scholarly journals ELKS1 Captures Rab6-Marked Vesicular Cargo in Presynaptic Nerve Terminals

Cell Reports ◽  
2020 ◽  
Vol 31 (10) ◽  
pp. 107712 ◽  
Author(s):  
Hajnalka Nyitrai ◽  
Shan Shan H. Wang ◽  
Pascal S. Kaeser
Keyword(s):  
Nerve Terminals ◽  
Presynaptic Nerve Terminals

Role of sodium-calcium exchange in regulation of intracellular calcium in nerve terminals

1987 ◽  
Vol 252 (6) ◽  
pp. C595-C603 ◽  
Author(s):  
S. Sanchez-Armass ◽  
M. P. Blaustein
Keyword(s):  
Hill Coefficient ◽  
Nerve Terminals ◽  
Physiological Load ◽  
Carbonyl Cyanide ◽  
Ca Uptake ◽  
Na Ions ◽  
Presynaptic Nerve Terminals ◽  
45Ca Efflux ◽  
Mitochondrial Uncoupler

Ca efflux from rat brain presynaptic nerve terminals (synaptosomes) was examined after loading the terminals with 45Ca during a brief depolarization, usually in media containing 20 microM Ca labeled with 45Ca, to assure a small (physiological) load. Efflux of 45Ca was very slow in the absence of external Na and Ca (approximately 0.5% of the load/s) and was greatly accelerated by Na and/or Ca (presumably Na+-Ca2+ and Ca2+-Ca2+ exchange, respectively). The dependence of 45Ca efflux on external Na was sigmoid, with a Hill coefficient of approximately 2.5; this implies that more than two external Na ions are required to activate the efflux of one Ca ion. The external Na (Nao)-dependent Ca efflux was inhibited by 1 mM external La, by low temperature (Q10 congruent to 2.3), and by raising external K (to depolarize the synaptosomes). With small Ca loads, the mitochondrial uncoupler, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP), had negligible effect on either Ca uptake or efflux; with large loads (greater than or equal to 5 nmol/mg protein), however, FCCP reduced the depolarization-stimulated Ca uptake and increased the Nao-dependent Ca efflux. These effects may be attributed to reduction of mitochondrial Ca sequestration. Mitochondria do not appear to sequester much Ca when the loads are smaller (and more physiological). Estimations of Ca efflux indicate that approximately 20% of a small 45Ca load (approximately 0.75 nmol Ca/mg protein) may be extruded via Na+-Ca2+ exchange within 1 s; this corresponds to a net Ca efflux of approximately 110 pmol Ca X mg protein-1 X s-1.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals TMEM16B regulates anxiety-related behavior and GABAergic neuronal signaling in the central lateral amygdala

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Ke-Xin Li ◽  
Mu He ◽  
Wenlei Ye ◽  
Jeffrey Simms ◽  
Michael Gill ◽  
...  
Keyword(s):  
Action Potential ◽  
Knockout Mice ◽  
Chloride Channel ◽  
Action Potential Duration ◽  
Fear Memory ◽  
Brain Regions ◽  
Gabaergic Neurons ◽  
Nerve Terminals ◽  
Lateral Amygdala ◽  
Presynaptic Nerve Terminals

TMEM16B (ANO2) is the Ca2+-activated chloride channel expressed in multiple brain regions, including the amygdala. Here we report that Ano2 knockout mice exhibit impaired anxiety-related behaviors and context-independent fear memory, thus implicating TMEM16B in anxiety modulation. We found that TMEM16B is expressed in somatostatin-positive (SOM+) GABAergic neurons of the central lateral amygdala (CeL), and its activity modulates action potential duration and inhibitory postsynaptic current (IPSC). We further provide evidence for TMEM16B actions not only in the soma but also in the presynaptic nerve terminals of GABAergic neurons. Our study reveals an intriguing role for TMEM16B in context-independent but not context-dependent fear memory, and supports the notion that dysfunction of the amygdala contributes to anxiety-related behaviors.

scholarly journals Direct Recording of Nicotinic Responses in Presynaptic Nerve Terminals

1997 ◽  
Vol 17 (15) ◽  
pp. 5798-5806 ◽  
Author(s):  
Jay S. Coggan ◽  
Jacques Paysan ◽  
William G. Conroy ◽  
Darwin K. Berg
Keyword(s):  
Nerve Terminals ◽  
Direct Recording ◽  
Presynaptic Nerve Terminals

scholarly journals Regulation of cytosolic free calcium concentration by intrasynaptic mitochondria.

1992 ◽  
Vol 3 (2) ◽  
pp. 235-248 ◽  
Author(s):  
A Martínez-Serrano ◽  
J Satrústegui
Keyword(s):  
Calcium Concentration ◽  
Adenine Nucleotides ◽  
Free Calcium ◽  
Nerve Terminals ◽  
Cytosolic Free Calcium ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Presynaptic Nerve Terminals

By the use of digitonin permeabilized presynaptic nerve terminals (synaptosomes), we have found that intrasynaptic mitochondria, when studied "in situ," i.e., surrounded by their cytosolic environment, are able to buffer calcium in a range of calcium concentrations close to those usually present in the cytosol of resting synaptosomes. Adenine nucleotides and polyamines, which are usually lost during isolation of mitochondria, greatly improve the calcium-sequestering activity of mitochondria in permeabilized synaptosomes. The hypothesis that the mitochondria contributes to calcium homeostasis at low resting cytosolic free calcium concentration ([Ca2+]i) in synaptosomes has been tested; it has been found that in fact this is the case. Intrasynaptic mitochondria actively accumulates calcium at [Ca2+]i around 10(-7) M, and this activity is necessary for the regulation of [Ca2+]i. When compared with other membrane-limited calcium pools, it was found that depending on external concentration the calcium pool mobilized from mitochondria is similar or even greater than the IP3- or caffeine-sensitive calcium pools. In summary, the results presented argue in favor of a more prominent role of mitochondria in regulating [Ca2+]i in presynaptic nerve terminals, a role that should be reconsidered for other cellular types in light of the present evidence.

The Calcium Signal for Transmitter Secretion from Presynaptic Nerve Terminals

1991 ◽  
Vol 635 (1 Calcium Entry) ◽  
pp. 365-381 ◽  
Author(s):  
GEORGE J. AUGUSTINE ◽  
E. M. ADLER ◽  
MILTON P. CHARLTONC
Keyword(s):  
Calcium Signal ◽  
Nerve Terminals ◽  
Transmitter Secretion ◽  
Presynaptic Nerve Terminals

scholarly journals The regulation of cytosolic pH in isolated presynaptic nerve terminals from rat brain.

1988 ◽  
Vol 91 (2) ◽  
pp. 289-303 ◽  
Author(s):  
D A Nachshen ◽  
P Drapeau
Keyword(s):  
Rat Brain ◽  
Parent Compound ◽  
Mammalian Brain ◽  
Fluorescence Signal ◽  
Nerve Terminals ◽  
Free Medium ◽  
Cytosolic Ph ◽  
Methyl Ester Derivative ◽  
Synaptosomal Membrane ◽  
Presynaptic Nerve Terminals

Cytosolic pH (pHi) was measured in presynaptic nerve terminals isolated from rat brain (synaptosomes) using a fluorescent pH indicator, 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The synaptosomes were loaded with BCECF by incubation with the membrane-permanent acetoxy-methyl ester derivative of BCECF, which is hydrolyzed by intracellular esterases to the parent compound. pHi was estimated by calibrating the fluorescence signal after permeabilizing the synaptosomal membrane by two different methods. Synaptosomes loaded with 15-90 microM BCECF were estimated to have a pHi of 6.94 +/- 0.02 (mean +/- standard error; n = 54) if the fluorescence signal was calibrated after permeabilizing with digitonin; a similar value was obtained using synaptosomes loaded with 10 times less BCECF (6.9 +/- 0.1; n = 5). When the fluorescence signal was calibrated by permeabilizing the synaptosomal membrane to H+ with gramicidin and nigericin, pHi was estimated to be 7.19 +/- 0.03 (n = 12). With the latter method, pHi = 6.95 +/- 0.09 (n = 14) when the synaptosomes were loaded with 10 times less BCECF. Thus, pHi in synaptosomes was approximately 7.0 and could be more precisely monitored using the digitonin calibration method at higher BCECF concentrations. When synaptosomes were incubated in medium containing 20 mM NH4Cl and then diluted into NH4Cl-free medium, pHi immediately acidified to a level of approximately 6.6. After the acidification, pHi recovered over a period of a few minutes. The buffering capacity of the synaptosomes was estimated to be approximately 50 mM/pH unit. Recovery was substantially slowed by incubation in an Na-free medium, by the addition of amiloride (KI = 3 microM), and by abolition of the Nao/Nai gradient. pHi and its recovery after acidification were not affected by incubation in an HCO3-containing medium; disulfonic stilbene anion transport inhibitors (SITS and DIDS, 1 mM) and replacement of Cl with methylsulfonate did not affect the rate of recovery of pHi. It appears that an Na+/H+ antiporter is the primary regulator of pHi in mammalian brain nerve terminals.

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