Mechanical sensitivity of carotid body glomus cells.

Cultured glomus cells from rat carotid bodies were prepared for optical studies of intracellular calcium using the Fura-2 dye. The baseline calcium had a mean of about 40 nM showing either a relatively steady level or large calcium spikes. Some cells did not show measurable levels of [Ca(2+)](i). Stirring the fluid bathing the cultures induced large increases in [Ca(2+)](i) which were abolished when the bathing medium had zero Ca(2+) and EGTA. It is concluded that glomus cells respond to mechanical stimulation when directly exposed to this stimulus and are not protected by supporting structures. It is unknown if the electrical properties of these cells are also affected by mechanical challenges.

Electric synapses in the carotid body-nerve complex.

Slices of rat carotid bodies, or cultured glomus cells, were used to study intercellular coupling. This phenomenon occurs because gap junctions allow passage of currents and dyes from one cell to another. There is a two-way resistive coupling between glomus cells (GC/GC coupling), which is accompanied by activity of intercellular channels. Coupling between glomus cells and nerve endings is more complex. Coupling is mostly resistive from cell to nerve (GC/NE) but it is mostly capacitive in the opposite direction (NE/GC). Thus, slow electric events originating in the glomus cells can be transferred to the nerve endings. But, only electric transients can pass from nerve to cell. There is also coupling between nerve endings (NE/NE), which is mostly capacitive in either direction. Chemoreceptor stimulants (acute and chronic hypoxia, hypercapnia, acidity, cholinergic agents and dopamine) uncouple most glomus cells, accompanied by cell depolarization and decreased amplitude of junction channels. Chronic hypobaric hypoxia increases GC/NE, NE/GC and NE/NE coupling. GC/GC uncoupling seems related to transmitter secretion. Transmission across chemical synapses is aided by increased coupling from glomus cell to nerve ending.

Electrophysiological properties of rat nodose ganglion neurons co-transplanted with carotid bodies into the chick chorioallantoic membrane.

The electrophysiological properties of nodose ganglion neurons were evaluated immediately after removing nodose ganglia from young adult rats and 3 to 10 days after nodose ganglia implantation -either alone or co-implanted with carotid bodies- onto the chick chorioallantoic membrane. Implanted and co-implanted nodose neurons were less excitable than acutely recorded nodose neurons. Co-implanted neurons also showed reduced amplitudes for both action potentials and spike after-hyperpolarizations relative to those found in. acutely recorded nodose ganglion neurons and a smaller time constant (T) than that found in implanted neurons. In addition, no spontaneous activity was recorded from nodose ganglion neurons co-implanted with carotid bodies during 3-9 days, which suggests that functional synapses between carotid glomus cells and nodose neurons were not yet established. Results indicate the feasibility of obtaining viable nodose neurons for up to 10 days grafted onto the chick chorioallantoic membrane, where they can conserve most of their passive and active membrane properties and also are susceptible to carotid bodies trophic influences. They also suggest that nodose neurons would need more time for the development of functional synapses when grafted with carotid body glomus cells.

Chemical and electric transmission in the carotid body chemoreceptor complex.

Carotid body chemoreceptors are complex secondary receptors. There are chemical and electric connections between glomus cells (GC/GC) and between glomus cells and carotid nerve endings (GC/NE). Chemical secretion of glomus cells is accompanied by GC/GC uncoupling. Chemical GC/NE transmission is facilitated by concomitant electric coupling. Chronic hypoxia reduces GC/GC coupling but increases G/NE coupling. Therefore, carotid body chemoreceptors use chemical and electric transmission mechanisms to trigger and change the sensory discharge in the carotid nerve.

Electrophysiological properties of rat nodose ganglion neurons co-transplanted with carotid bodies into the chick chorioallantoic membrane

The electrophysiological properties of nodose ganglion neurons were evaluated immediately after removing nodose ganglia from young adult rats and 3 to 10 days after nodose ganglia implantation _either alone or co-implanted with carotid bodies_ onto the chick chorioallantoic membrane. Implanted and co-implanted nodose neurons were less excitable than acutely recorded nodose neurons. Co-implanted neurons also showed reduced amplitudes for both action potentials and spike after-hyperpolarizations relative to those found in acutely recorded nodose ganglion neurons and a smaller time constant (ô) than that found in implanted neurons. In addition, no spontaneous activity was recorded from nodose ganglion neurons co-implanted with carotid bodies during 3-9 days, which suggests that functional synapses between carotid glomus cells and nodose neurons were not yet established. Results indicate the feasibility of obtaining viable nodose neurons for up to 10 days grafted onto the chick chorioallantoic membrane, where they can conserve most of their passive and active membrane properties and also are susceptible to carotid bodies trophic influences. They also suggest that nodose neurons would need more time for the development of functional synapses when grafted with carotid body glomus cells.

Chemical and electric transmission in the carotid body chemoreceptor complex

Carotid body chemoreceptors are complex secondary receptors. There are chemical and electric connections between glomus cells (GC/GC) and between glomus cells and carotid nerve endings (GC/NE). Chemical secretion of glomus cells is accompanied by GC/GC uncoupling. Chemical GC/NE transmission is facilitated by concomitant electric coupling. Chronic hypoxia reduces GC/GC coupling but increases G/NE coupling. Therefore, carotid body chemoreceptors use chemical and electric transmission mechanisms to trigger and change the sensory discharge in the carotid nerve.