Surangin B: Insecticidal Properties and Mechanism Underlying Its Transmitter-Releasing Action in Nerve-Terminal Fractions Isolated from Mammalian Brain

1995 ◽  
Vol 53 (3) ◽  
pp. 152-163 ◽  
Author(s):  
R.A. Nicholson ◽  
A.G. Zhang
2016 ◽  
Vol 212 (6) ◽  
pp. 721-736 ◽  
Author(s):  
Jianmin Su ◽  
Jiang Chen ◽  
Kumiko Lippold ◽  
Aboozar Monavarfeshani ◽  
Gabriela Lizana Carrillo ◽  
...  

Inhibitory synapses comprise only ∼20% of the total synapses in the mammalian brain but play essential roles in controlling neuronal activity. In fact, perturbing inhibitory synapses is associated with complex brain disorders, such as schizophrenia and epilepsy. Although many types of inhibitory synapses exist, these disorders have been strongly linked to defects in inhibitory synapses formed by Parvalbumin-expressing interneurons. Here, we discovered a novel role for an unconventional collagen—collagen XIX—in the formation of Parvalbumin+ inhibitory synapses. Loss of this collagen results not only in decreased inhibitory synapse number, but also in the acquisition of schizophrenia-related behaviors. Mechanistically, these studies reveal that a proteolytically released fragment of this collagen, termed a matricryptin, promotes the assembly of inhibitory nerve terminals through integrin receptors. Collectively, these studies not only identify roles for collagen-derived matricryptins in cortical circuit formation, but they also reveal a novel paracrine mechanism that regulates the assembly of these synapses.


2018 ◽  
Author(s):  
Matthew S. Scarnati ◽  
Rahul Kataria ◽  
Mohana Biswas ◽  
Kenneth G. Paradiso

AbstractPresynaptic neuronal activity requires the localization of thousands of proteins that are typically synthesized in the soma and transported to nerve terminals. Local translation for some dendritic proteins occurs, but local translation in mammalian presynaptic nerve terminals is difficult to demonstrate. Here, we present evidence for local presynaptic protein synthesis in the mammalian brain at a glutamatergic nerve terminal. We show an essential ribosomal component, 5.8s rRNA, in terminals. We also show active translation in nerve terminals, in situ, in brain slices demonstrating ongoing presynaptic protein synthesis. After inhibiting translation for ~1 hour, the presynaptic terminal exhibits increased spontaneous release, and increased evoked release with an increase in vesicle recycling during stimulation trains. Postsynaptic response, shape and amplitude were not affected. We conclude that ongoing protein synthesis limits vesicle release at the nerve terminal which reduces the need for presynaptic vesicle replenishment, thus conserving energy required for maintaining synaptic transmission.


Author(s):  
Steven R. Childers ◽  
Peter Nijssen ◽  
Pauline Nadeau ◽  
Page Buckhannan ◽  
Phi-Van Le ◽  
...  

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