Localization of m4 muscarinic receptors on direct ⪢ indirect striatal projection neurons

Life Sciences ◽  
1999 ◽  
Vol 64 (6-7) ◽  
pp. 584
Author(s):  
M.P. Santiago ◽  
L.T. Potter
Keyword(s):  
Muscarinic Receptors ◽  
Projection Neurons ◽  
Striatal Projection Neurons

scholarly journals KV7 Channels Regulate Firing during Synaptic Integration in GABAergic Striatal Neurons

2015 ◽  
Vol 2015 ◽  
pp. 1-18 ◽  
Author(s):  
M. Belén Pérez-Ramírez ◽  
Antonio Laville ◽  
Dagoberto Tapia ◽  
Mariana Duhne ◽  
Esther Lara-González ◽  
...  
Keyword(s):  
Muscarinic Receptors ◽  
Synaptic Integration ◽  
Projection Neurons ◽  
Striatal Neurons ◽  
Kv7 Channels ◽  
Striatal Projection Neurons ◽  
Voltage Dependent ◽  
Cognitive Information ◽  
Firing Properties ◽  
The Impact

Striatal projection neurons (SPNs) process motor and cognitive information. Their activity is affected by Parkinson’s disease, in which dopamine concentration is decreased and acetylcholine concentration is increased. Acetylcholine activates muscarinic receptors in SPNs. Its main source is the cholinergic interneuron that responds with a briefer latency than SPNs during a cortical command. Therefore, an important question is whether muscarinic G-protein coupled receptors and their signaling cascades are fast enough to intervene during synaptic responses to regulate synaptic integration and firing. One of the most known voltage dependent channels regulated by muscarinic receptors is theKV7/KCNQ channel. It is not known whether these channels regulate the integration of suprathreshold corticostriatal responses. Here, we study the impact of cholinergic muscarinic modulation on the synaptic response of SPNs by regulatingKV7 channels. We found thatKV7 channels regulate corticostriatal synaptic integration and that this modulation occurs in the dendritic/spines compartment. In contrast, it is negligible in the somatic compartment. This modulation occurs on sub- and suprathreshold responses and lasts during the whole duration of the responses, hundreds of milliseconds, greatly altering SPNs firing properties. This modulation affected the behavior of the striatal microcircuit.

scholarly journals Inhibition of Phosphodiesterase 10A Increases the Responsiveness of Striatal Projection Neurons to Cortical Stimulation

2008 ◽  
Vol 328 (3) ◽  
pp. 785-795 ◽  
Author(s):  
Sarah Threlfell ◽  
Stephen Sammut ◽  
Frank S. Menniti ◽  
Christopher J. Schmidt ◽  
Anthony R. West
Keyword(s):  
Cortical Stimulation ◽  
Projection Neurons ◽  
Striatal Projection Neurons ◽  
Phosphodiesterase 10A

Differences in synaptic integration between direct and indirect striatal projection neurons: Role of CaV 3 channels

Synapse ◽  
2018 ◽  
Vol 73 (4) ◽  
pp. e22079 ◽  
Author(s):  
Brisa García-Vilchis ◽  
Paola Suárez ◽  
Miguel Serrano-Reyes ◽  
Mario Arias-García ◽  
Dagoberto Tapia ◽  
...  
Keyword(s):  
Synaptic Integration ◽  
Projection Neurons ◽  
Striatal Projection Neurons

scholarly journals Fronto-striatal projections regulate approach-avoidance conflict

2020 ◽  
Author(s):  
Adrienne C. Loewke ◽  
Adelaide R. Minerva ◽  
Alexandra B. Nelson ◽  
Anatol C. Kreitzer ◽  
Lisa A. Gunaydin
Keyword(s):  
Anxiety Disorders ◽  
Avoidance Behavior ◽  
D1 Receptor ◽  
Projection Neurons ◽  
Medium Spiny Neurons ◽  
Neural Pathways ◽  
Spiny Neurons ◽  
Striatal Projection Neurons ◽  
Neural Computations ◽  
Approach Avoidance

ABSTRACTThe dorsomedial prefrontal cortex (dmPFC) has been linked to approach-avoidance behavior and decision-making under conflict, key neural computations thought to be altered in anxiety disorders. However, the heterogeneity of efferent prefrontal projections has obscured identification of the specific top-down neural pathways regulating these anxiety-related behaviors. While the dmPFC-amygdala circuit has long been implicated in controlling reflexive fear responses, recent work suggests that this circuit is less important for avoidance behavior. We hypothesized that dmPFC neurons projecting to the dorsomedial striatum (DMS) represent a subset of prefrontal neurons that robustly encode and drive approach-avoidance behavior. Using fiber photometry recording during the elevated zero maze (EZM) task, we show heightened neural activity in prefrontal and fronto-striatal projection neurons, but not fronto-amydalar projection neurons, during exploration of the anxiogenic open arms of the maze. Additionally, through pathway-specific optogenetics we demonstrate that this fronto-striatal projection preferentially excites postsynaptic D1 receptor-expressing medium spiny neurons in the DMS and bidirectionally controls avoidance behavior. We conclude that this striatal-projecting subpopulation of prefrontal neurons regulates approach-avoidance conflict, supporting a model for prefrontal control of defensive behavior in which the dmPFC-amygdala projection controls reflexive fear behavior and the dmPFC-striatum projection controls anxious avoidance behavior. Our findings identify this fronto-striatal circuit as a valuable therapeutic target for developing interventions to alleviate excessive avoidance behavior in anxiety disorders.

scholarly journals What is the true discharge rate and pattern of the striatal projection neurons in Parkinson’s disease and Dystonia?

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Dan Valsky ◽  
Shai Heiman Grosberg ◽  
Zvi Israel ◽  
Thomas Boraud ◽  
Hagai Bergman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Cluster Analysis ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Discharge Rate ◽  
Spontaneous Discharge ◽  
Projection Neurons ◽  
Pathological State ◽  
Striatal Projection Neurons ◽  
Deep Brain

Dopamine and striatal dysfunctions play a key role in the pathophysiology of Parkinson’s disease (PD) and Dystonia, but our understanding of the changes in the discharge rate and pattern of striatal projection neurons (SPNs) remains limited. Here, we recorded and examined multi-unit signals from the striatum of PD and dystonic patients undergoing deep brain stimulation surgeries. Contrary to earlier human findings, we found no drastic changes in the spontaneous discharge of the well-isolated and stationary SPNs of the PD patients compared to the dystonic patients or to the normal levels of striatal activity reported in healthy animals. Moreover, cluster analysis using SPN discharge properties did not characterize two well-separated SPN subpopulations, indicating no SPN subpopulation-specific (D1 or D2 SPNs) discharge alterations in the pathological state. Our results imply that small to moderate changes in spontaneous SPN discharge related to PD and Dystonia are likely amplified by basal ganglia downstream structures.

Muscarinic presynaptic modulation in GABAergic pallidal synapses of the rat

2015 ◽  
Vol 113 (3) ◽  
pp. 796-807 ◽  
Author(s):  
Ricardo Hernández-Martínez ◽  
José J. Aceves ◽  
Pavel E. Rueda-Orozco ◽  
Teresa Hernández-Flores ◽  
Omar Hernández-González ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Projection Neurons ◽  
Quantal Content ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Striatal Projection Neurons ◽  
Muscarinic Cholinergic ◽  
Muscarinic Modulation

The external globus pallidus (GPe) is central for basal ganglia processing. It expresses muscarinic cholinergic receptors and receives cholinergic afferents from the pedunculopontine nuclei (PPN) and other regions. The role of these receptors and afferents is unknown. Muscarinic M1-type receptors are expressed by synapses from striatal projection neurons (SPNs). Because axons from SPNs project to the GPe, one hypothesis is that striatopallidal GABAergic terminals may be modulated by M1 receptors. Alternatively, some M1 receptors may be postsynaptic in some pallidal neurons. Evidence of muscarinic modulation in any of these elements would suggest that cholinergic afferents from the PPN, or other sources, could modulate the function of the GPe. In this study, we show this evidence using striatopallidal slice preparations: after field stimulation in the striatum, the cholinergic muscarinic receptor agonist muscarine significantly reduced the amplitude of inhibitory postsynaptic currents (IPSCs) from synapses that exhibited short-term synaptic facilitation. This inhibition was associated with significant increases in paired-pulse facilitation, and quantal content was proportional to IPSC amplitude. These actions were blocked by atropine, pirenzepine, and mamba toxin-7, suggesting that receptors involved were M1. In addition, we found that some pallidal neurons have functional postsynaptic M1 receptors. Moreover, some evoked IPSCs exhibited short-term depression and a different kind of modulation: they were indirectly modulated by muscarine via the activation of presynaptic cannabinoid CB1 receptors. Thus pallidal synapses presenting distinct forms of short-term plasticity were modulated differently.

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