Phase-Transition-Driven Synaptic Exocytosis: A Hypothesis and Its Physiological and Evolutionary Implications

2001 ◽  
Vol 21 (6) ◽  
pp. 801-830 ◽  
Author(s):  
Dmitri P. Kharakoz

It is proposed that the plasma membrane in the active zones of synaptic terminals contains self-assembling cooperative domains whose Ca2+-induced solidification may be the driving force of the fast neurotransmitter release in the central synapses. This hypothesis and a qualitative model of the phase-transition-driven exocytosis provide formulation of a unitary approach to a number of general problems in the physiology of animals. It allows answering the following questions, among others: (i) What is the physical reason for the existence of a narrow optimum range of body temperatures in warm-blooded species? (ii) What is the physical reason for the inevitable necessity of regular sleep in animals? (iii) Does there indeed exist any general mechanism of general anesthesia?

RSC Advances ◽  
2014 ◽  
Vol 4 (83) ◽  
pp. 44056-44064 ◽  
Author(s):  
Valentina Domenici ◽  
Jerneja Milavec ◽  
Alexej Bubnov ◽  
Damian Pociecha ◽  
Blaž Zupančič ◽  
...  

A new series of liquid single crystal elastomers having a nematic–SmA and a direct isotropic–SmA phase transition.


2020 ◽  
Vol 117 (41) ◽  
pp. 25830-25839
Author(s):  
Beril Kiragasi ◽  
Pragya Goel ◽  
Sarah Perry ◽  
Yifu Han ◽  
Xiling Li ◽  
...  

Presynaptic glutamate receptors (GluRs) modulate neurotransmitter release and are physiological targets for regulation during various forms of plasticity. Although much is known about the auxiliary subunits associated with postsynaptic GluRs, far less is understood about presynaptic auxiliary GluR subunits and their functions. At theDrosophilaneuromuscular junction, a presynaptic GluR,DKaiR1D, localizes near active zones and operates as an autoreceptor to tune baseline transmission and enhance presynaptic neurotransmitter release in response to diminished postsynaptic GluR functionality, a process referred to as presynaptic homeostatic potentiation (PHP). Here, we identify an auxiliary subunit that collaborates with DKaiR1D to promote these synaptic functions. This subunit, dSol-1, is the homolog of theCaenorhabditis elegansCUB (Complement C1r/C1s, Uegf, Bmp1) domain protein Sol-1. We find thatdSol-1functions in neurons to facilitate baseline neurotransmission and to enable PHP expression, properties shared withDKaiR1D. Intriguingly, presynaptic overexpression ofdSol-1is sufficient to enhance neurotransmitter release through aDKaiR1D-dependent mechanism. Furthermore,dSol-1is necessary to rapidly increase the abundance of DKaiR1D receptors near active zones during homeostatic signaling. Together with recent work showing the CUB domain protein Neto2 is necessary for the homeostatic modulation of postsynaptic GluRs in mammals, our data demonstrate that dSol-1 is required for the homeostatic regulation of presynaptic GluRs. Thus, we propose that CUB domain proteins are fundamental homeostatic modulators of GluRs on both sides of the synapse.


2008 ◽  
pp. 2834-2839
Author(s):  
Hiroshi Kawabe ◽  
Frederique Varoqueaux ◽  
Nils Brose

Open Physics ◽  
2013 ◽  
Vol 11 (3) ◽  
Author(s):  
Nikolay Oskolkov ◽  
Jakob Bohr

AbstractHelical structures with Lennard-Jones self-interactions are studied for optimal conformations. For this purpose, their self-energy is analyzed for extrema with respect to the geometric parameters of the helices. It is found that Lennard-Jones helices exhibit a first order phase transition from a state with large curvature of the helical backbone to one with a small curvature. I.e. from a dense helix to an extended helix. A transition from one helical structure to another is a phenomenon known to take place in self-assembling helices formed in multicomponent solutions with cholesterol.


Neuron ◽  
2000 ◽  
Vol 27 (3) ◽  
pp. 539-550 ◽  
Author(s):  
Miguel Morales ◽  
Michael A Colicos ◽  
Yukiko Goda

2008 ◽  
Vol 100 (4) ◽  
pp. 2089-2100 ◽  
Author(s):  
ChiHye Chung ◽  
Ferenc Deák ◽  
Ege T. Kavalali

Noncanonical secretagogues such as hypertonicity or α-latrotoxin have been extremely informative in studying neurotransmission. Lanthanum and lanthanides can also trigger neurotransmitter release through an unknown mechanism. Here, we studied the effect of lanthanides on neurotransmission in hippocampal cultures. Application of 2 mM La3+ caused rapid and robust neurotransmitter release within seconds. In addition, transient application of La3+ uncovered a sustained facilitation of miniature neurotransmission. The response to La3+ was detectable at 2 μM and increased in a concentration-dependent manner ≤2 mM. Rapid effect of La3+ was independent of extracellular and intracellular Ca2+ and did not require La3+ entry into cells or activation of phospholipaseCβ. Synapses deficient in synaptobrevin-2, the major synaptic vesicle soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein in the brain, did not display any rapid release in response to La3+, whereas the slow facilitation of release detected after La3+ removal remained intact. In contrast, preincubation with intracellular Ca2+ chelators selectively attenuated the delayed release triggered by La3+. Moreover, synapses deficient in synaptotagmin-1 maintained a rapid response to La3+, suggesting that La3+-triggered neurotransmitter release does not require synaptotagmin-1 as a sensor. Therefore La3+ has two separate effects on synaptic transmission. For its rapid action, La3+ interacts with a target on the surface membrane, and unlike other forms of release, it triggers strictly synaptobrevin-2–dependent fusion, implying that in central synapses synaptobrevin-2 function is secretagogue specific. For the delayed action, La3+ may act intracellularly after its entry or through intracellular Ca2+ via a mechanism that does not require synaptobrevin-2.


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