Biomedical subjects

W Precht

Publications and source records attributed to W Precht.

At least 91 records · Page 5Linked to original sources

PubMed1976

Electron microscopic investigation of the vestibular projection to the cat trochlear nuclei.

Ultrastructural degeneration studies were carried out on the cat trochlear nucleus following lesion of the vestibulo-trochlear pathway in order to characterize the location and type of presynaptic endings involved in this pathway. Four types of boutons are found in the normal trochlear nucleus. Types I and II are large and demonstrate typical en passant profiles with small diameter synaptic vesicles (35 and 40 nm). These terminals are characterized by the absence of neurofilaments in the Type II endings. Types III and IV are smaller boutons, located more axondendritically, and contain larger diameter synaptic vesicles (45 nm). Type V terminals contain large, granulated vesicles and occur only rarely. Following the interruption of the ascending projection from the ipsilateral superior and medial vestibular nuclei by parasagittal medullary lesions, degeneration of Type II boutons was commonly encountered in the ipsilateral trochlear nucleus. Predominantly Type III degeneration was found in the contralateral trochlear nucleus. Electrical stimulation of the vestibular nerve showed that these lesions resulted in (1) a complete loss of inhibition in the ipsilateral trochlear nucleus and (2) a significant (75-90%) reduction in the contralateral excitatory pathway to the trochlear nucleus. Midline sagittal lesions in the floor of the fourth ventricle interrupting the decussating fiber projection from the bilateral medial vestibular nuclei resulted in selective degeneration of only Type III boutons in both trochlear nuclei. We conclude that inhibitory vestibular neurons eminating from the superior vestibular nucleus terminate on trochlear motoneurons with Type II boutons and excitatory vestibular neurons from the contralateral medial vestibular nucleus end on trochlear motoneurons with Type III boutons.

Animals↗

PubMed1976

Electrical properties of frog motoneurons in the in situ spinal cord.

Electrical properties of the spinal motoneurons of Rana temporaria and R. esculenta were investigated in the in situ spinal cord at 20-22 degrees C by means of intracellular recording and current injection. Input resistance values depended on the method of measurement in a given cell but were generally inversely related to axon conduction velocity. The membrane-potential response to a subthreshold current pulse was composed of at least two exponentials with mean time constants of 2.5 and 20 ms. The membrance potential reached by the peak of a spike depended on the mode of spike initiation and membrane potential. Preceding a suprathreshold depolarization by a hyperpolarizing pulse could delay and eliminate spike initiation, similar to effects reported in certain invertebrate neurons. Antidromic invasion frequently failed in motoneurons of normal resting potential. Antidromic spike components (m,IS, SD) were similar to those of cat motoneurons. The delayed depolarization and the long afterhyperpolarization following an antidromic spike had many properties in common with the analogous afterpotentials of cat motoneurons. The reversal potential of the short afterhyperpolarization occurring immediately after the spike varied with resting potential and could not be used to determine potassium equilibrium potential. Sustained rhythmic firing could be evoked by continuous synaptic drive or long pulses of injected current. The plot of firing rate versus current strength had a substantial linear region. Both steady firing and adaptation properties varied markedly with motoneuron input resistance.

Animals↗

PubMed1976

Evidence for electrotonic coupling between frog motoneurons in the in situ spinal cord.

A recurrent EPSP was observed on antidromic stimulation of motoneurons in the in situ spinal cord of Rana temporaria and R. esculenta at 20-22C. The EPSP was finely graded and not refractory following full or partial antidromic spike components in a given neuron. The EPSP amplitude varied in parallel with the antidromic field potential under different conditions, suggesting transmission of the EPSP to the recorded motoneuron depended on invasion of the somadendritic membrane or neighboring motoneurons by the antidromic spike. The latency of the EPSP with respect to antidromic invasion of the local motoneuron pool was too short for the EPSP to be mediated by chemical transmission. It was concluded the EPSP was electrically transmitted between the somadendritic membranes of the motoneurons. Under certain conditions, the EPSP magnitude could be made to vary with membrane potential in a direction opposite to that expected from a chemical EPSP. Dendritic spikes were sometimes associated with the EPSP.

Animals↗

PubMed1975

Cerebellar control of vestibular neurons of the frog.

Intra- and extracellular potentials were recorded from vestibular neurons of the frog following stimulation of the ipsilateral cerebellar cortex (auricular lobe). Single neurons were identified as vestibular neurons by their location within the borders of the vestibular nuclei and by their activation via stimulation of the anterior branch of the VIIIth nerve. 2. Stimulation of the cerebellar auricular lobe provoked in some vestibular neurons apparently pure IPSPs with latencies as short as 1.5 msec suggesting a monosynaptic linkage between Purkinje cells and vestibular neuron. Vestibular-evoked responses were inhibited by cerebellar conditioning stimuli for as long as 50 msec. 3. Cerebellar stimulation also elicited an EPSP-IPSP sequence or occasionally pure EPSPs in vestibular neurons. These EPSPs were probably generated by axon reflex activation via the excitation of axons of primary and secondary vestibular neurons terminating in the cerebellum since they persisted after chronic VIIIth nerve section. Some vestibular evoked resonses were facilitated by cerebellar stimuli for 40-50 msec. 4. Occasionally an inhibitory effect was also induced in vestibular neurons by paired ipsilateral VIIIth nerve stimulation; it's latency of onset and time course suggested that a vestibulo-cerebello-vestibular loop was mainly responsible for the inhibition.

Animals↗

PubMed1975

Responses of neurons of lizard's, Lacerta viridis, vestibular nuclei to electrical stimulation of the ipsi- and contralateral VIIIth nerves.

Field and intracellular potentials were recorded in the vestibular nuclei of the lizard following stimulation of the ipsi- and contralateral vestibular nerves. The field potentials induced by ipsilateral VIIIth nerve stimulation consisted of an early negative or positive-negative wave (presynaptic component) followed by a slow negativity (transsynaptic component). The spatial distribution of the field potential complex closely paralleled the extension of the vestibular nuclei. Mono- and polysynaptic EPSPs were recorded from vestibular neurons after ipsilateral VIIIth nerve stimulation. In some neurons early depolarizations preceded the EPSPs. These potentials may be elicited by electrical transmission. Often spikelike partial responses were superimposed on the EPSPs. It is assumed that these potentials represent dendritic spikes. Contralateral VIIIth nerve stimulation generated disynaptic and polysynaptic IPSPs in some neurons and EPSPs in others. The possible role of commissural inhibition in phylogeny is discussed. In a group of vestibular neurons stimulation of the ipsilateral VIIIth nerve evoked full action potentials with latencies ranging from 0.25-1.1msec. These potentials are caused by antidromic activation of neurons which send their axons to the labyrinth.

Action Potentials↗

PubMed1975