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Biomedical subjects

P Paggi

Publications and source records attributed to P Paggi.

36 records · Page 2Linked to original sources
PubMed1984

Degeneration and regeneration of neuromuscular junctions in chicken iris muscle after crush of the ciliary nerves: a study of ultrastructural changes and of cholinergic enzymes.

Degeneration of neuromuscular junctions in the iris muscle was observed to have occurred 4 days after ciliary nerve crush. By day 10 reinnervation had commenced and by day 30 the maturation of neuromuscular junctions was nearly complete. The loss and recovery of acetylcholinesterase activity in the iris muscle paralleled the denervation-reinnervation process, with recovery being completed by day 30, whereas the loss in the activity of choline acetyltransferase had not yet completely recovered at this time. The acetylcholinesterase activity localized cytochemically at synaptic sites followed the same trend as the total activity in the iris muscle, whereas acetylcholinesterase localized at myo-muscular junctions showed only slight changes. The acetylcholinesterase molecular forms displayed changes in their relative proportions, which could be related to the time course of the denervation-reinnervation process and to the cytochemical localization of the activity.

Acetylcholinesterase↗
PubMed1979

Acetylcholine receptors in the ciliary ganglion and in the iris muscle of the chick: specific binding and effect on the synaptic transmission of the neurotoxin from Naja naja siamensis.

1 A specific binding of Naja naja siamensis neurotoxin was found both in the iris and in the ciliary ganglion of the chick. 2 Naja-toxin (125 nM) caused a complete block of the iris muscle contraction induced by carbamylcholine. 3 Naja-toxin had a different effect on the two neuronal populations present in the ganglion: it blocked the synaptically evoked response of the ciliary cells, while the response of the choroid ones was only slightly reduced. The effects were the same in a wide range of concentrations (125 to 2500 nM). 4 The results obtained in the iris show the existence of an acetylcholine receptor population similar to the nicotinic receptor of the skeletal muscle. 5 In the ciliary ganglion the results confirm the existence of different acetylcholine receptors on the two cell types.

Animals↗
PubMedDate not supplied

Neuronal compartments and axonal transport of synapsin I.

Studies on the transport kinetics and the posttranslational modification of synapsin I in mouse retinal ganglion cells were performed to obtain an insight into the possible factors involved in forming the structural and functional differences between the axon and its terminals. Synapsin I, a neuronal phosphoprotein associated with small synaptic vesicles and cytoskeletal elements at the presynaptic terminals, is thought to be involved in modulating neurotransmitter release. The state of phosphorylation of synapsin I in vitro regulates its interaction with both synaptic vesicles and cytoskeletal components, including microtubules and microfilaments. Here we present the first evidence that in the mouse retinal ganglion cells most synapsin I is transported down the axon, together with the cytomatrix proteins, at the same rate as the slow component b of axonal transport, and is phosphorylated at both the head and tail regions. In addition, our data suggest that, after synapsin I has reached the nerve endings, the relative proportions of variously phosphorylated synapsin I molecules change, and that these changes lead to a decrease in the overall content of phosphorus. These results are consistent with the hypothesis that, in vivo, the phosphorylation of synapsin I along the axon prevents the formation of a dense network that could impair organelle movement. On the other hand, the dephosphorylation of synapsin I at the nerve endings may regulate the clustering of small synaptic vesicles and modulate neurotransmitter release by controlling the availability of small synaptic vesicles for exocytosis.

Animals↗