Morphologically distinct classes of inhibitory synapses arise from the same neurons: ultrastructural identification from crossed vestibular interneurons intracellularly stained with HRP.
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Biomedical subjects
Publications and source records attributed to H Korn.
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Binomial predictions provided a better description than the Poisson law of fluctuating unitary inhibitory postsynaptic potentials evoked in the goldfish Mauthner cell by impulses in presynaptic interneurons. The number of terminal boutons established on this target cell by each horseradish peroxidase-filled interneuron corresponded to the value of the binomial parameter n.
Transneuronal transport of horseradish peroxidase (HRP) was observed by electron microscopy following intracellular injection of the enzyme into single interneurons inhibiting the teleost Mauthner cell. Complex membrane infolding, associating protrusions of the stained cells with adjacent indentations of the postsynaptic neuron, favours the interpretation that transport of HRP is brought about by an active process of extrusion and consecutive micropinocytosis of HRP by the target cell.
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In the goldfish Mauthner cell, inhibitory postsynaptic currents evoked by intracellular stimulation of presynaptic neurons decay exponentially, with a mean time constant of 6.65 milliseconds. Analysis of membrane conductance fluctuations induced by iontophoresis of glycine and gamma-aminobutyric acid indicates a mean inhibitory channel lifetime of 7.15 milliseconds. The results thus suggest that the relaxation kinetics of activated inhibitory channels are rate-limiting during decay of the inhibitory postsynaptic current.
Cell acidification was obtained by exposing to carbon dioxide the lateral giant axon of the crayfish and the buccal ganglion of Navanax inermis; electrophysiological measurements show that the resulting intracellular pH uncouples neurons and that this uncoupling is the consequence of increased junctional resistance at the level of the gap junctions. Conditions under which the uncoupling is reversible are also described.
Differentiated contacts were identified by electron microscopy between glia and axons as they enter the axon cap which surrounds the initial segment of the teleost's Mauthner cell. At these regions, the cleft of adjacent membranes is 20-25 nm wide and contains clods of electron-dense material with a pseudo-periodicity of 10-30 nm. These junctions, referred to as 'septate-like junctions', presumably contribute to the compartmentalization of the axon cap and, therefore, to its elevated resistivity which underlies the generation of field effect inhibitions.
Monosynaptic activation of cerebellar Purkinje cells by a volley of parallel-fiber impulses is followed by a powerful disynaptic chemical inhibition mediated by molecular layer interneurons, including basket cells. Active zone established by basket preterminal axons on the body surface of the Purkinje cell account for this inhibition. However, morphological studies indicate that branches of the presynaptic fibers further descend along the initial segment of the Purkinje axon. Terminals from several basket cells converge and encapsulate each initial segment with a peculiar architectural structure that is reminiscent of that characterizing the axon cap of the teleost Mauthner cell. Because no function has yet been attributed to this pinceau, we have reanalyzed the successive Purkinje cell responses to activation of their presynaptic elements. Electrophysiological data provided by field-potential and single-unit measurements indicate that the classical phases of excitation and inhibition after a parallel-fiber volley are preceded by a brief inhibition of the Purkinje cells. Transmembrane hyperpolarizing potentials that exhibit the characteristics expected of electrically mediatd potentials underlie this early phase of inhibition; their properties are consistent with the hypothesis that they are generated by currents through terminals of nearby basket cells. Therefore, these hyperpolarizations, which are similar in their mechanism of generation to those described in the Mauthner cell system, represent a known case of electrical inhibition in the mammalian central nervous system.
Intracellular injections of horseradish peroxidase provided a basis for morphological identification of inhibitory interneurons belonging to the recurrent collateral network of the Mauthner cell. Their axons dilate to form unusually large bulbs surrounding the axon cap. The morphological appearance of these bulbs as well as intracellular recordings at their level indicate that they behave as nodes and serve as a final source of current for electrical inhibition of the Mauthner cell. The axon of each interneuron gives rise to two different groups of fibres which are respectively fitted for the mediation of electrical and chemical inhibitions of their target cell.
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Horseradish peroxydase was injected intracellularly in some of the medullary neurons which, in Fish, exhibit a passive hyperpolarizing potential after spinal cord stimulation (this indicates that such neurons both electrical and chemical inhibitions of the Mauthner cells). With positive staining, commissural vestibular neurons were identified; their axons cross the midline and they establish connexions with the Mauthner cell and with vestibular neurons of both sides. Thus the existence of a crossed vestibular inhibitory pathway, previously suggested by electrophysiological studies in lower Vertebrates as well as in Mammals, is now correlated with histological evidence.
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Identified goldfish medullary interneurons previously shown to inhibit the Mauthner cell electrically also produce a classical postsynaptic inhibition of that cell. Failure of active spike propagation in the processes of these interneurons underlies generation of the electrical component, and the resultant electrotonic terminal depolarization is sufficient to evoke inhibitory transmitter release.
Cardiazol induces in the Mauthner cell the paroxysmal depolarizing shifts which are characteristic of epilepsia at the neuronal level. The period of depolarizations is preceded and, later, accompanied by an increased transmission at the electrotonic synapses which are established upon this neuron by primary afferent vestibular fibers. Increased excitability of the chemical synapses occurs subsequently.
Cerebrally-induced responses of pontine nuclei cells (PN cells) were studied in cats anesthetized with pentobarbitone sodium and with the midbrain transected bilaterally sparing only the cerebral penuncles. After stimulating the subcortical white matter, the internal capsule or the cerebral peduncle, mass potentials were recorded from the cut end of fibres in the brachium pontis (BP) and in the pyramid at the level of the trapezoid body. These potentials were regarded as indicating, respectively, the size of an output volley of PN cells and the size of its causative input volley through the pyramidal tract. BP responses consisted of short- and long-latency potentials which were caused by fast and slow conducting pyramidal tract volleys, respectively. The input-output relations for fast component responses took a characteristic S-shaped form resembling those obtained from the monosynaptic spinal reflex. The input-output relations for slow component responses were almost linear. Both fast and slow BP responses were remarkably potentiated after single or relatively brief repetitive peduncular stimulation, but were depressed after long-lasting high-frequency activation. During repetitive stimulation with varied frequencies, fast and slow BP responses showed different patterns of frequency-dependence of their amplitudes. These results suggest the existence of two separate transmission lines with different properties in cerebro-ponto-cerebellar pathways.
Extracellular and intracellular recordings were made from single cells in the pontine nuclei (PN) of the cat. PN cells were identified by antidromic invasion from the cerebellum by stimulating either the brachium pontis (BP) or the white matter near the cerebellar nuclei. The cerebrally-induced impulses excited PN cells postsynaptically with a monosynaptic latency. Both fast and slow conducting cortical fibres contributed to the corticopontine excitation, so that the latency varied over a wide range. Measurements of the latencies for antidromic and corticopontine excitation and of the distances between stimulated sites permitted the calcuation of conduction velocities of PN cell axons and of their cortical input fibres. PN cells with fast conducting axons received convergence from both fast and slow cortical fibres, whereas PN cells with slow axons were innervated only by slow cortical fibres. The majority of PN cells were also excited by stimulating the medullary pyramid through collaterals of the pyramidal tract. Evidence of abundant pyramidal collaterals was provided by the collision technique. The functional role of the PN is discussed in connection with the cerebro-cerebellar loop circuits.
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