PubMed · 9616949
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A Fernández de Molina. 1997. [Contacts, network systems, synapses].. https://pubmed.ncbi.nlm.nih.gov/9616949/
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The Characeae internodal cell is excitable and generates an action potential. The depolarizing phase of the action potential primarily reflects the activation of Cl- channels, which takes place in a Ca2+-dependent manner. Namely, an increase in the Ca2+ influx takes place at the very beginning of the action potential and heightens the Ca2+ concentration in the cytoplasm ([Ca2+]c). The high [Ca2+]c activates Cl- channels at the plasmalemma, resulting in a large depolarization. The high [Ca2+]c also acts as a signal to induce a tonoplast action potential and the instantaneous cessation of cytoplasmic streaming; the tonoplast action potential also is caused by Ca2+-induced activation of Cl- channels at the tonoplast, and the cessation is a result of inhibition of the actin-myosin interaction by Ca2+. When the cytoplasm of the Characeae cell, especially in Nitella flexilis, is hydrated rapidly, [Ca2+], also increases through Ca2+ release from an intracellular store(s). The release may be triggered by the stretching of endomembranes caused by osmotic swelling of the Ca2+ store lumens. Although the origin of Ca2+ is different from that in the case of an action potential, high [Ca2+]c not only induces membrane depolarization through activation of the Cl- channel in a Ca2+-dependent manner but also inhibits cytoplasmic streaming in Characeae.
In the salamander Plethodon jordani, the morphology and axonal projections of thalamic (TH) neurons and their responses to electrical optic nerve stimulation were determined by intracellular recording and biocytin labeling under in vitro, whole-brain conditions. Based on their axonal projections, labeled neurons (n = 76) were divided into the following groups: TH1 neurons, with mostly ipsilateral projections to the striatum; TH2 neurons, with ipsilateral or bilateral projections to the medial amygdala and nucleus accumbens; TH3 neurons, with bilateral projections to the medial and dorsal pallium; TH4 neurons, with mostly ipsilateral projections to the striatum and ipsilateral projections to the tectum opticum, tegmentum, and rostral medulla oblongata; and TH5 neurons, with ipsilateral projections to the tegmentum, medulla oblongata, and rostral spinal cord without (TH5.1) or with (TH5.2) additional projections to the optic tectum. TH1-TH4 neurons are found in the dorsal thalamus and around the sulcus medialis, and TH5 neurons are found in the ventral thalamus. Labeled neurons with ascending projections, i.e., the more dorsally situated TH1-TH4 neurons, are mostly inhibited by electrical stimulation of the optic nerve and have significantly longer latencies (mean +/- S.D., 42.1 +/- 11.6 msec) than neurons with exclusively descending projections, i.e., the ventrally located TH5 neurons (8.5 +/- 6.1 msec), which receive the bulk of retinal afferents and show excitation at electrical optic nerve stimulation. Neurons recorded without labeling in the dorsal thalamus likewise exhibit mostly inhibition and have significantly longer latencies (35.7 +/- 18.9 msec) than those recorded in the ventral thalamus (10.9 +/- 7.7 msec), which mostly show excitation. None of the neurons recorded in the dorsal thalamus followed repetitive stimulation of the optic nerve. Thus, neurons situated in the dorsal thalamus and projecting to pallial or subpallial telencephalic targets are unlikely to receive monosynaptic or oligosynaptic, excitatory retinal input. Accordingly, no retino-thalamo-telencephalic pathway homologous to that found in amniotes appears to exist in salamanders.
Relationships between presynaptic function and short- and long-term plasticity were investigated at adult corticostriatal synapses. Wide variability was observed in the expression of short- and long-term synaptic plasticity. Intracellular records from 47 cells produced 17 examples of LTD (<90% of control), 10 examples of no long-term change (between 90-110% of control), and 20 examples of LTP (>110% of control). Similar variation existed in paired-pulse and posttetanic plasticities. The variability expressed in all three forms of plasticity appears to be related, based on correlations found between the paired-pulse ratio (PPR) and tetanus-induced short- (3 min posttetanus) and long-term plasticities (16-20 min posttetanus). These data suggest that tetanus-induced changes in synaptic strength are related to the intrinsic, preconditioned behavior of synapses. Every cell showing paired-pulse depression also expressed LTD in response to high-frequency activation of its afferents. Those synapses showing paired-pulse potentiation tended to express LTP, although exceptions did exist. Similar relationships were found in a parallel analysis of population spikes. PPR also changed in association with the expression of posttetanic and long-term depression. Greater paired-pulse potentiation was observed in medial intracellular recordings, but no medial to lateral differences were seen in posttetanic plasticities. Field recordings also showed a medial bias toward paired-pulse and posttetanic potentiation, but not in long-term plasticity. Block of postsynaptic L-type Ca(2+) channels with nifedipine eliminated LTD expression, but overall no differences were found between nifedipine and control cells.