scholarly journals Psychostimulants depress excitatory synaptic transmission in the nucleus accumbens via presynaptic D1-like dopamine receptors

1996 ◽  
Vol 16 (5) ◽  
pp. 1591-1604 ◽  
Author(s):  
SM Nicola ◽  
SB Kombian ◽  
RC Malenka
Keyword(s):  
Nucleus Accumbens ◽  
Synaptic Transmission ◽  
Dopamine Receptors ◽  
Excitatory Synaptic Transmission

Substance P Depresses Excitatory Synaptic Transmission in the Nucleus Accumbens Through Dopaminergic and Purinergic Mechanisms

2003 ◽  
Vol 89 (2) ◽  
pp. 728-737 ◽  
Author(s):  
Samuel B. Kombian ◽  
Kethireddy V. V. Ananthalakshmi ◽  
Subramanian S. Parvathy ◽  
Wandikayi C. Matowe
Keyword(s):  
Nucleus Accumbens ◽  
Substance P ◽  
Synaptic Transmission ◽  
Input Resistance ◽  
Nmda Receptor Antagonist ◽  
Excitatory Synaptic Transmission ◽  
Nk1 Receptor ◽  
Dose Dependent Decrease ◽  
Neurokinin 1 ◽  
Synaptic Effects

Substance P (SP) is an undecapeptide that is co-localized with conventional transmitters in the nucleus accumbens (NAc). Its neurochemical and behavioral effects resemble those of cocaine and amphetamine. How SP accomplishes these effects is not known, partly because its cellular and synaptic effects are not well characterized. Using whole cell and nystatin-perforated patch recording in rat forebrain slices, we show here that SP, an excitatory neuropeptide, depresses evoked excitatory postsynaptic currents (EPSCs) and potentials (EPSPs) in NAc through intermediate neuromodulators. SP caused a partially reversible, dose-dependent decrease in evoked EPSCs. This effect was mimicked by a neurokinin-1 (NK1) receptor-selective agonist, [Sar9, Met (O2)11]-SP and blocked by a NK1 receptor-selective antagonist, L 732 138. Both the SP- and [Sar9, Met (O2)11]-SP-induced synaptic depressions were accompanied by increases in paired pulse ratio (PPR), effects that were also blocked by L 732 138. In contrast to its effect on PPR, SP did not produce significant changes in the holding current, input resistance, EPSC decay rate (τ), and steady-state I-V curves of the recorded cells. The SP-induced synaptic depressions were prevented by dopamine receptor blockade using SCH23390 and haloperidol, but not by sulpiride. In addition, the SP-induced synaptic depression was blocked by an adenosine A1 receptor blocker 8-cyclopentyltheophylline (8-CPT) but not the N-methyl-d-aspartate (NMDA) receptor antagonist d-APV. These data show that SP, by activating presynaptic NK1 receptors, depresses excitatory synaptic transmission indirectly by enhancing extracellular dopamine and adenosine levels. Since the cellular and synaptic effects of SP resemble those of cocaine and amphetamine, it may serve as an endogenous psychogenic peptide.

scholarly journals Exposure to Cocaine Alters Dynorphin-Mediated Regulation of Excitatory Synaptic Transmission in Nucleus Accumbens Neurons

2011 ◽  
Vol 69 (3) ◽  
pp. 228-235 ◽  
Author(s):  
Ping Mu ◽  
Peter A. Neumann ◽  
Jaak Panksepp ◽  
Oliver M. Schlüter ◽  
Yan Dong
Keyword(s):  
Nucleus Accumbens ◽  
Synaptic Transmission ◽  
Excitatory Synaptic Transmission

scholarly journals Effect of Aggressive Experience in Female Syrian Hamsters on Glutamate Receptor Expression in the Nucleus Accumbens

2020 ◽  
Vol 14 ◽  
Author(s):  
Johnathan M. Borland ◽  
Ellen Kim ◽  
Samuel P. Swanson ◽  
Patrick E. Rothwell ◽  
Paul G. Mermelstein ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Synaptic Transmission ◽  
Glutamate Receptors ◽  
Social Relationships ◽  
Well Being ◽  
Receptor Expression ◽  
Excitatory Synaptic Transmission ◽  
Common Mechanism ◽  
Syrian Hamsters ◽  
Group I

Our social relationships determine our health and well-being. In rodent models, there is now strong support for the rewarding properties of aggressive or assertive behaviors to be critical for the expression and development of adaptive social relationships, buffering from stress and protecting from the development of psychiatric disorders such as depression. However, due to the false belief that aggression is not a part of the normal repertoire of social behaviors displayed by females, almost nothing is known about the neural mechanisms mediating the rewarding properties of aggression in half the population. In the following study, using Syrian hamsters as a well-validated and translational model of female aggression, we investigated the effects of aggressive experience on the expression of markers of postsynaptic structure (PSD-95, Caskin I) and excitatory synaptic transmission (GluA1, GluA2, GluA4, NR2A, NR2B, mGluR1a, and mGluR5) in the nucleus accumbens (NAc), caudate putamen and prefrontal cortex. Aggressive experience resulted in an increase in PSD-95, GluA1 and the dimer form of mGluR5 specifically in the NAc 24 h following aggressive experience. There was also an increase in the dimer form of mGluR1a 1 week following aggressive experience. Aggressive experience also resulted in an increase in the strength of the association between these postsynaptic proteins and glutamate receptors, supporting a common mechanism of action. In addition, 1 week following aggressive experience there was a positive correlation between the monomer of mGluR5 and multiple AMPAR and NMDAR subunits. In conclusion, we provide evidence that aggressive experience in females results in an increase in the expression of postsynaptic density, AMPARs and group I metabotropic glutamate receptors, and an increase in the strength of the association between postsynaptic proteins and glutamate receptors. This suggests that aggressive experience may result in an increase in excitatory synaptic transmission in the NAc, potentially encoding the rewarding and behavioral effects of aggressive interactions.

Kappa Opioid Receptor Inhibition of Glutamatergic Transmission in the Nucleus Accumbens Shell

2001 ◽  
Vol 85 (3) ◽  
pp. 1153-1158 ◽  
Author(s):  
Gregory O. Hjelmstad ◽  
Howard L. Fields
Keyword(s):  
Nucleus Accumbens ◽  
Synaptic Transmission ◽  
Opioid Receptor ◽  
Receptor Activation ◽  
Kappa Opioid Receptor ◽  
Excitatory Synaptic Transmission ◽  
Nucleus Accumbens Shell ◽  
Receptor Agonists ◽  
Κ Receptor

Microinjection of κ-opioid receptor agonists into the nucleus accumbens produces conditioned place aversion. While attention has focused primarily on the inhibition of dopamine release by κ-receptor agonists as the synaptic mechanism underlying this effect, recent anatomical studies have raised the possibility that regulation of noncatecholaminergic transmission also contribute. We have investigated the effects of κ-receptor activation on fast excitatory synaptic transmission in an in vitro slice preparation using whole cell voltage-clamp or extracellular field recordings in the shell region of the nucleus accumbens. The κ-receptor agonist U69593 produces a pronounced, dose-dependent inhibition of glutamatergic excitatory postsynaptic currents (EPSCs) that can be reversed by 100 nM nor-BNI. Furthermore, U69593 causes an increase in the paired-pulse ratio as well as a decrease in the frequency of spontaneous miniature events, suggesting a presynaptic site of action. Despite anatomical evidence for κ-receptor localization on dendritic spines of nucleus accumbens neurons, no electrophysiological evidence of a postsynaptic effect was found. This presynaptic inhibition of excitatory synaptic transmission in the nucleus accumbens shell provides a novel mechanism that may contribute to the κ-receptor–mediated aversion observed in intact animals.

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