Abstract
The role of the Merkel cell-neurite complex in the
transduction process in slowly adapting type 1 {SA1)
cutaneous mechanoreceptors is unresolved. One hypothesis,
based largely on the ultrastrueture of Merkel cell-neurite
complexes, suggests that chemosynaptic transmission occurs
between the Merkel cell and its subjacent nerve terminal.
This idea was investigated by mechanically stimulating SA1
mechanoreceptors exposed to pharmacologically active
agents in several experimental preparations; an in vivo
rat model, and in vivo feline isolated hind limb perfusion
model and a novel isolated rat skin-nerve preparation.
After exposure to the calcium channel blockers Mg2+,
Cd2+ and verapamil hydrochloride there was a dose
dependent decline in the response of the SA1
mechanoreceptors to mechanical stimulation. Given that an
influx of Ca2+ ions is required for stimulus-secretion
coupling, these results suppo rt the hypothesis of
chemosynaptic transmission.
Immunohistochemical studies have shown that a metenkephalin-like substance is associated with the dense
cored vesicles in rodent Merkel cells. The idea that metenkephalin was the transmitter substance in rat Merkel
cell-neurite complexes was tested using the opiate
antagonist naloxone and the agonist met-enkephalin in the
isolated rat skin-nerve preparation. Met-enkephalin
caused a dose dependent decline in the response of the SAl
mechanoreceptors to mechanical stimulation. This effect
was antagonised by naloxone, indicating the presence of
functional opioid receptors in the SAl sensory receptor.
However, this result indicates that met-enkephalin is not
the excitatory transmitter substance in rat Merkel cellneurite complexes, though it does have a modulatory role.
The results presented in this thesis support the
hypothesis that chemosynaptic transmission is involved in
the transduction process in the Merkel cell-neurite
complex.
