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Biomedical subjects

H Korn

Publications and source records attributed to H Korn.

At least 145 records · Page 8Linked to original sources
PubMed1975

Vestibular nystagmus and teleost oculomotor neurons: functions of electrotonic coupling and dendritic impulse initiation.

1. Nystagmus in the horizontal plane is evoked in fish by mechanical stimulation of the ampulla of the horizontal semicircular canal or by electrical stimulation of the nerve from this canal. The movements are conjugate and the slow phase is away from the side of stimulation. 2. Medial rectus motoneurons were recorded from intracellularly, during nystagmus. During the slow phase (induced by ipsilateral stimulation), impulses arise abruptly from the base line and appear to arise at a distance from the cell body. During the fast phase (evoked by contralateral stimulation), impulses appear to arise from large PSPs that must be generated at or near the cell body. 3. In the curarized fish, stimulation of the nerve from the contralateral horizontal canal evokes spikes that arise from large EPSPs and that are blocked relatively easily by hyperpolarizing currents. Stimulation of the nerve from the ipsilateral horizontal canal evokes spikes that arise abruptly from the base line and that are much more difficult to block by hyperpolarizing currents. Little if any underlying PSP is observed when these impulses are delayed or blocked. Thus impulses evoked by stimulation of contralateral and ipsilateral side are initiated near to and far from the cell soma, respectively. 4. If impulses evoked by contralateral stimulation fail to excite the cell body due to injury, antidromic spikes are not occluded. Thus contralateral stimulation initiates impulses in the dendrites. 5. Cell bodies of neighboring motoneurons are coupled electrotonically, and graded antidromic stimulation evokes graded depolarizing potentials which result from electrotonic spread of spike activity from adjacent neurons. These depolarizing potentials are adequate to excite the cells in the presence of a background EPSP evoked by contralateral canal stimulation. In this manner coupling tends to synchronize cells during the fast phase of the nystagmus. 6. Antidromic responses of neighboring cells fail to interact with dendritic inputs to a particular cell, although indirect evidence indicates antidromic spikes invade the impulse-initiating regions in the dendrites. Thus coupling between dendrites is negligible and dendritic inputs can mediate the smoothly graded movements of the slow nystagmic phase. Coupling between somata is too weak to cause significant interaction between dendritically evoked impulses (unless the cell bodies are depolarized by EPSPs). 7. Rhythmic firing can be recorded in a single presynaptic fiber corresponding to either the slow or the fast phase of nystagmus, but not to both. Oculomotor neurons appear to be "relay cells" that, during the fast phase of the nystagmus receive a synchronized synaptic input which is initiated in a higher level command nucleus.

Animals↗
PubMed1975

An electrically mediated inhibition in goldfish medulla.

1. Passive hyperpolarizing potentials (PHPs) have been recorded intracellularly from goldfish medullary neurons in the vicinity of the Mauthner cell (M-cell). They are evoked when this cell is activated antidromically by stimulation of the spinal cord, and orthodromically via the ipsilateral eighth nerve; when appropriately timed they block or delay spikes induced both directly and transsynaptically. 2. Since the PHPs and the M-cell spike have the same latency, time course, and all-or-none character, they cannot be generated by chemically mediated synaptic transmission. This conclusion is further supported by the evidence that PHP amplitude and time course are independent of membrane potential. 3. The analysis of the mechanism underlying PHP generation has been based on the hypothesis that they are brought about by the extracellular currents flowing to the axon cap during an M-cell action potential. Specifically, it was postulated that some of this current is channeled back to the axon cap region intracellularly through processes of PHP-exhibiting neurons, and that these cells are passively hyperpolarized by the associated inward transmembrane current flow. This model would require that PHP-exhibiting neurons send processes into the axon cap. This hypothesis is confirmed by the following: a) When the PHP is timed to occur during the conductance increase associated with a spike after hyperpolarization, it is reduced, as would be expected for a passive current flow across a membrane resistance. b) PHPs are not found in all medullary neurons in the vicinity of the M-cell, but rather in a specific neuronal population. c) PHP-exhibiting neurons have been identified following Procion yellow injections; as predicted, they issue one process, presumably the axon, which projects toward the M-cell axon cap area. d) The PHP can be stimulated by passing a cathodal current from a microelectrode located in the axon cap; it is not mimicked when the cathodal electrode is moved outside this region. The currents necessary to mimic a PHP are comparable to the estimated current flowing back to the axon cap during an M-cell action potential. 4. The input resistance of PHP-exhibiting neurons is in the range of 4 M alpha, and their estimated specific membrane resistance is in the range of 900-2,000 alpha-cm-2, which is not an unusually low value for neuronal membranes. By contrast, the intracellular channeling of current during a PHP can rather be attributed to a high extracellular tissue resistance within the axon cap, which was found to be at least 2.5 times that of the surrounding medullary tissue..

Action Potentials↗
PubMed1973

A neuronal inhibition mediated electrically.

When the goldfish Mauthner cell fires an impulse there is a simultaneous hyperpolarization of adjacent medullary neurons as far as 200 micrometers from its soma. This hyperpolarization is due to an inward transmembrane flow of some of the current generated by the Mauthner cell spike and is sufficiently large to block spikes evoked both directly or transsynaptically.

Action Potentials↗