% (MP) and 27.02 ± 1.73% (OSP) for simultaneous CART and AChT expression and 94.18 ± 0.93% (MP) and 88.21 ± 0.81% (OSP) for CART and NOS co-localization. These data confirm that the examined neurotransmitters have a role in traumatic and inflammatory responses of enteric neurons.

Resiniferatoxin and tetrodotoxin induced NPY and TH immunoreactivity changes within the paracervical ganglion neurons supplying the urinary bladder.

Both resiniferatoxin (RTX) and tetrodotoxin (TTX) have been reported to be effective in several urinary bladder dysfunction clinical trials. The aim of this study was to establish the effect of intravesical administration of RTX and TTX on neuropeptides Y (NPY) and tyrosine hydroxylase (TH) relationship in the paracervical ganglion (PCG) neurons supplying the urinary bladder in the pig. TH is an enzyme responsible for catalyzing the conversion of the amino acid L-tyrosine to dihydroxyphenylalanine (DOPA) and is used as a marker of catecholaminergic neurons. NPY augments the vasoconstrictor effects of noradrenergic neurons, and is involved in pathophysiological processes as a neuromodulator. To identify the PCG neurons supplying urinary bladder Fast Blue (FB) was injected into the bladder wall prior to intravesical RTX or TTX administration. Consequent application of immunocytochemical methods revealed that in control group 64.08 % of FB-positive PCG neurons contain NPY and 4.25 % TH. Intravesical infusion of RTX resulted upregulation of the NPY-IR neurons to 82.97 % and TH-IR to 43.78 %. Also administration of TTX induced further increase number of TH-IR neurons to 77.49 % but induced decrease number of NPY-IR neurons to 57.45 %. Both neurotoxins affect chemical coding of the PCG neural somata supplying urinary bladder, but the effects of their action are different. This results shed light on possible involvement of RTX and TTX on curing tissue, and potentially could help us to broaden our neurourological armamentarium.