scholarly journals Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

2002 ◽  
Vol 83 (4) ◽  
pp. 895-903 ◽  
Author(s):  
Simona Scheggi ◽  
Benedetta Leggio ◽  
Flavio Masi ◽  
Silvia Grappi ◽  
Carla Gambarana ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Synaptic Transmission ◽  
Chronic Stress

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.

Decreases in rat locomotor activity as a result of changes in synaptic transmission to neurons within the mesencephalic locomotor region

1993 ◽  
Vol 71 (5-6) ◽  
pp. 394-406 ◽  
Author(s):  
Stefan M. Brudzynski ◽  
Michael Wu ◽  
Gordon J. Mogenson
Keyword(s):  
Nucleus Accumbens ◽  
Synaptic Transmission ◽  
Synaptic Input ◽  
Cobalt Chloride ◽  
Critical Role ◽  
Ventral Pallidum ◽  
Functional Region ◽  
Mesencephalic Locomotor Region ◽  
Freely Behaving

The mesencephalic locomotor region is defined as a functional region sending signals to the spinal cord generators of rhythmical limb movements for locomotion. It has been shown that the mesencephalic locomotor region plays a critical role in locomotion initiated from the nucleus accumbens or from the subpallidal region. However, there are conflicting data on whether synaptic input from the nucleus accumbens – subpallidal region to the mesencephalic locomotor region mediates locomotion. The purpose of the study was to determine the role of synaptic input to different subregions of the mesencephalic locomotor region in locomotion induced by injecting dopamine into the nucleus accumbens or by injecting picrotoxin into the subpallidal region in freely behaving rats. Synaptic transmission in the mesencephalic locomotor region was eliminated by excitotoxic lesions or was reversibly interrupted by injecting cobalt chloride, which can block synaptic transmission. Excitotoxic lesions or injections of cobalt into subregions of the mesencephalic locomotor region significantly decreased, although did not completely block, locomotion. The most effective sites for cobalt- and lesion-induced reduction in locomotion were consistent with localization of the mesencephalic locomotor region. Effective sites for cobalt and lesions markedly overlapped but were not identical. The results indicate that synaptic transmission within the mesencephalic locomotor region contributes to dopamine- or picrotoxin-induced locomotion.Key words: locomotion, mesencephalic locomotor region, nucleus accumbens, ventral pallidum, dopamine, picrotoxin, excitotoxins, cobalt chloride.

Opioid peptides reduce synaptic transmission in the nucleus accumbens

1992 ◽  
Vol 134 (2) ◽  
pp. 223-228 ◽  
Author(s):  
Xiaoru Yuan ◽  
Samuel Madamba ◽  
George Robert Siggins
Keyword(s):  
Nucleus Accumbens ◽  
Synaptic Transmission ◽  
Opioid Peptides

scholarly journals GABAergic neurons in nucleus accumbens are correlated to resilience and vulnerability to chronic stress for major depression

Oncotarget ◽  
2017 ◽  
Vol 8 (22) ◽  
pp. 35933-35945 ◽  
Author(s):  
Zhaoming Zhu ◽  
Guangyan Wang ◽  
Ke Ma ◽  
Shan Cui ◽  
Jin-Hui Wang
Keyword(s):  
Nucleus Accumbens ◽  
Major Depression ◽  
Chronic Stress ◽  
Gabaergic Neurons

scholarly journals Chronic Morphine Treatment Alters NMDA Receptor-Mediated Synaptic Transmission in the Nucleus Accumbens

1999 ◽  
Vol 19 (20) ◽  
pp. 9081-9089 ◽  
Author(s):  
Gilles Martin ◽  
Serge H. Ahmed ◽  
Thomas Blank ◽  
Joachim Spiess ◽  
George F. Koob ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Morphine Treatment ◽  
Chronic Morphine ◽  
Chronic Morphine Treatment

scholarly journals Dendritic Spines in Depression: What We Learned from Animal Models

2016 ◽  
Vol 2016 ◽  
pp. 1-26 ◽  
Author(s):  
Hui Qiao ◽  
Ming-Xing Li ◽  
Chang Xu ◽  
Hui-Bin Chen ◽  
Shu-Cheng An ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Chronic Stress ◽  
Dendritic Spines ◽  
Mild Stress ◽  
Spine Density ◽  
Chronic Social Defeat Stress ◽  
Underlying Mechanisms ◽  
Dendritic Atrophy ◽  
Stress Models

Depression, a severe psychiatric disorder, has been studied for decades, but the underlying mechanisms still remain largely unknown. Depression is closely associated with alterations in dendritic spine morphology and spine density. Therefore, understanding dendritic spines is vital for uncovering the mechanisms underlying depression. Several chronic stress models, including chronic restraint stress (CRS), chronic unpredictable mild stress (CUMS), and chronic social defeat stress (CSDS), have been used to recapitulate depression-like behaviors in rodents and study the underlying mechanisms. In comparison with CRS, CUMS overcomes the stress habituation and has been widely used to model depression-like behaviors. CSDS is one of the most frequently used models for depression, but it is limited to the study of male mice. Generally, chronic stress causes dendritic atrophy and spine loss in the neurons of the hippocampus and prefrontal cortex. Meanwhile, neurons of the amygdala and nucleus accumbens exhibit an increase in spine density. These alterations induced by chronic stress are often accompanied by depression-like behaviors. However, the underlying mechanisms are poorly understood. This review summarizes our current understanding of the chronic stress-induced remodeling of dendritic spines in the hippocampus, prefrontal cortex, orbitofrontal cortex, amygdala, and nucleus accumbens and also discusses the putative underlying mechanisms.

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