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N Dieringer

Publications and source records attributed to N Dieringer.

61 records · Page 4Linked to original sources
PubMed1979

Mechanisms of compensation for vestibular deficits in the frog. I. Modification of the excitatory commissural system.

In hemilabyrinthectomized frogs excitatory responses of central vestibular neurons to electrical stimulation of the remaining vestibular nerve were recorded extra- and intracellulary at different stages (0, 3, and 60 days) after the operation. The output pattern of ipsilateral vestibular neurons sending an axon across the midline via the vestibular commissure to the deafferented nucleus did not change postoperatively. The synaptic efficacy of these commissural axons ending on partially deafferented vestibular neurons on the lesioned side increased with time. This enhanced synaptic potency was associated with a shortening in time to peak and duration and an increase in amplitude of the evoked EPSPs. As a result most vestibular neurons were readily excited by single shock stimulation of the contralateral vestibular nerve, a finding which was rarely observed in control animals. These plastic changes are explained by the assumption of reactive synaptogenesis. The consequences of this modification for the readjustment of static and dynamic vestibular reflexes are discussed.

Afferent Pathways↗
PubMed1979

Mechanisms of compensation for vestibular deficits in the frog. II. Modification of the inhibitory Pathways.

In hemilabyrinthectomized frogs inhibitory responses of central vestibular neurons to electrical stimulation of the remaining vestibular nerve were recorded extra- and intracellularly at different stages (0, 3, and 60 days) after the operation. In acute animals inhibition of vestibular neurons following stimulation of the VIIIth nerve is rarely observed. In chronic animals about 30% of the vestibular neurons on the partially deafferented side and about 15% of the vestibular neurons on the intact side are inhibited. The distribution of the latencies of these inhibitory responses is bimodal with ranges from 4 to 14 ms and 18 to 24 ms. Removal of the cerebellum reduced the number of inhibited vistibular neurons and picrotoxin abolished all inhibitory responses. The vestibular input to the cerebellar dorsal rim is bilateral. In chornic animals excitation of Purkinje cells was similar as in acute preparations but many more cells were disfacilitated. Inhibition of partially deafferented vestibular neurons by cerebellar and brain stem neurons increases in parallel with their excitatory commissural input. The balance between these plastic changes may be crucial for the functional recovery of appropriate compensatory reflexes.

Afferent Pathways↗
PubMed1979

Timing of bilateral cerebellar output evoked by unilateral vestibular stimulation in the frog.

Electrical stimulation of one VIIIth nerve evoked simple spike activity in Purkinje cells located on either side of the cerebellum. This cellebullar output was delayed by ca. 10 ms with respect to its mossy fiber-parallel fiber input. The onset of the cerebellar output occurs on the average simultaneously on either side of the corpus cerebelli. The delay is explained by slowly rising EPSPs in PC induced by primary afferent and by second and higher order vestibular fibers. The latter inputs are stronger and terminate ipsi- and contralaterally in the granular layer.

Action Potentials↗
PubMed1979

Biophysical mechanisms contributing to inking behavior in Aplysia.

1. The release of ink from the ink gland of Aplysia californica in response to noxious stimuli is mediated by three electrically coupled motor neurons, L14A, L14B, L14C, whose cell bodies are located in the abdominal ganglion. The initial synaptic input to the ink motor neurons is relatively ineffective in firing the cells. As a result, a pause of 1--3 s often occurs before the cells attain their maximum firing frequency and cause the release of ink. Using current and voltage-clamp techniques we have analyzed the mechanisms underlying the firing pattern of these cells. 2. The presence of a fast transient K+ current appears to play an important role in mediating the firing pattern of the ink motor neurons. Their high resting potential (-75 mV) ensures that the steady-state level of inactivation of the conductance channels for the fast K+ current will normally be low. Thus a train of EPSPs or a depolarizing current pulse can activate this current maximally, thereby reducing the initial effectiveness of the excitatory input. 3. In addition to the fast transient K+ current, four other currents were identified: 1) a fast transient tetrodotoxin-sensitive inward current, presumed to be carried by Na+; 2) a slower tetrodotoxin-insensitive inward current, presumed to be carried by Ca2+; 3) a slow transient outward tetraethylammonium- (TEA) sensitive current; and 4) a very slow TEA-insensitive outward current. 4. A decreased conductance EPSP, which turns on over a several-second period, contributes to a late acceleration of spike discharge in the L14 cells. 5. The results suggest that a unique combination of biophysical properties of the L14 cells and the features of the synaptic input cause them to act as a low-pass filter in the reflex pathway for inking. Their high resting potential, which ensures minimal inactivation of the fast transient K+ current channel, makes these cells preferentially responsive to strong and long-lasting stimuli. The delayed recruitment of a decreased conductance EPSP augments the tendency of the L14 cells to fire in an accelerating burst pattern.

Aggression↗
PubMed1978

Connections of behaviorally identified cat omnipause neurons.

The afferent and efferent connections of omnipause neurons involved in saccadic eye movements were studied electrophysiologically in ketamine anesthetized cats. Omnipause neurons were identified by their characteristic discharge pattern which was qualitatively unaltered by ketamine anesthesia.

Action Potentials↗