PubMed · 7434593
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P Lennie. 1980. Parallel visual pathways: a review.. https://doi.org/10.1016/0042-6989(80)90115-7
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Dorsal root ganglion (DRG) neurons from control rats or from rats in which the sciatic nerve had been sectioned were studied by whole-cell recording techniques. Noradrenaline (10-100 micro;M) activated beta-adrenoceptors and increased L-type Ca2+ channel current in control DRG cells, but this had little effect on excitability (the number of action potentials generated by a pulse of current at rheobasic strength). By contrast, in cells from nerve-damaged animals, noradrenaline activated alpha2-adrenoceptors, suppressed N-type Ca2+ channel current, and increased excitability. In axotomized cells, it also reduced total outward current recorded at +70 mV. Because noradrenaline did not affect total outward current recorded in the presence of the Ca2+ channel blocker Cd2+ (0. 5-1 mM), its effects on excitability may result from reduction of Ca2+-sensitive K+-conductance(s) following suppression of N-type Ca2+ channel current. The strongest effects of noradrenaline were seen in small cells and in cells from animals that exhibited autotomy, a self-mutilatory behavior that can accompany peripheral nerve damage. Because many of these small DRG cells may be involved in the transmission of nociceptive information, changes in coupling between Ca2+ channels and adrenoceptors may contribute to the generation of the ectopic sensory nerve activity that has been implicated in the etiology of neuropathic pain.
Microphotolysis and confocal microscopy were used to investigate the timing of calcium release and of the electrical response in Limulus polyphemus ventral photoreceptors. The fluorescent dyes Fluo-3 and Calcium Green-5N were used to monitor local Ca2+ elevations. Photolysis of caged inositol trisphosphate (InsP3) close to the plasma membrane of the light-sensitive rhabdomeral (R-) lobe resulted in Ca2+ elevation within 10-20 msec, 20-45 msec before the physiological response to light normally would be detected. Inward ionic current flow and depolarization followed InsP3-induced calcium release within 2.5 +/- 3.3 msec. Voltage-clamping the cells and removal of extracellular Ca2+ did not affect the timing of the Ca2+ elevation that followed the photolysis of caged InsP3 or its relationship to the electrical response. In contrast to the physiological response to light, which only released calcium within the R-lobe, photolysis of InsP3 elevated Cai in both lobes, although with much greater effect in the R-lobe, as compared with the bulk of the A-lobe, suggesting the presence of InsP3-sensitive calcium stores in both lobes. Photolysis of caged calcium [o-nitrophenyl EGTA (NPE)] at the edge of the R-lobe activated an inward ionic current within 1.8 +/- 0.7 msec. This NPE-induced current reversed at a membrane potential of 10 +/- 6 mV in the range typical of that of the light-activated current under physiological conditions. Calcium release, therefore, activates an inward current rapidly enough to contribute to the electrical response to light.
The modulation of the pyloric rhythm of the stomatogastric ganglion of the crab, Cancer borealis, by crustacean cardioactive peptide (CCAP) is described. CCAP activated pyloric rhythms in most silent preparations, and altered the phase relationships of pyloric motor neuron firing in all preparations. In CCAP, the pyloric rhythms were characterized by long lateral pyloric (LP) neuron bursts of action potentials. The threshold for CCAP action was approximately 10(-10) M, with increasing effects at higher CCAP concentrations. The changes in motor pattern evoked by CCAP produced significant changes in LP-innervated muscle movement. These movements were additionally potentiated by CCAP applications to isolated nerve-muscle preparations. Thus, enhanced motor neuron firing and increase of the gain of the neuromuscular junctions are likely to operate coordinately in response to hormonally released CCAP. High CCAP concentrations sometimes resulted in modification of the normal 1:1 alternation between the pyloric dilator (PD) and LP neurons to patterns of 2:1, 3:1, or 4:1 alternation. CCAP seems to activate slow intrinsic oscillations in the LP neuron, as well as enhance faster oscillations in the pacemaker group of PD/anterior burster (AB) neurons. Simulations of fast and slow oscillators with reciprocal inhibitory coupling suggest mechanisms that could account for the mode switch from 1:1 alternation to multiple PD bursts alternating with one LP neuron burst.