Effects of intermittent and continuous cocaine administration on dopamine release and uptake regulation in the striatum: in vitro voltammetric assessment

1996 ◽  
Vol 126 (4) ◽  
pp. 331-338 ◽  
Author(s):  
S. R. Jones ◽  
R. M. Wightman ◽  
T. H. Lee ◽  
E. H. Ellinwood
Keyword(s):  
Dopamine Release ◽  
Cocaine Administration ◽  
Continuous Cocaine

scholarly journals Stimulation-Evoked Dopamine Release in the Nucleus Accumbens Following Cocaine Administration in Rats Perinatally Exposed to Polychlorinated Biphenyls

2013 ◽  
Vol 136 (1) ◽  
pp. 144-153 ◽  
Author(s):  
Jenna R. Fielding ◽  
Tiffany D. Rogers ◽  
Abby E. Meyer ◽  
Mellessa M. Miller ◽  
Jenna L. Nelms ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Polychlorinated Biphenyls ◽  
Dopamine Release ◽  
Cocaine Administration

scholarly journals Room D, 10/17/2000 9: 00 AM - 11: 00 AM (PS) Nitrous Oxide Induced Met-enkephalin Release Provokes Dopamine Release in Rat Adrenal Medulla Cultured In Vitro 

2000 ◽  
Vol 93 (3A) ◽  
pp. A-758
Author(s):  
Shin-ichi Inomata ◽  
Mervyn Maze ◽  
Toshikazu Hashimoto ◽  
Matthew Jones ◽  
Masahiko Fujinaga
Keyword(s):  
Nitrous Oxide ◽  
Adrenal Medulla ◽  
Dopamine Release

Characteristics of Electrically Evoked Somatodendritic Dopamine Release in Substantia Nigra and Ventral Tegmental Area In Vitro

1997 ◽  
Vol 77 (2) ◽  
pp. 853-862 ◽  
Author(s):  
M. E. Rice ◽  
S. J. Cragg ◽  
S. A. Greenfield
Keyword(s):  
Electrical Stimulation ◽  
Substantia Nigra ◽  
Ventral Tegmental Area ◽  
Dopamine Release ◽  
Substantia Nigra Pars Compacta ◽  
Frequency Dependent ◽  
Body Regions ◽  
Ventral Tegmental ◽  
Da Release

Rice, M. E., S. J. Cragg, and S. A. Greenfield. Characteristics of electrically evoked somatodendritic dopamine release in substantia nigra and ventral tegmental area in vitro. J. Neurophysiol. 77: 853–862, 1997. Somatodendritic dopamine (DA) release from neurons of the midbrain represents a nonclassical form of neuronal signaling. We assessed characteristics of DA release during electrical stimulation of the substantia nigra pars compacta (SNc) in guinea pig midbrain slices. With the use of parameters optimized for this region, we compared stimulus-induced increases in extracellular DA concentration ([DA]o) in medial and lateral SNc, ventral tegmental area (VTA), and dorsal striatum in vitro. DA release was monitored directly with carbon-fiber microelectrodes and fast-scan cyclic voltammetry. Detection of DA in SNc was confirmed by electrochemical, pharmacological, and anatomic criteria. Voltammograms of the released substance had the same peak potentials as those of DA obtained during in vitro calibration, but different from those of the indoleamine 5-hydroxytryptamine. Similar voltammograms were also obtained in the DA-rich striatum during local electrical stimulation. Contribution from the DA metabolite 3,4-dihydroxyphenylacetic acid to somatodendritic release was negligible, as indicated by the lack of effect of the monoamine oxidase inhibitor pargyline (20 μM) on the signal. Lastly, DA voltammograms could only be elicited in regions that were subsequently determined to be positive for tyrosine hydroxylase immunoreactivity (TH-ir). The frequency dependence of stimulated DA release in SNc was determined over a range of 1–50 Hz, with a constant duration of 10 s. Release was frequency dependent up to 10 Hz, with no further increase at higher frequencies. Stimulation at 10 Hz was used in all subsequent experiments. With this paradigm, DA release in SNc was tetrodotoxin insensitive, but strongly Ca2+ dependent. Stimulated [DA]o in the midbrain was also site specific. At the midcaudal level examined, DA efflux was significantly greater in VTA (1.04 ± 0.05 μM, mean ± SE) than in medial SNc (0.52 ± 0.05 μM), which in turn was higher than in lateral SNc (0.35 ± 0.03 μM). This pattern followed the apparent density of TH-ir, which was also VTA > medial SNc > lateral SNc. This report has introduced a new paradigm for the study of somatodendritic DA release. Voltammetric recording with electrodes of 2–4 μm tip diameter permitted highly localized, direct detection of endogenous DA. The Ca2+ dependence of stimulated release indicated that the process was physiologically relevant. Moreover, the findings that somatodendritic release was frequency dependent across a range characteristic of DA cell firing rates and that stimulated [DA]o varied markedly among DA cell body regions have important implications for how dendritically released DA may function in the physiology and pathophysiology of substantia nigra and VTA.

scholarly journals CSPα reduces aggregates and rescues striatal dopamine release in αsynuclein transgenic mice

2020 ◽  
Author(s):  
L Caló ◽  
E Hidari ◽  
M Wegrzynowicz ◽  
JW Dalley ◽  
BL Schneider ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Early Stage ◽  
Synaptic Function ◽  
Snare Complex ◽  
Early Event ◽  
Vesicle Recycling ◽  
Cysteine String Protein ◽  
And Function

AbstractαSynuclein aggregation at the synapse is an early event in Parkinson’s disease and is associated with impaired striatal synaptic function and dopaminergic neuronal death. The cysteine string protein (CSPα) and αsynuclein have partially overlapping roles in maintaining synaptic function and mutations in each cause neurodegenerative diseases. CSPα is a member of the DNAJ/HSP40 family of co-chaperones and like αsynuclein, chaperones the SNARE complex assembly and neurotransmitter release. αSynuclein can rescue neurodegeneration in CSPαKO mice. However, whether αsynuclein aggregation alters CSPα expression and function is unknown. Here we show that αsynuclein aggregation at the synapse induces a decrease in synaptic CSPα and a reduction in the complexes that CSPα forms with HSC70 and STGa. We further show that viral delivery of CSPα rescues in vitro the impaired vesicle recycling in PC12 cells with αsynuclein aggregates and in vivo reduces synaptic αsynuclein aggregates restoring normal dopamine release in 1-120hαsyn mice. These novel findings reveal a mechanism by which αsynuclein aggregation alters CSPα at the synapse, and show that CSPα rescues αsynuclein aggregation-related phenotype in 1-120hαsyn mice similar to the effect of αsynuclein in CSPαKO mice. These results implicate CSPα as a potential therapeutic target for the treatment of early-stage PD.

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