Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices

1986 ◽  
Vol 64 (12) ◽  
pp. 1507-1514 ◽  
Author(s):  
S. J. McKay ◽  
J. N. Reynolds ◽  
W. J. Racz
Keyword(s):  
Calcium Homeostasis ◽  
Sulfonic Acid ◽  
Synaptic Function ◽  
Spontaneous Release ◽  
Striatal Slices ◽  
Dopaminergic Neurotransmission ◽  
Calcium Dependent ◽  
Mercury Compounds ◽  
Dependent Processes ◽  
Mercuric Mercury

The effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices have been examined. All mercury compounds examined produced concentration-dependent increases in the spontaneous release of [3H]dopamine, with an order of potency of methylmercury > mercuric (Hg2+) mercury >p-choloromercuribenzene sulfonic acid. Methylmercury had no effect on the 25 mM potassium evoked release of [3H]dopamine in the presence of 1.3 mM calcium. However, in calcium-free conditions, methylmercury significantly increased the potassium-evoked release of [3H]dopamine. Mercuric mercury significantly reduced the 25 mM potassium evoked release of [3H]dopamine in the presence of 1.3 mM calcium, and this response was not reversible with brief washing of the tissue. In calcium-free conditions, mercuric mercury significantly elevated the evoked release of [3H]dopamine, similar to the result obtained with methylmercury. It is suggested that mercury compounds alter dopaminergic synaptic function, possibly by disrupting calcium homeostasis or calcium-dependent processes, and that methylmercury and mercuric mercury can have differential effects to alter dopaminergic neurotransmission.

scholarly journals Loss of Non-Apoptotic Role of Caspase-3 in the PINK1 Mouse Model of Parkinson’s Disease

2019 ◽  
Vol 20 (14) ◽  
pp. 3407 ◽  
Author(s):  
Paola Imbriani ◽  
Annalisa Tassone ◽  
Maria Meringolo ◽  
Giulia Ponterio ◽  
Graziella Madeo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Caspase 3 ◽  
Cysteine Proteases ◽  
Synaptic Function ◽  
Adult Brain ◽  
Striatal Slices

Caspases are a family of conserved cysteine proteases that play key roles in multiple cellular processes, including programmed cell death and inflammation. Recent evidence shows that caspases are also involved in crucial non-apoptotic functions, such as dendrite development, axon pruning, and synaptic plasticity mechanisms underlying learning and memory processes. The activated form of caspase-3, which is known to trigger widespread damage and degeneration, can also modulate synaptic function in the adult brain. Thus, in the present study, we tested the hypothesis that caspase-3 modulates synaptic plasticity at corticostriatal synapses in the phosphatase and tensin homolog (PTEN) induced kinase 1 (PINK1) mouse model of Parkinson’s disease (PD). Loss of PINK1 has been previously associated with an impairment of corticostriatal long-term depression (LTD), rescued by amphetamine-induced dopamine release. Here, we show that caspase-3 activity, measured after LTD induction, is significantly decreased in the PINK1 knockout model compared with wild-type mice. Accordingly, pretreatment of striatal slices with the caspase-3 activator α-(Trichloromethyl)-4-pyridineethanol (PETCM) rescues a physiological LTD in PINK1 knockout mice. Furthermore, the inhibition of caspase-3 prevents the amphetamine-induced rescue of LTD in the same model. Our data support a hormesis-based double role of caspase-3; when massively activated, it induces apoptosis, while at lower level of activation, it modulates physiological phenomena, like the expression of corticostriatal LTD. Exploring the non-apoptotic activation of caspase-3 may contribute to clarify the mechanisms involved in synaptic failure in PD, as well as in view of new potential pharmacological targets.

scholarly journals Methamphetamine increases dopamine release in the nucleus accumbens through calcium-dependent processes

2020 ◽  
Vol 237 (5) ◽  
pp. 1317-1330 ◽  
Author(s):  
Jordan T. Yorgason ◽  
David M. Hedges ◽  
J. Daniel Obray ◽  
Eun Young Jang ◽  
Kyle B. Bills ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Dopamine Release ◽  
Calcium Dependent ◽  
Dependent Processes

P2-333: Enhanced spontaneous release of neurotransmitter underlies early changes in synaptic function by beta-amyloid

2010 ◽  
Vol 6 ◽  
pp. S411-S411
Author(s):  
Mauro Fa ◽  
Elena Leznik ◽  
Ipe Ninan ◽  
Fabrizio Trinchese ◽  
Shumin Liu ◽  
...  
Keyword(s):  
Beta Amyloid ◽  
Synaptic Function ◽  
Spontaneous Release

Glycine stimulates the spontaneous release of newly synthesized 3H-dopamine in rat striatal slices

1979 ◽  
Vol 60 (1) ◽  
pp. 101-104 ◽  
Author(s):  
M.F. Giorguieff-Chesselet ◽  
M.L. Kemel ◽  
D. Wandscheer ◽  
J. Glowinski
Keyword(s):  
Spontaneous Release ◽  
Striatal Slices

Phagocytosis and Phagosome Maturation Are Regulated by Calcium in J774 Macrophages Interacting with Unopsonized Prey

2002 ◽  
Vol 22 (5-6) ◽  
pp. 529-540 ◽  
Author(s):  
Katarina Tejle ◽  
Karl-Eric Magnusson ◽  
Birgitta Rasmusson
Keyword(s):  
Leishmania Donovani ◽  
Inhibitory Effect ◽  
Phagosome Maturation ◽  
Calcium Dependent ◽  
Proper Functioning ◽  
Phagosomal Maturation ◽  
Macrophage Phagocytosis ◽  
Dependent Processes

Phagocytosis by neutrophils, macrophages, and other professional phagocytes requires rapid remodeling of actin. Early phagosomes are surrounded by a rim of F-actin that is disassembled during phagosomoal maturation. Breakdown of periphagosomal F-actin and phagolysosome fusion are calcium dependent processes in neutrophils interacting with serum-opsonized prey, but appears to be calcium independent in macrophages interacting with serum- or IgG-opsonized prey. In the present study, we found that calcium was necessary for phagocytosis, breakdown of periphagosomal F-actin, and phagosomal maturation in J774 macrophages interacting with unopsonized prey. We also observed that lipophosphoglycan (LPG) from Leishmania donovani promastigotes required calcium to exert its inhibitory effect on macrophage phagocytosis and periphagosomal F-actin breakdown. We conclude that calcium is essential for phagocytosis, depolymerization of periphagosomal F-actin, and phagosomal maturation in J774 macrophages interacting with unopsonized prey, as well as for proper functioning of LPG.

Effect of yttrium on calcium-dependent processes in vertebrate myocardium

2014 ◽  
Vol 50 (3) ◽  
pp. 221-226 ◽  
Author(s):  
I. V. Shemarova ◽  
K. V. Sobol’ ◽  
S. M. Korotkov ◽  
V. P. Nesterov
Keyword(s):  
Calcium Dependent ◽  
Dependent Processes

scholarly journals DYNAMICS OF NEUROMUSCULAR TRANSMISSION REPRODUCED BY CALCIUM-DEPENDENT SERIAL TRANSITIONS IN THE VESICLE FUSION COMPLEX

2021 ◽  
Author(s):  
Alejandro Martínez-Valencia ◽  
Guillermo Ramírez-Santiago ◽  
Francisco F. De-Miguel
Keyword(s):  
Experimental Data ◽  
Kinetic Model ◽  
Electrical Activity ◽  
Rate Constant ◽  
Rate Constants ◽  
Resting State ◽  
Neuromuscular Transmission ◽  
Spontaneous Release ◽  
Calcium Dependent ◽  
Vesicle Pool

Neuromuscular transmission, from spontaneous release to facilitation and depression was accurately reproduced by a mechanistic kinetic model of sequential maturation transitions in the molecular fusion complex. The model incorporates three predictions. First, sequential calcium-dependent forward transitions take vesicles from docked to pre-primed to primed states, followed by fusion. Second, pre-priming and priming are reversible. Third, fusion and recycling are unidirectional. The model was fed with experimental data from previous studies while the backward (β) and recycling (ρ) rate constant values were fitted. Classical experiments were successfully reproduced when every forward (α) rate constant had the same value, and both backward rate constants were 50-100 times larger. Such disproportion originated an abruptly decreasing gradient of resting vesicles from docked to primed states. Simulations also predict that: i. Spontaneous release reflects primed to fusion spontaneous transitions. ii. Calcium elevations synchronize the series of forward transitions that lead to fusion. iii Facilitation reflects a transient increase of priming following calcium-dependent transitions. iv. Backward transitions and recycling restore the resting state. v. Depression reflects backward transitions and slow recycling after intense release. Such finely-tuned kinetics offers a mechanism for collective non-linear transitional adaptations of a homogeneous vesicle pool to an ever-changing pattern of electrical activity.

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