A light microscopical, histochemical and electron microscopical investigation of the frog neuromuscular junction has been performed on muscles from animals in different functional states of activity. The combined staining of axon terminals and cholinesterase (ChE) allows a precise description of the nerve terminal arborization and its synaptic contacts. Most terminal arborizations form long continuous contacts with the muscle cell. Distinquishable from these are nerve branches (usually of small diameter)d or distal endings of branches with one or several small and isolated contacts. It is assumed that these are sprouts with newly-formed synaptic sites. Other sprouts end without apparent synaptic contact. At the uttrastructural levet, nerve sprouts end without apparent synaptic contact. At the uttrastructural levet, nerve sprouts growing into empty, well-differentiated synaptic gutters or inducing the formation of new synaptic sites were observed. In other sites, ChE is apparently located at postsynaptic gutters with no nerve present. Similarly, in the electron microscope, well-differentiated synaptic gutters lacking any nerve or Schwann cell elements were observed. In addition, synaptic gutters only partially occupied by the nerve were frequently seen. These features have been interpreted as signs of regression of the nerve terminals. Nerve regression and sprouting were found in animals chronically paralysed with curare over several weeks as well as in untreated frogs (winter and summer frogs, laboratory frogs, fed and unfed). When quantitatively evaluating the occurence of presumed features of nerve sprouting and nerve regression, differences were found between different experimental groups. From this it is concluded that, in addition to developmental changes, the degree of nerve sprouting and regression is controlled by external factors such as muscle activity and seasonal variations. Signs of sprouting and nerve regression can be simultaneously present in a single synapse. It appears that the frog neuromuscular synapse is not a static structure, but is in a state of permenent remodelling.
Combination of Karnovsky's cholinesterase staining with silver impregnation of axons (modified Bodian's technique) offers a new means of studying the relation between the pre- and postsynaptic elements in the frog neuromuscular junction. The method can be applied to whole muscles so that synapses of individual superficial muscle fibers which have previously been investigated by electrophysiological techniques can be identified after staining. In this way synaptic activity can be correlated with such synaptic features as number of axon branches, length of the occupied synaptic gutter, axonal sprouts, etc. The distinction between occupied and unoccupied parts of the synaptic gutters is useful when studying reinnervation, regression, or growth of a synapse.
BACKGROUNDParkinson’s disease (PD) neuropathology is characterized by intraneuronal protein aggregates composed of misfolded α-Synuclein (α-Syn), as well as degeneration of substantia nigra dopamine neurons. Deficits in olfactory perception and aggregation of α-Syn in the olfactory bulb (OB) are observed during early stages of PD, and have been associated with the PD prodrome, before onset of the classic motor deficits. α-Syn fibrils injected into the OB of mice cause progressive propagation of α-Syn pathology throughout the olfactory system and are coupled to olfactory perceptual deficits.OBJECTIVEWe hypothesized that accumulation of pathogenic α-Syn in the OB impairs neural activity in the olfactory system.METHODSTo address this, we monitored spontaneous and odor-evoked local field potential dynamics in awake wild type mice simultaneously in the OB and piriform cortex (PCX) one, two, and three months following injection of pathogenic preformed α-Syn fibrils in the OB.RESULTSWe detected α-Syn pathology in both the OB and PCX. We also observed that α-Syn fibril injections influenced odor-evoked activity in the OB. In particular, α-Syn fibril-injected mice displayed aberrantly high odor-evoked power in the beta spectral range. A similar change in activity was not detected in the PCX, despite high levels of α-Syn pathology.CONCLUSIONSTogether, this work provides evidence that synucleinopathy impacts in vivo neural activity in the olfactory system at the network-level.
Background: Parkinson’s disease (PD) neuropathology is characterized by intraneuronal protein aggregates composed of misfolded α-Synuclein (α-Syn), as well as degeneration of substantia nigra dopamine neurons. Deficits in olfactory perception and aggregation of α-Syn in the olfactory bulb (OB) are observed during early stages of PD, and have been associated with the PD prodrome, before onset of the classic motor deficits. α-Syn fibrils injected into the OB of mice cause progressive propagation of α-Syn pathology throughout the olfactory system and are coupled to olfactory perceptual deficits. Objective: We hypothesized that accumulation of pathogenic α-Syn in the OB impairs neural activity in the olfactory system. Methods: To address this, we monitored spontaneous and odor-evoked local field potential dynamics in awake wild type mice simultaneously in the OB and piriform cortex (PCX) one, two, and three months following injection of pathogenic preformed α-Syn fibrils in the OB. Results: We detected α-Syn pathology in both the OB and PCX. We also observed that α-Syn fibril injections influenced odor-evoked activity in the OB. In particular, α-Syn fibril-injected mice displayed aberrantly high odor-evoked power in the beta spectral range. A similar change in activity was not detected in the PCX, despite high levels of α-Syn pathology. Conclusion: Together, this work provides evidence that synucleinopathy impacts in vivo neural activity in the olfactory system at the network-level.
Twelve hours after injection of 125I labelled tetanus toxin into the shank of one hindlimb of mice radioactivity was found in the end-plate region of soleus muscles. The ratio between the radioactivity of the end-plate and the end-plate-free region was 2.5 +/- 0.4 S.D. Autoradiographs showed intense labelling of end-plates and a slight but clear labelling of axons. When 125I tetanus toxin was injected 3 days after denervation of the soleus muscle the former end-plate region still accumulated a higher radioactivity (ratio 2.0 +/- 0.5 S.D.), however, autoradiographs showed a diffuse distribution of labelled tetanus toxin. It can be concluded that tetanus toxin binds to the presynaptic nerve terminal. This binding is not dependent on activity of the nerve terminal or transmitter release.
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