Effects of imipramine on raphe nuclei and prefrontal cortex extracellular serotonin levels in the rat

1997 ◽  
Vol 134 (4) ◽  
pp. 401-405 ◽  
Author(s):  
S. Maione ◽  
E. Palazzo ◽  
M. Pallotta ◽  
J. Leyva ◽  
L. Berrino ◽  
...  
2000 ◽  
Vol 279 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Lionella Palego ◽  
Annalisa Giromella ◽  
Maria Rosa Mazzoni ◽  
Donatella Marazziti ◽  
Antonio Giuseppe Naccarato ◽  
...  

2020 ◽  
Vol 17 (3) ◽  
pp. 319-326
Author(s):  
Mehmet Bostanciklioğlu

Memory retrieval is mediated by discharges of acetylcholine, glutamate, gammaaminobutyric acid, norepinephrine, and serotonin/5-hydroxytryptamine circuits. These projections and memory interact through engram circuits, neurobiological traces of memory. Increased excitability in engram circuits of the medial prefrontal cortex and hippocampus results in remote and recent memory retrievals, respectively. However, due to degenerated neurotransmitter projections, the excitability state of engram circuits is decreased in the patient with dementia; and thus, acquired- memory cannot be retrieved by natural cues. Here, we suggest that artificial neuropharmacological stimulations of the acquired-memory with an excitation potential higher than a natural cue can excite engram circuits in the medial prefrontal cortex, which results in the retrieval of lost memories in dementia. The neuropharmacological foundations of engram cell-mediated memory retrieval strategy in severe dementia, in line with this has also been explained. We particularly highlighted the close interactions between periaqueductal gray, locus coeruleus, raphe nuclei, and medial prefrontal cortex and basolateral amygdala as treatment targets for memory loss. Furthermore, the engram circuits projecting raphe nuclei, locus coeruleus, and pontomesencephalic tegmentum complex could be significant targets of memory editing and memory formation in the absence of experience, and a well-defined study of the neural events underlying the interaction of brain stem and memory will be relevant for such developments. We anticipate our perspective to be a starting point for more sophisticated in vivo models for neuropharmacological modulations of memory retrieval in Alzheimer’s dementia.


2020 ◽  
Vol 32 (3) ◽  
pp. 159-165 ◽  
Author(s):  
Jakob Näslund ◽  
Erik Studer ◽  
Staffan Nilsson ◽  
Elias Eriksson

AbstractObjective:Although the assessment of expression of serotonin-related genes in experimental animals has become a common strategy to shed light on variations in brain serotonergic function, it remains largely unknown to what extent the manipulation of serotonin levels causes detectable changes in gene expression. We therefore chose to investigate how sub-acute depletion or elevation of brain serotonin influences the expression of a number of serotonin-related genes in six brain areas.Methods:Male Wistar rats were administered a serotonin synthesis inhibitor, para-chlorophenylalanine (p-CPA), or a serotonin reuptake inhibitor, paroxetine, for 3 days and then sacrificed. The expression of a number of serotonin-related genes in the raphe nuclei, hypothalamus, amygdala, striatum, hippocampus and prefrontal cortex was investigated using real-time quantitative PCR (rt-qPCR).Results:While most of the studied genes were uninfluenced by paroxetine treatment, we could observe a robust downregulation of tryptophan hydroxylase-2 in the brain region where the serotonergic cell bodies reside, that is, the raphe nuclei. p-CPA induced a significant increase in the expression of Htr1b and Htr2a in amygdala and of Htr2c in the striatum and a marked reduction in the expression of Htr6 in prefrontal cortex; it also enhanced the expression of the brain-derived neurotrophic factor (Bdnf) in raphe and hippocampus.Conclusion:With some notable exceptions, the expression of most of the studied genes is left unchanged by short-term modulation of extracellular levels of serotonin.


1993 ◽  
Vol 161 (2) ◽  
pp. 149-152 ◽  
Author(s):  
Masae Hosogai ◽  
Satoshi Matsuo ◽  
Shozo Nakao

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