Tandospirone potentiates the fluoxetine-induced increases in extracellular dopamine via 5-HT1A receptors in the rat medial frontal cortex

@article{Yoshino2002TandospironePT,
  title={Tandospirone potentiates the fluoxetine-induced increases in extracellular dopamine via 5-HT1A receptors in the rat medial frontal cortex},
  author={Tatsuki Yoshino and Koichi Nisijima and Satoshi Katoh and Kunio Yui and Mitsutaka Nakamura},
  journal={Neurochemistry International},
  year={2002},
  volume={40},
  pages={355-360}
}

The role of 5-HT1A receptors in phencyclidine (PCP)-induced novel object recognition (NOR) deficit in rats

TLDR
Results indicate that 5-HT1A agonism is adequate to ameliorate the PCP-induced impairment in NOR and suggest further study of utilizing the combination of a 5- HT 1A agonist and an atypical APD to amaliorate some types of cognitive impairment in schizophrenia.

Role of tandospirone, a 5-HT1A receptor partial agonist, in the treatment of central nervous system disorders and the underlying mechanisms

TLDR
The beneficial effect of tandospirone has been revealed on improvement of motor dysfunction of Parkinson's disease and cognitive deficits of schizophrenia either in monotherapy or in combination with other drugs.

Comparative effect of lurasidone and blonanserin on cortical glutamate, dopamine, and acetylcholine efflux: role of relative serotonin (5‐HT)2A and DA D2 antagonism and 5‐HT1A partial agonism

TLDR
The ability to increase cortical DA efflux was the only shared effect of the compounds which ameliorates the deficit in cognition in rodents following phencyclidine.

Is milnacipran a promising agent to suppress impulsive behavior

TLDR
This is the first report that demonstrates a critical role for D1-like receptors of the vmPFC in milnacipran-enhanced control of impulsive action.

Serotonin control of central dopaminergic function: focus on in vivo microdialysis studies.

Tandospirone activates neuroendocrine and ERK (MAP kinase) signaling pathways specifically through 5-HT1A receptor mechanisms in vivo

TLDR
The results are the first evidence that systemic 5-HT1A receptor agonist administration produces a rapid increase in p-ERK levels in vivo, providing further insight into the signaling mechanisms of the 5- HT1A receptors.

References

SHOWING 1-10 OF 20 REFERENCES

Buspirone Enhances Duloxetine‐ and Fluoxetine‐Induced Increases in Dialysate Levels of Dopamine and Noradrenaline, but Not Serotonin, in the Frontal Cortex of Freely Moving Rats

TLDR
The interaction of buspirone with two SSRIs on extra‐cellular levels of 5‐HT, dopamine, and noradrenaline in single dialysate samples of freely moving rats supports the hypothesis that a reinforcement in dopaminergic transmission in the FCX contributes to the actions of SSR Is and other antidepressant drugs.

Potentiation of the Fluoxetine‐Induced Increase in Dialysate Levels of Serotonin (5‐HT) in the Frontal Cortex of Freely Moving Rats by Combined Blockade of 5‐HT1A and 5‐HT1B Receptors with WAY 100,635 and GR 127,935

TLDR
5‐HT1A/1B antagonism may represent a novel strategy for the improvement in the therapeutic profile of 5‐ HT reuptake inhibitor antidepressant agents and that 5‐HT may be primarily involved in such interactions.

In vivo biogenic amine efflux in medial prefiontal cortex with imipramine, fluoxetine, and fluvoxamine

TLDR
The data suggest that the SSRIs are not entirely selective for serotonin in vivo, as compared with the standard tricyclic antidepressant imipramine and the two selective serotonin reuptake inhibitors, fluoxetine and fluvoxamine.

Fluoxetine Increases Extracellular Dopamine in the Prefrontal Cortex by a Mechanism Not Dependent on Serotonin

TLDR
The results clearly show that the effects of fluoxetine and of high concentrations of citalopram on extracellular dopamine do not depend on their effects on serotonin.

Differential effects of phencyclidine and methamphetamine on dopamine metabolism in rat frontal cortex and striatum as revealed by in vivo dialysis

TLDR
The present results clearly demonstrate the differential effects of PCP on cortical and striatalDA transmission, suggesting that PCP may facilitate DA release in the medial frontal cortex by increasing impulse flow in the DA neurons projecting to the cortical area, whereas PCP‐induced elevation of extracellular DA in the striatum may be caused mainly by reuptake inhibition of DA liberated by basal activity of the striatal DA neurons.

Blockade of the Noradrenaline Carrier Increases Extracellular Dopamine Concentrations in the Prefrontal Cortex: Evidence that Dopamine Is Taken up In Vivo by Noradrenergic Terminals

TLDR
It is suggested that reuptake into NA terminals is an important mechanism by which DA is cleared from the extracellular space in a NA‐rich area such as the prefrontal cortex and may play a role in the therapeutic effects of these drugs.