Activation of dopamine D1 receptors in the medial prefrontal cortex produces bidirectional effects on cocaine-induced locomotor activity in rats: effects of repeated stress

Neuroscience ◽  
2004 ◽  
Vol 127 (1) ◽  
pp. 187-196 ◽  
Author(s):  
B.A Sorg ◽  
N Li ◽  
W Wu ◽  
T.M Bailie
Keyword(s):  
Prefrontal Cortex ◽  
Locomotor Activity ◽  
Medial Prefrontal Cortex ◽  
D1 Receptors ◽  
Dopamine D1 Receptors ◽  
Repeated Stress ◽  
Bidirectional Effects

scholarly journals Morphine selectively promotes glutamate release from glutamatergic terminals of projection neurons from medial prefrontal cortex to dopamine neurons of ventral tegmental area

2017 ◽  
Author(s):  
Li Yang ◽  
Ming Chen ◽  
Ping Zheng
Keyword(s):  
Prefrontal Cortex ◽  
Locomotor Activity ◽  
Ventral Tegmental Area ◽  
Medial Prefrontal Cortex ◽  
Lateral Hypothalamus ◽  
Basolateral Amygdala ◽  
Glutamate Release ◽  
Dopamine Neurons ◽  
Projection Neurons ◽  
Ventral Tegmental

AbstractRecently, we found that morphine promoted presynaptic glutamate release of dopamine (DA) neurons in the ventral tegmental area (VTA), which constituted the main mechanism for morphine-induced increase in VTA-DA neuron firing and related behaviors (Chen et al., 2015). However, what source of presynaptic glutamate release of DA neurons in the VTA is promoted by morphine remains unknown. To address this question, we used optogenetic strategy to selectively activate glutamatergic inputs from different projection neurons and then observed the effect of morphine on them. The result shows that morphine promotes glutamate release from glutamatergic terminals of projection neurons from the medial prefrontal cortex (mPFC) to VTA DA neurons, but has no effect on that from the basolateral amygdala (BLA) or the lateral hypothalamus (LH) to VTA DA neurons, and the inhibition of glutamatergic projection neurons from the mPFC to the VTA significantly reduces morphine-induced increase in locomotor activity of mice.

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