Prefrontocortical serotonin depletion results in plastic changes of prefrontocortical pyramidal neurons, underlying a greater efficiency of short-term memory

Vega, M.I. Pérez; Feria‐Velasco, Alfredo; González-Burgos, Ignacio

doi:10.1016/s0361-9230(00)00344-0

Cited by 48 publications

(20 citation statements)

References 43 publications

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“…Recently, we found that selective 5,7-DHT induced prefrontal 5-HT depletion in PFC caused in cytoarchitectural alterations of the prefrontocortical pyramidal neurons and partially the greater efficiency observed in the shortterm memory behavioral performance [27].…”

Section: Discussionmentioning

confidence: 96%

“…In this sense, previous studies from our laboratory have shown a better behavioral performance in a task requiring the animals to evoke acquired short-term information, following generalized 5-HT depletion [14]. Yet, 5,7-dyhydroxytryptamine-induced prefrontal 5-HT depletion leaded to a time-related improve in short-term memory, concomitantly with an increase in the spine density and the proportion of thin spines in prefrontal third-layer pyramidal neurons [27], suggesting an over-excitability of these cells as revealed by previous multiunitary activity recording studies (in preparation). These morphological and electrophysiological mechanisms underlying the abnormally efficient short-term memory could be strongly related to possible plastic changes in the activity of 5-HT 2A receptors or in their affinity for their ligand, and also may be by mediation of the 5-HT 2A receptors.…”

Section: Introductionmentioning

confidence: 81%

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Prefrontal Serotonergic Denervation Induces Increase in the Density of 5-HT2A Receptors in Adult Rat Prefrontal Cortex

et al. 2008

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The 5-HTergic system and particularly 5-HT(2A) receptors have been involved in prefrontal cognitive functions, but the underlying mechanisms by which the serotonin (5-HT) system modulates these processes are still unclear. In this work, the effects of prefrontal 5-HTergic denervation on the density and expression levels of 5-HT(2A) receptors were evaluated by immunohistochemical and molecular biology studies in the prefrontal cortex (PFC). The [(3)H]-Ketanserin binding study revealed an increase in the B(max), along with no change in the binding affinity (K(D)) for 5-HT(2A) receptors. The increase in PFC of 5-HT(2A) receptor density in response to denervation was accompanied by increase in 5-HT(2A) receptor mRNA and protein levels. This increase in the number of 5-HT(2A) receptors may be interpreted as an adaptive plastic change, i.e., hypersensitivity; resulting from the selective pharmacological lesion of the raphe-proceeding 5-HTergic fibers to the PFC. Based on previous evidence, this could be strongly related to the abnormal expression of short-term memory.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 81%

Prefrontal Serotonergic Denervation Induces Increase in the Density of 5-HT2A Receptors in Adult Rat Prefrontal Cortex

et al. 2008

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“…Earlier studies have shown that coping up with stress increases the 5-HT metabolism in the PFC of male rats (Duchesne et al 2009). Lesioning the dorsal raphe nucleus results in atrophy of the layer III PFC neurons (Perez-Vega et al 2000) and stress blunts 5-HT responses of layer III PFC neurons (Liu and Aghajanian 2008). Thus, it appears that 5-HT impacts the structure and function of the PFC neurons and the effects of ICSS could be mediated in part due to restoration of 5-HT levels.…”

Section: Discussionmentioning

confidence: 99%

Reversal of stress-induced dendritic atrophy in the prefrontal cortex by intracranial self-stimulation

et al. 2011

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The mammalian prefrontal cortex (PFC) has been implicated in a variety of motivational and emotional processes underlying working memory, attention and decision making. The PFC receives dopaminergic projections from the ventral tegmental area (VTA) and contains high density of D1 and D2 receptors and these projections are important in higher integrative cortical functions. The neurons of the PFC have been shown to undergo atrophy in response to stress. In an earlier study, we demonstrated that the chronic stress-induced atrophy of hippocampal neurons and behavioral impairment in the T-maze task were reversed by the activation of dopaminergic pathway by intracranial self-stimulation (ICSS) of the VTA. The stress-induced decrease in hippocampal dopamine (DA) levels was also restored by ICSS. Whether the reversal of stress-induced behavioral deficits by ICSS involves changes in the morphology of PFC neurons is unknown and the current study addresses this issue. Male Wistar rats underwent 21 days of restraint stress followed by ICSS for 10 days. The dendritic morphology of the PFC neurons was studied in Golgi-impregnated sections. Stress produced atrophy of the layer II/III and V PFC pyramidal neurons and ICSS to naïve rats significantly increased the dendritic arborization of these neurons compared to control. Interestingly, ICSS of stressed rats resulted in the reversal of the dendritic atrophy. Further, these structural changes were associated with a restored tissue levels of DA, norepinephrine and serotonin in the PFC. These results indicate that the behavioral restoration in stressed rats could involve changes in the plasticity of the PFC neurons and these results further our understanding of the role of dopaminergic neurotransmitter system in the amelioration of stress-induced deficits.

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“…5-HT regulates the excitability of glutamatergic cortical neurons, and of their cholinergic afferences by means of presynaptic inhibitory contacts (Wilson and Molliver 1991). DRN-prefrontocortical serotonergic depletion, using 5,7-DHT, was observed to induce facilitation in a short-term memory task in rats, associated with cytoarchitectural alterations in cortical pyramidal cells, a result that the authors interpreted as the expression of an "undermodulated" excitatory cholinergic activity due to 5-HT depletion (Perez-Vega et al 2000). Thus, among possible mechanisms linking 5-HT to memory, the interaction with the cholinergic system constitutes a key factor.…”

Section: -Ht In Memory: Basic Neurobiological Datamentioning

confidence: 99%

Spatial Learning in the 5-HT1B Receptor Knockout Mouse: Selective Facilitation/Impairment Depending on the Cognitive Demand

Buhot

Wolff²,

Benhassine³

et al. 2003

Learn. Mem.

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Age-related memory decline is associated with a combined dysfunction of the cholinergic and serotonergic systems in the hippocampus and frontal cortex, in particular. The 5-HT1B receptor occupies strategic cellular and subcellular locations in these structures, where it plays a role in the modulation of ACh release. In an attempt to characterize the contribution of this receptor to memory functions, 5-HT1B receptor knockout (KO) mice were submitted to various behavioral paradigms carried out in the same experimental context (water maze), which were aimed at exposing mice to various levels of memory demand. 5-HT1BKO mice exhibited a facilitation in the acquisition of a hippocampal-dependent spatial reference memory task in the Morris water maze. This facilitation was selective of task difficulty, showing thus that the genetic inactivation of the 5-HT1B receptor is associated with facilitation when the complexity of the task is increased, and reveals a protective effect on age-related hippocampal-dependent memory decline. Young-adult and aged KO and wild-type (WT) mice were equally able to learn a delayed spatial matching-to-sample working memory task in a radial-arm water maze with short (0 or 5 min) delays. However, 5-HT1BKO mice, only, exhibited a selective memory impairment at intermediate and long (15, 30, and 60 min) delays. Treatment by scopolamine induced the same pattern of performance in wild type as did the mutation for short (5 min, no impairment) and long (60 min, impairment) delays. Taken together, these studies revealed a beneficial effect of the mutation on the acquisition of a spatial reference memory task, but a deleterious effect on a working memory task for long delays. This 5-HT1BKO mouse story highlights the problem of the potential existence of "global memory enhancers." Data from cognitive psychology, neuropsychology, and behavioral neuroscience no longer conceive memory as a unitary process (e.g., Cohen and Squire 1980;Cohen 1984;Graf and Schacter 1985;Kesner 1986;Tulving 1987). Based on neuropsychological studies in humans, different memory systems have been defined on the basis of (1) the cognitive operations that they enable and (2) the structures of the central nervous system that are implicated therein. In the declarative system, long-term memory ensures the consolidation of information for long-term retrieval or recognition, and short-term memory allows the maintenance of information during short periods of time to execute a particular action or sequential actions (Baddeley 1995). Studies in humans may not be directly applicable to rodents. However, there may be some homologies that experiments in rodents reveal. Hence, if the hippocampus is conceived as a key structure involved in long-term, especially spatial memory (O'Keefe and Nadel 1978), but also in working memory (Olton et al. 1979), the prefrontal cortex is also considered as a key structure to complete working memory tasks (Fuster 1989;Tulving 1991), especially those that are sensitive to interferences.In humans as well as...

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Prefrontocortical serotonin depletion results in plastic changes of prefrontocortical pyramidal neurons, underlying a greater efficiency of short-term memory

Cited by 48 publications

References 43 publications

Prefrontal Serotonergic Denervation Induces Increase in the Density of 5-HT2A Receptors in Adult Rat Prefrontal Cortex

Prefrontal Serotonergic Denervation Induces Increase in the Density of 5-HT2A Receptors in Adult Rat Prefrontal Cortex

Reversal of stress-induced dendritic atrophy in the prefrontal cortex by intracranial self-stimulation

Spatial Learning in the 5-HT1B Receptor Knockout Mouse: Selective Facilitation/Impairment Depending on the Cognitive Demand

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