PubMed · 9097639
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O Hasegawa. 1997. [Sensory nerve conduction studies].. https://pubmed.ncbi.nlm.nih.gov/9097639/
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In the first step toward identifying the neurotransmitter released from spiking interneurons of both local and intersegmental groups in the crayfish terminal abdominal ganglion, the authors examined whether spiking local interneurons and ascending intersegmental interneurons contain the transmitter gamma-aminobutyric acid (GABA). In this paper, 17 identified ascending interneurons and three spiking local interneurons were stained by intracellular injection of Lucifer yellow and subsequently treated for immunocytochemical staining against GABA. Double-labeling experiments revealed that six identified ascending interneurons are GABAergic, but no spiking local interneurons show GABA-like immunoreactivity. Four ascending interneurons with GABA-like immunoreactivity (reciprocal closing ascending neuron 5 [RC-5], reciprocal opening ascending neuron 6 [RO-6], variable-effect ascending interneuron 1 [VE-1], and no-effect ascending interneuron 4[NE-4]) had cell bodies that formed a cluster on the ventral surface of the rostral edge of the ganglion, whereas two GABAergic interneurons (coinhibiting ascending interneuron 2 [CI-2] and NE-2) had cell bodies in a caudal region around the cell body of the seventh flexor inhibitor (FI) motor neuron. Another four rostral interneurons (RC-2, RC-3, RC-4, and NE-3) and seven caudal interneurons (CI-3, RC-7, RO-1, RO-2, RO-3, RO-4, and NE-1) had no GABA-like immunoreactivity. Because VE-1 is known to make direct inhibitory connections with other ascending interneurons, whereas RC-3 and RO-1 are known to make direct excitatory connections, the immunocytochemical results from this study are consistent with previous physiological studies. Although many spiking local interneurons (including spiking local interneuron 1 of the anterior group [sp-ant1]) made direct inhibitory connections with nonspiking local interneurons, three spiking local interneurons (sp-ant1, spiking local interneuron 6 of the medial group [sp-med6], and spiking interneuron 5 of the posterior group [sp-post]) do not show GABA-like immunoreactivity. These results suggest that the inhibitory transmitter released from spiking local interneurons is not GABA but that another substance mediates the inhibitory action of these interneurons. J. Comp. Neurol. 410:677-688.
1. Calcium sparks were examined in enzymatically dissociated mouse cardiac ventricular cells using the calcium indicator fluo-3 and confocal microscopy. The properties of the mouse cardiac calcium spark are generally similar to those reported for other species. 2. Examination of the temporal relationship between the action potential and the time course of calcium spark production showed that calcium sparks are more likely to occur during the initial repolarization phase of the action potential. The latency of their occurrence varied by less than 1.4 ms (s.d.) and this low variability may be explained by the interaction of the gating of L-type calcium channels with the changes in driving force for calcium entry during the action potential. 3. When fixed sites within the cell are examined, calcium sparks have relatively constant amplitude but the amplitude of the sparks was variable among sites. The low variability of the amplitude of the calcium sparks suggests that more than one sarcoplasmic reticulum (SR) release channel must be involved in their genesis. Noise analysis (with the assumption of independent gating) suggests that > 18 SR calcium release channels may be involved in the generation of the calcium spark. At a fixed site, the response is close to 'all-or-none' behaviour which suggests that calcium sparks are indeed elementary events underlying cardiac excitation-contraction coupling. 4. A method for selecting spark sites for signal averaging is presented which allows the time course of the spark to be examined with high temporal and spatial resolution. Using this method we show the development of the calcium spark at high signal-to-noise levels.
Primary afferent depolarizations (PADs) are associated with presynaptic inhibition in both vertebrates and invertebrates. In the present study, we have used both anatomical and electrophysiological techniques to analyze the relative importance of shunting mechanisms versus sodium channel inactivation in mediating the decrease of action potential amplitude, and thereby presynaptic inhibition. Experiments were performed in sensory afferents of a stretch receptor in an in vitro preparation of the crayfish. Lucifer yellow intracellular labeling of sensory axons combined with GABA immunohistochemistry revealed close appositions between GABA-immunoreactive (ir) fibers and sensory axons. Most contacts were located on the main axon at the entry zone of the ganglion, close to the first branching point within the ganglion. By comparison, the output synapses of sensory afferents to target neurons were located on distal branches. The location of synaptic inputs mediating spontaneous PADs was also determined electrophysiologically by making dual intracellular recordings from single sensory axons. Inputs generating PADs appear to occur around the first axonal branching point, in agreement with the anatomical data. In this region, small PADs (3-15 mV) produced a marked reduction of action potential amplitude, whereas depolarization of the membrane potential by current injection up to 15 mV had no effect. These results suggest that the decrease of the amplitude of action potentials by single PADs results from a shunting mechanism but does not seem to involve inactivation of sodium channels. Our results also suggest that GABAergic presynaptic inhibition may act as a global control mechanism to block transmission through certain reflex pathways.