The use of antisera directed against conjugates of histamine and serotonin has revealed the locations of neurons labeling for these transmitters in the nervous system of barnacles. Photoreceptors label for histamine but not serotonin and also satisfy a number of other criteria indicating that histamine is their neurotransmitter. Photoreceptors also take up radioactively labeled histamine but not serotonin. Within the barnacle's brain no somata are consistently found that label with antiserum against histamine, but one to three pairs of small cells, depending on species, label with antiserum against serotonin. The most impressive serotonin-like immunoreactivity in the brain, however, is in a pair of large fibers ascending through the circumesophageal connectives and ramifying extensively. Within the ventral ganglion, the only other ganglion in the barnacle, ten pairs of cells label with antiserum against histamine. These neurons are confined to the posterior portion of the ganglion but ramify extensively throughout the ganglion. Antiserum against serotonin labels about 15 cell pairs, depending on species, located throughout the ganglion. The positions of the arbors of many of these cells suggest that these amines have a role in modulating either the motor pathways underlying feeding or the visual pathways responsible for the detection of shadows.

Animals↗

PubMedDate not supplied

Internal herniation involving the sigmoid mesocolon.

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Aged↗

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Currents in the presynaptic terminal arbors of barnacle photoreceptors.

We have described the currents flowing across the presynaptic membranes of the four median photoreceptors of the giant barnacle, Balanus nubilus, using a quasi-voltage clamp arrangement. Membrane potential, measured in the terminal region of one photoreceptor, was controlled in all four terminals by feedback current supplied through the nerve containing the photoreceptors' axons. The [Ca2+]o in the saline was reduced to decrease the Ca2+ current, enabling better voltage control, and tetraethylammonium ion (TEA, 20 mM) was added to block a fast voltage-dependent K+ conductance. Depolarizing voltage steps from the resting potential in the dark (-60 mV) evoked slow, inward Ca(2+)-dependent currents which could be blocked by Co2+, Mg2+, or Cd2+. The Ca2+ currents were followed by large outward currents that persisted for many seconds after the offset of moderate or large pulses. These tail currents increased in magnitude and duration with pulse duration and reversed at about -80 mV, consistent with previous evidence for a Ca(2+)-activated K+ conductance in this membrane. When the Ca(2+)-activated outward current was reduced to zero by increasing the [K+]o so as to set EK at -20 mV, and then stepping the voltage to this value, the step evoked a steady inward Ca2+ current. Thus, the Ca2+ current did not show voltage- or Ca(2+)-dependent inactivation. When Ba2+ was substituted for Ca2+, 500-ms depolarizing steps evoked steady inward currents but no outward currents. In any given experiment, the activation voltage of the Ca2+ or Ba2+ current did not depend on holding potential. At the barnacle photoreceptor's synapse, the postsynaptic cell adapts to maintained presynaptic voltage by a mechanism that is not understood. We conclude that neither Ca2+ current inactivation nor a shift in activation voltage with holding potential can account for this adaptation.

Adaptation, Physiological↗