scholarly journals Prolonged Consumption of Sucrose in a Binge-Like Manner, Alters the Morphology of Medium Spiny Neurons in the Nucleus Accumbens Shell

2016 ◽  
Vol 10 ◽  
Author(s):  
Paul M. Klenowski ◽  
Masroor R. Shariff ◽  
Arnauld Belmer ◽  
Matthew J. Fogarty ◽  
Erica W. H. Mu ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Medium Spiny Neurons ◽  
Nucleus Accumbens Shell ◽  
Spiny Neurons

scholarly journals Morphine differentially alters the synaptic and intrinsic properties of D1R- and D2R-expressing medium spiny neurons in the nucleus accumbens

2019 ◽  
Author(s):  
Dillon S. McDevitt ◽  
Benjamin Jonik ◽  
Nicholas M. Graziane
Keyword(s):  
Nucleus Accumbens ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
D1 Receptor ◽  
Medium Spiny Neurons ◽  
Nucleus Accumbens Shell ◽  
Membrane Excitability ◽  
Action Potential Firing ◽  
Spiny Neurons ◽  
Functional Output

AbstractExposure to opioids reshapes future reward and motivated behaviors partially by altering the functional output of medium spiny neurons (MSNs) in the nucleus accumbens shell. Here, we investigated how morphine, a highly addictive opioid, alters synaptic transmission and intrinsic excitability on dopamine D1-receptor (D1R) expressing and dopamine D2-receptor (D2R) expressing MSNs, the two main output neurons in the nucleus accumbens shell. Using whole-cell electrophysiology recordings, we show, that 24 h abstinence following repeated non-contingent administration of morphine (10 mg/kg, i.p.) in mice reduces miniature excitatory postsynaptic current (mEPSC) frequency and miniature inhibitory postsynaptic current (mIPSC) frequency on D2R-MSNs, with concomitant increases in D2R-MSN intrinsic membrane excitability. We did not observe any changes on synaptic or intrinsic changes on D1R-MSNs. Lastly, in an attempt to determine the integrated effect of the synaptic and intrinsic alterations on the overall functional output of D2R-MSNs, we measured the input-output efficacy by measuring synaptically-driven action potential firing. We found that both D1R-MSN and D2R-MSN output was unchanged following morphine treatment.

scholarly journals The Ethanol Metabolite Acetic Acid Activates Mouse Nucleus Accumbens Shell Medium Spiny Neurons

2021 ◽  
Author(s):  
Andrew D. Chapp ◽  
Paul G Mermelstein ◽  
Mark J Thomas
Keyword(s):  
Acetic Acid ◽  
Nucleus Accumbens ◽  
Neuronal Excitability ◽  
Ethanol Consumption ◽  
Synaptic Activity ◽  
Medium Spiny Neurons ◽  
Nucleus Accumbens Shell ◽  
Spiny Neurons ◽  
The Impact ◽  
Reward Circuit

While ethanol consumption leads to an array of neurophysiological alterations involving the neural circuits for reward, the underlying mechanisms remain unclear. Acetic acid is a major metabolite of ethanol with high bioactivity and potentially significant pharmacological importance in regulating brain function. Yet the impact of acetic acid on reward circuit function has not been well explored. Given the rewarding properties associated with ethanol consumption, we investigated the acute effects of ethanol and/or acetic acid on the neurophysiological function of medium spiny neurons of the nucleus accumbens shell, a key node in the mammalian reward circuit. We find that acetic acid, but not ethanol, provided a rapid and robust boost in neuronal excitability at physiologically relevant concentrations, while both compounds enhanced glutamatergic synaptic activity. These effects were consistent across both sexes in C57BL/6J mice. Overall, our data suggest acetic acid is a promising candidate mediator for ethanol effects on mood and motivation that deserves further investigation.

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