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PubMed1991

Avian locomotion activated by brainstem infusion of neurotransmitter agonists and antagonists. I. Acetylcholine excitatory amino acids and substance P.

Previous studies have demonstrated that focal electrical stimulation of regions within the brainstem of a decerebrate bird will elicit all the normal patterns of avian locomotion. However, electrical stimulation can activate a variety of neuronal elements within the radius of effective current spread, including axons of passage traversing the stimulation point. To restrict activation to neuronal cell bodies within the immediate vicinity, we have utilized direct intracerebral injection of neurotransmitters, their agonists and antagonists, into identified brainstem locomotor regions. To undertake these studies, birds (geese or ducks) were placed in a stereotaxic frame and decerebrated under halothane anesthesia. After completion of surgery, several discrete locomotor regions were first identified with electrical microstimulation. Acetylcholine (ACh) and excitatory amino acid (EAA) agonists and antagonists, as well as Substance P were then slowly infused into each brainstem region. Any change in locomotor behavior was recorded by electromyographic techniques. When injected into a variety of sites, carbachol (an ACh nicotinic (AChN) and muscarinic (AChM) agonist) and pilocarpine (an AChM agonist) evoked locomotion, whereas atropine (an AChM antagonist) blocked locomotion. N-methyl-D-aspartate NMDA), but not glutamate, also elicited locomotion or reduced the current intensity threshold for electrically-evoked locomotion. The NMDA-induced locomotion evoked locomotion. The NMDA-induced locomotion could be blocked by the injection of glutamic acid diethyl ester (GDEE, an EAA antagonist) or D-2-amino-5-phosphonopentanoic acid (AP5) into the same site. Finally. Substance P also evoked locomotion. The above observations strongly suggest that brainstem electrically-stimulated locomotion in decerebrate birds is not due to activation of fibers traversing a brainstem locomotor region, but instead, is due to the activation of receptors located on neuronal cell bodies, dendrites or presynaptic terminals in the immediate vicinity of the micropipette tip. After correlating our findings with similar lamprey and mammalian studies, the comparable discoveries serve to underscore the suggestion that the neuroanatomical substrates underlying the brainstem control of locomotion appear to be highly conserved in all vertebrates.

Acetylcholine↗
PubMed1983

Differential sensitivity of individual primary afferents to glutamic and gamma-aminobutyric acids in the amphibian spinal cord in vitro.

In the isolated amphibian spinal cord the responses to glutamate and GABA recorded intracellularly from individual primary afferents differed considerably according to the fibre type. Muscle afferents giving rise to direct sensory-motor synapses were strongly depolarized by glutamate, whereas GABA produced smaller and inconsistent depolarization. In contrast, fibres both of muscle and cutaneous origin establishing polysynaptic connections with motoneurones were relatively insensitive to glutamate but very sensitive to GABA. These observations suggest that the effects of glutamate on fibres synapsing with motoneurones are probably mediated via the depolarization of motoneurones electrically coupled with them and do not result from direct activation of presynaptic terminals by glutamate.

Afferent Pathways↗
PubMed1982

Effects of climbing fiber destruction on large dendrite spines of Purkinje cells.

The number and freeze-fracture membrane organization of spines on Purkinje cell dendrites were studied in rats after destruction, by intraperitoneal injection of 3-acetyl-pyridine (3-AP), of the climbing fiber afferents to the cerebellum. The results obtained show that: (1) there is a 1.6 fold increase in the total number of dendritic spines in the 3-AP-treated animals as compared to controls, but no change in the total number of spine synaptic profiles; (2) the spines from main dendrites in both control and 3-AP-treated animals have more than 1,000 IMP/micron 2 of P-face membrane; and, (3) the spines formed on Purkinje cell dendrites in the absence of their presynaptic axons have the same P-face membrane organization (i.e. more than 1,000 IMP/micron 2) as spines normally innervated by afferent climbing fibers. These data suggest that each type of Purkinje cell spine has a specific P-face membrane organization which does not appear to be influenced by presynaptic terminals.

Afferent Pathways↗
PubMed1993

Colocalization of retinal dystrophin and actin in postsynaptic dendrites of rod and cone photoreceptor synapses.

In this paper we demonstrate immunostaining specific for dystrophin in photoreceptor synapses of human, bovine and rat retinas. Cryosections of retinas incubated with dystrophin-specific monoclonal antibodies displayed a punctuate staining pattern in the outer plexiform layer. This pattern resulted from binding of the antibodies to synaptic complexes of both rods and cones, shown by double-labelling with antibodies to either synaptophysin or actin. Confocal laser fluorescence microscopy demonstrated that dystrophin staining colocalized predominantly with actin, which is concentrated in the postsynaptic portions of the synaptic complex. No significant dystrophin immunolabel was seen in the presynaptic terminals labelled with antibodies to synaptophysin, a marker of synaptic vesicles. Immunoblot analysis confirmed the presence of approximately 420 kDa and approximately 360 kDa dystrophin-like polypeptide bands associated with membranes of the bovine retina. We speculate that retinal dystrophin is involved in the linkage of actin filaments to the postsynaptic plasma membrane. Such a linkage may be important for the generation of synaptic microdomains and for certain phenomena of synaptic plasticity. The absence of dystrophin in patients suffering from Duchenne's muscular dystrophy is accompanied by visual problems and abnormalities of the electroretinogram. Therefore it is likely that retinal dystrophin plays a role in certain stages of synaptic transmission between photoreceptors and the postsynaptic dendritic complex formed by horizontal and bipolar cells.

Actins↗
PubMed1990

Selective vulnerability in the gerbil hippocampus: morphological changes after 5-min ischemia and long survival times.

The morphology of the hippocampus of Mongolian gerbils was investigated by light and electron microscopy after 5-min forebrain ischemia and survival times of up to 10 months. After 3 weeks recirculation only 5.8% of pyramidal neurons of the CA1 (cornu ammonis 1) sector had survived but the thickness of the inner and outer hippocampal layers did not change. After recirculation times of 6 and 10 months the number of surviving neurons declined no further but all layers of the CA1 subfield shrank markedly. Ultrastructurally, many but not all surviving CA1 neurons were altered. After 3 weeks both "dark" and "pale" type neurons were present, while after 6 and 10 months only the "pale" type of injury persisted. Axonal enlargements and myelin breakdown were observed at all survival times up to 10 months of recirculation. The astrocytes of CA1 sector contained numerous glial fibrils which were most pronounced after the longer recirculation times. The stratum radiatum presented intact presynaptic terminals densely packed with an abundance of clear vesicles even after survival of 10 months. Initially, morphologically damaged postsynaptic structures were still attached to these terminals but they disappeared after longer recirculation times. However, even after 10 months some intact synapses were observed involving dendrites which probably originated from surviving CA1 neurons. In CA3 sector and dentate gyrus no ultrastructural changes occurred at any survival time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Deposition of beta/A4 protein along neuronal plasma membranes in diffuse senile plaques.

The origin of the extracellular beta-amyloid protein (beta/A4) found in senile plaques and the cellular mechanisms responsible for its deposition in cerebral tissues are still an unresolved issue in Alzheimer's disease. In this study we analyzed in detail the distribution of various epitopes of beta/A4 in relation to local cellular elements in diffuse plaques of the hippocampal region. We also correlated our findings with the presence and distribution of non-beta/A4 epitopes of the amyloid precursor protein (APP) and with synaptophysin immunoreactivity in the cortical neuropil. Discontinuous beta/A4-immunoreactive deposits were found along dendrites, and around the soma of neurons included in the plaques. Furthermore, increased synaptophysin reactivity with slightly dilated synaptophysin-immunolabeled presynaptic terminals were found in diffuse plaques. APP epitopes could not be found in diffuse plaques. However, some of the APP antibodies, mainly those to the C-terminal portion of APP, and antibodies to beta/A4 recognized clusters of flat vesicular profiles (0.6-1.4 micron in width and 2-3 microns in length) in the neuropil of cortical areas where plaques had developed. Our findings are compatible with a neuronal origin of beta/A4 in diffuse plaques and with a primary release of beta/A4 at synaptic sites along the immunostained neurites. They also suggest that diffuse plaques might be preceded by minute lesions of the neuropil where beta/A4 is not yet released from the precursor molecule.

Aged↗
PubMed1991

Scrapie inoculation of mice: light and electron microscopy of the superior colliculi.

Ultrastructural examination of the superior colliculi of mice intraocularly inoculated with the ME7 strain of scrapie showed vacuolation early in the course of infection. Brains were examined between 85-260 days after monocular inoculation with scrapie. The mean incubation period for the development of clinical disease was 302 days. Vacuolation was seen initially in the contralateral superior colliculus and subsequently in the ipsilateral colliculus. In coded trials light microscopical vacuolation was seen from 218 days but ultrastructural examination showed that sparse vacuoles were inconsistently present in either or both of the ipsilateral and contralateral colliculi from 85 days; frequent vacuoles were seen from 190 days. Scrapie-induced vacuoles were differentiated from vacuoles present in control tissue by the presence of loculation or by a limiting double membrane which showed protrusion or proliferation of the innermost lamella. Vacuolation was seen in neuronal perikarya, myelinated fibres, dendrites and axonal presynaptic terminals. Vacuoles of myelinated fibres were observed within myelin and possibly also in the inner tongue of oligodendroglial cytoplasm. Whorled membrane configurations were also seen. Tubulovesicular particles, 40 nm in diameter, were recognised in two scrapie-infected mice. It is suggested that some scrapie vacuoles arise as a result of incorporation of abnormal membrane into organelles, possibly mitochondria, in neuronal perikarya and neurites and probably also within oligodendroglial cytoplasm and myelin.

Animals↗
PubMed1984

Ectopic photoreceptor cells and cell death in the developing rat retina.

To confirm the identity of presumed photoreceptor-like neurones displaced from their normal location in the developing retina we have examined their morphology and extent of occurrence in the Long-Evans hooded rat aged one to six weeks postnatally. Displaced photoreceptor cells (PR) in the inner nuclear layer showed changing nuclear chromatin patterns during retinal development akin to those occurring in PR cells in the outer nuclear layer. PR cell cytoplasmic specializations included outer segments in various stages of formation and presynaptic terminal features including synaptic ribbons and vesicles. Processes abutting on PR cell terminals did not have postsynaptic specializations. Displaced PR cells may have arisen from PR progenitors which failed to retain a foothold at the retina's ventricular surface. The incidence of displaced PR cells determined from quantification of their planimetric densities decreased from 18% of the INL cell population at day 9 postnatally to less than 2% at day 15. A few such cells remained even at 36 days. Their fate appeared to be migration to the ONL and, or, in situ degeneration. Counts of necrotic cells carried out at ages preceding, during, and following the period during which ectopic PR cells were most numerous indicated that the decline in numbers of displaced PR cells coincided temporally with the period during which cell degeneration in the INL was most prominent. Degeneration of cells in the INL, including ectopic PR cells, was sufficient to account for a considerable proportion of the retinal thinning that occurred during development. Results suggest that future studies of retinal development in genetically or experimentally manipulated animals should consider abnormalities in cell migration and death.

Animals↗
PubMed1986

Ultrastructure of marginal zone during prenatal development of human spinal cord.

Electron microscopic studies were conducted in the marginal zone (lamina I) in human fetuses ranging from 8-25 weeks of gestational age. At 8 weeks the neurons have indented nuclei and sparse organelles in the cytoplasm. The neuropil shows contacts between the axons and dendritic profiles. Some of them are well defined synapses with post synaptic thickening and agranular spherical vesicles in the presynaptic terminal. At 18 weeks compactly packed organelles with long cisternae of rough endoplasmic reticulum could be visualized in the neuronal cytoplasm. At 25 weeks the neurons have heterochromatin patches in the nuclei. Axosomatic, dendrodendritic, axoaxonic, symmetrical, asymmetrical and multisynaptic contacts with agranular and dense core vesicles are seen at different sequential age periods.

Axons↗
PubMed1985

Improvement in neuromuscular transmission in myasthenia gravis by 3,4-diaminopyridine.

3,4-Diaminopyridine (3,4-DAP), a potent potentiator of action potential evoked release of acetylcholine from presynaptic terminals in the neuromuscular junction was given i.v. and p.o. to two patients with myasthenia gravis. Effects were monitored electrophysiologically by repetitive nerve stimulation and by standardized clinical testing. Administration of 8 mg and 9 mg 3,4-DAP i.v. produced a clear improvement in the neuromuscular transmission after approximately 20 min. When 3,4-DAP was given p.o. 24 mg was shown to be effective. At a dosage of 18-24 mg p.o. 3,4-DAP significantly potentiated the effect of the cholinesterase inhibitor pyridostigmine at an optimal dose. The maximal effect of 3,4-DAP p.o. was obtained after 2.5-3 h. No significant CNS side-effects were found which is in contrast to those reported for 4-aminopyridine. The results suggest that 3,4-DAP may be useful as an addition to the conventional treatment with cholinesterase inhibitors when immunosuppressive treatment is considered contraindicated or when it has not yet reached its full effect.

4-Aminopyridine↗
PubMed1981

Amphetamine-, scopolamine- and caffeine-induced locomotor activity following 6-hydroxydopamine lesions of the mesolimbic dopamine system.

As previously reported, 6-hydroxydopamine (6-OHDA) lesions to the region of the nucleus accumbens blocked the locomotor activation induced by low doses of d-amphetamine, and produced a supersensitive locomotor response to the dopamine (DA) agonist, apomorphine. This same lesion, however, failed to block the locomotor activation induced by scopolamine or caffeine. These results suggest that scopolamine and caffeine activate locomotion in the rat by acting independently of presynaptic terminals in the mesolimbic DA system.

Animals↗
PubMed1981

[Neurobiologic aspects of nerve regeneration (author's transl)].

This review is focusing on the cell biology of regeneration in neurons of the peripheral nervous system, mainly the motoneuron. The retrograde or axonal reaction in these cells is characterized by an increase in the RNA and protein metabolism and is associated with morphological and cytochemical changes. The neuronal events are accompanied by changes in the microenvironment of the complete motor nucleus. Presynaptic terminal, glial cells and the capillaries participate in this process. Axonal sprouting occurs in the proximal stump of regenerating nerve. This event has been studied by scanning electron microscopy as well as with histochemical methods. Wallerian degeneration in the distal stump is viewed on as an important prerequisite for regeneration. Some aspects of current research in the field are briefly discussed, for instance: signal for chromatolysis, search for regeneration factors, role of axonal transport and intercellular communication.

Axons↗
PubMed1980

On the postsynaptic action of glutamate in frog spinal motoneurons.

In the isolated frog spinal cord depolarization of motoneurons (MNs) induced by glutamate (GLUT) was not accompanied by measurable changes of neuronal input resistance when chemical synaptic transmission was blocked by Mn2+ or Mg2+. The GLUT depolarization was, however, paralleled by a considerable increase in K+ in the extracellular space. To clarify, whether the GLUT depolarization was exclusively due to a reduction of the transmembrane K+ gradient or whether ion conductances not detectable by measurements of neuronal input resistance were involved, membrane potential (MP) was plotted semilogarithmically versus extracellular K+ activity (aKe+). During experimental elevation of aKe+ the function delta MP/dec. delta aKe+ was found to agree fairly with the Nernst equation. The slope of this function was much steeper during GLUT superfusion, indicating an influx of positive ions. The elevation of aKe+ during the GLUT action can mimic postsynaptic effects by release of transmitter from presynaptic terminals synapsing with the recorded cell. In vivo preparations do not allow blockade of chemical synaptic transmission. Therefore, it is impossible to decide, whether the recorded cell is depolarized either postsynaptically by GLUT or by K+ release from surrounding GLUT sensitive cells. As an experimental proof of the postsynaptic GLUT action is not feasible in such preparations, the ubiquitous action of GLUT in the CNS may have been overestimated.

Amino Acids↗
PubMed1984

Presynaptic currents in frog motor endings.

Membrane currents were recorded from non-myelinated frog endings by external electrodes. Changes in shape of the signals recorded at varying distances from the myelin end could be explained by assuming a non uniform distribution of Na and K channels along the presynaptic terminal. Specific channel blocking agents revealed that Na channels are present in highest density in the first half of each terminal branch and at almost undetectable levels near the extreme end, while K channels show a more widespread distribution with higher density at medial parts. Suppression of K conductance revealed Ca current which was seen as outward current near the myelin end.

4-Aminopyridine↗
PubMed1988

Study of axonal dystrophy. III. Posterior funiculus and posterior column of ageing and old rats.

Axonal dystrophy in normal ageing can be studied in experimental animals. Primary sensory neurones show two different kinds of change with ageing, i.e. axonal dystrophy and axonal atrophy (degeneration). This paper reports the chronology and topography of these two processes in relation to growth and involution of these neurones throughout the lifespan of the rats used in this study. Axonal spheroids preferentially form at presynaptic terminal regions in many of the collaterals of central branches of the axons, i.e. in the posterior funiculus nuclei, posterior column and posterior funiculus. Axonal dystrophy in normal ageing is essentially a morbid process restricted to the terminal parts of the axon. It shows little tendency to expand retrogradely along the axon. Evidence is presented that spheroids in posterior funiculus also derive from terminal axons. Preference is also noted in the lumbosacral rather than cervical neurons, and in longer (posterior funiculus nuclei) rather than shorter (posterior column) collaterals. Quantitative study of myelinated fibres in posterior funiculus shows that they increase in number until middle age (400 days) of the animals, before beginning to decline. On the other hand, axonal atrophy begins to appear early in small numbers, and increases in numbers with age. Atrophy involves the whole length of the axon within the posterior funiculus from the start, suggesting, therefore, that it does not belong to a dying-back process. It is noteworthy that the main development of axonal dystrophy lies in the earlier half of the animals' life, while that of axonal atrophy lies in the latter half. This fact adds to the evidence that axonal dystrophy, as far as in normal ageing is concerned, is more related to the positive side of neuronal activity, e.g. one form of growth abnormality of axon.

Aging↗
PubMed1980

Changes in the contralateral dentate gyrus in Mongolian gerbils subjected to unilateral cerebral ischemia.

Distinct morphological changes were demonstrated in the contralateral hemisphere in the brains of Mongolian gerbils that were subjected to transient unilateral cerebral ischemia. The alterations were most obvious in a narrow region of the contralateral dentate gyrus (fascia dentata), where commissural inputs to the dentate gyrus are known to form synapses with the dentate granule cells. Electron microscopic examination revealed that these changes were caused by degenerative processes which took place in presynaptic terminals of the commissural inputs. An interesting fact was that the degenerated terminals were detected by light microscopy without the aid of special silver impregnation methods. After 1 week, these alterations almost disappeared, and after 3 months the dentate gyrus was undistinguishable from normal. These results strongly suggest that the changes were closely related to axonal degeneration and subsequent repair mechanisms of the brain. The present study indicates the importance of such anatomo-pathological study to delineate the effect of focal ischemia upon distant areas of the brain.

Animals↗
PubMed1983

Methylmercury poisoning of the developing nervous system: morphological changes in neuronal mitochondria.

Neonatal rats received s.c. injections of methylmercuric chloride (MeHg) in physiological saline (1.5 mg Hg/kg b.wt.) at 48-h intervals from postnatal day 2 to day 50. Littermate controls were injected with an equivalent volume of saline. All animals were perfused on day 51 and blocks of cerebral cortex were prepared for electron microscopy. Ultrastructural changes in mitochondria were evident in the dendrites, axons and presynaptic terminals of cortical neurones in the MeHg-treated animals. Many mitochondria were condensed with an increased electron density of the inner matrix. Some profiles exhibited regressive alterations, including a disruption of cristae and the inner membrane with an accumulation of electron-opaque material in the matrix. Membranous whorls were found in association with the most degenerate mitochondria. A morphometric analysis of mitochondrial profiles in the neuropil of layer I revealed a 24% decrease in average profile area and a 16% increase in the number of profiles per micrograph in the MeHg-treated animals. These pathological changes in mitochondrial ultrastructure are consistent with an inhibition of mitochondrial respiration. The observed increase in the number of mitochondrial profiles may reflect a compensation by cortical neurons for the reduced efficiency of aerobic metabolism in the individual organelle.

Animals↗
PubMed1979

Skin and conjunctival biopsies in infantile neuroaxonal dystrophy.

The diagnosis of infantile neuro-axonal dystrophy (INAD) in a 5-year-old patient was confirmed by the ultrastructural study of neuromuscular, skin and conjunctival biopsy specimens. Abnormal networks of smooth membranous, lamellar and tubular profiles were found in presynaptic terminals and in conjunctival and dermal axons. INAD is the first neurological disease outside the group of storage disorders in which skin and conjunctival biopsies contribute significiantly to the diagnosis.

Axons↗