scholarly journals Striatal Dopamine Release Is Triggered by Synchronized Activity in Cholinergic Interneurons

Neuron ◽  
2012 ◽  
Vol 75 (1) ◽  
pp. 58-64 ◽  
Author(s):  
Sarah Threlfell ◽  
Tatjana Lalic ◽  
Nicola J. Platt ◽  
Katie A. Jennings ◽  
Karl Deisseroth ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Striatal Dopamine ◽  
Cholinergic Interneurons ◽  
Striatal Dopamine Release

scholarly journals Cell-intrinsic effects of TorsinA(ΔE) disrupt dopamine release in a mouse model of DYT1-TOR1A dystonia

2020 ◽  
Author(s):  
Anthony M. Downs ◽  
Xueliang Fan ◽  
Radhika Kadakia ◽  
Yuping Donsante ◽  
H.A. Jinnah ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Ex Vivo ◽  
Dopamine Neurons ◽  
Striatal Dopamine ◽  
Cholinergic Interneurons ◽  
Base Pair Deletion ◽  
Presynaptic Mechanisms ◽  
Conditional Expression ◽  
Striatal Dopamine Release

ABSTRACTDYT1-TOR1A dystonia is an inherited dystonia caused by a three base-pair deletion in the TOR1A gene (TOR1AΔE). Although the mechanisms underlying the dystonic movements are largely unknown, abnormalities in striatal dopamine and acetylcholine neurotransmission are consistently implicated whereby dopamine release is reduced while cholinergic tone is increased. Because striatal cholinergic neurotransmission mediates dopamine release, it is not known if the dopamine release deficit is mediated indirectly by abnormal acetylcholine neurotransmission or if Tor1a(ΔE) acts directly within dopaminergic neurons to attenuate release. To dissect the microcircuit that governs the deficit in dopamine release, we conditionally expressed Tor1a(ΔE) in either dopamine neurons or cholinergic interneurons in mice and assessed striatal dopamine release using ex vivo fast scan cyclic voltammetry or dopamine efflux using in vivo microdialysis. Conditional expression of Tor1a(ΔE) in cholinergic neurons did not affect striatal dopamine release. In contrast, conditional expression of Tor1a(ΔE) in dopamine neurons reduced dopamine release to 50% of normal, which is comparable to the deficit in Tor1a+/ΔE knockin mice that express the mutation ubiquitously. Despite the deficit in dopamine release, we found that the Tor1a(ΔE) mutation does not cause obvious nerve terminal dysfunction as other presynaptic mechanisms, including electrical excitability, vesicle recycling/refilling, Ca2+ signaling, D2 dopamine autoreceptor function and GABAB receptor function, are intact. Although the mechanistic link between Tor1a(ΔE) and dopamine release is unclear, these results clearly demonstrate that the defect in dopamine release is caused by the action of the Tor1a(ΔE) mutation within dopamine neurons.

scholarly journals Axonal mechanisms mediating γ-aminobutyric acid receptor type A (GABA-A) inhibition of striatal dopamine release

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Paul F Kramer ◽  
Emily L Twedell ◽  
Jung Hoon Shin ◽  
Renshu Zhang ◽  
Zayd M Khaliq
Keyword(s):  
Dopamine Release ◽  
Branching Processes ◽  
Striatal Dopamine ◽  
Gaba A ◽  
Cholinergic Interneurons ◽  
Adult Mice ◽  
Receptor Modulation ◽  
Channel Inactivation ◽  
Mechanism Of Inhibition ◽  
Striatal Dopamine Release

Axons of dopaminergic neurons innervate the striatum where they contribute to movement and reinforcement learning. Past work has shown that striatal GABA tonically inhibits dopamine release, but whether GABA-A receptors directly modulate transmission or act indirectly through circuit elements is unresolved. Here, we use whole-cell and perforated-patch recordings to test for GABA-A receptors on the main dopaminergic neuron axons and branching processes within the striatum of adult mice. Application of GABA depolarized axons, but also decreased the amplitude of axonal spikes, limited propagation and reduced striatal dopamine release. The mechanism of inhibition involved sodium channel inactivation and shunting. Lastly, we show the positive allosteric modulator diazepam enhanced GABA-A currents on dopaminergic axons and directly inhibited release, but also likely acts by reducing excitation from cholinergic interneurons. Thus, we reveal the mechanisms of GABA-A receptor modulation of dopamine release and provide new insights into the actions of benzodiazepines within the striatum.

scholarly journals Insulin enhances striatal dopamine release by activating cholinergic interneurons and thereby signals reward

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Melissa A. Stouffer ◽  
Catherine A. Woods ◽  
Jyoti C. Patel ◽  
Christian R. Lee ◽  
Paul Witkovsky ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Striatal Dopamine ◽  
Cholinergic Interneurons ◽  
Striatal Dopamine Release

scholarly journals Axonal mechanisms mediating GABA-A receptor inhibition of striatal dopamine release

2020 ◽  
Author(s):  
Paul F. Kramer ◽  
Emily L. Twedell ◽  
Jung Hoon Shin ◽  
Renshu Zhang ◽  
Zayd M. Khaliq
Keyword(s):  
Dopaminergic Neuron ◽  
Dopamine Release ◽  
Branching Processes ◽  
Striatal Dopamine ◽  
Gaba A ◽  
Cholinergic Interneurons ◽  
Receptor Modulation ◽  
Mechanism Of Inhibition ◽  
Midbrain Dopaminergic Neurons ◽  
Striatal Dopamine Release

AbstractAxons of midbrain dopaminergic neurons innervate the striatum where they contribute to movement and reinforcement learning. Past work has shown that striatal GABA tonically inhibits dopamine release, but whether GABA-A receptors directly modulate transmission or act indirectly through circuit elements is unresolved. Here, we use whole-cell and perforated-patch recordings to test for GABA-A receptors on the main dopaminergic neuron axons and branching processes within striatum. Application of GABA depolarized axons, but also decreased the amplitude of axonal spikes, limited propagation and reduced striatal dopamine release. The mechanism of inhibition involved sodium channel inactivation and shunting. Lastly, we show that the positive allosteric modulator diazepam enhanced GABA-A currents on dopaminergic neuron axons and directly inhibited release, but also likely acts by reducing excitatory drive from cholinergic interneurons. Thus, we reveal the mechanisms of GABA-A receptor modulation of dopamine release and provide new insight into the actions of benzodiazepines within the striatum.

VENTRAL STRIATAL DOPAMINE RELEASE AND SENSORIMOTOR GATING

1998 ◽  
Vol 9 (Supplement) ◽  
pp. S95
Author(s):  
L. S. Wilkinson ◽  
T. Humbya ◽  
M. A. Geyer
Keyword(s):  
Dopamine Release ◽  
Sensorimotor Gating ◽  
Striatal Dopamine ◽  
Striatal Dopamine Release
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