5-HT1A receptors direct the orientation of plasticity in layer 5 pyramidal neurons of the mouse prefrontal cortex

Meunier, C; Amar, Muriel; Lanfumey, Laurence; Hamon, Michel; Fossier, Philippe

doi:10.1016/j.neuropharm.2013.03.003

Cited by 22 publications

(31 citation statements)

References 57 publications

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“…Layer 2–3 electrical stimulation typically produced a fast excitatory conductance followed by a long‐lasting inhibitory conductance. Integrals of excitatory and inhibitory conductances were expressed as a percentage of the integral of the total conductance to determine the E‐I balance (32, 34, 36). Quantification of these somatic conductances showed that the evoked composite signal at the soma was composed of 19.3 ± 1.1% of excitation and 80.7 ± 1.1% of inhibition in the PFC of C57BL/6 mice (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The access resistance was compensated offline in voltage-clamp mode and neurons exhibiting .10% of access resistance were rejected. Analysis of the synaptic response and decomposition of synaptic conductance changes were performed as extensively described in previous publications (32)(33)(34)(35)(36)(37). 5 Hz, each burst containing 4 pulses at 100 Hz, for a total duration of 2 min), whereas the L5PyN was under the current clamp condition.…”

Section: Slice Preparation and Electrophysiological Recordingsmentioning

confidence: 99%

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A multiscale analysis in CD38 ^−/− mice unveils major prefrontal cortex dysfunctions

et al. 2019

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Autism Spectrum Disorder (ASD) is characterized by early onset of behavioural and cognitive alterations. Low plasma levels of oxytocin have also been found in ASD patients and recently, a critical role for the enzyme CD38 in the regulation of oxytocin release was demonstrated. CD38 is important in regulating several Ca2+ dependent pathways, but beyond its role in regulating oxytocin secretion, it is not known whether a deficit in CD38 expression leads to functional modifications of the prefrontal cortex, a structure involved in social behaviour. Here, we report that CD38-/- male mice show an abnormal cortex development, an excitation-inhibition balance shifted towards a higher excitation, and impaired synaptic plasticity in the prefrontal cortex such as those observed in various mouse models of ASD. We also show that a lack of CD38 alters social behaviour and emotional responses. Finally, examining neuromodulators known to control behavioural flexibility, we found elevated monoamine levels in the prefrontal cortex of CD38-/- adult mice. Overall our study unveiled major changes in prefrontal cortex physiological mechanisms and provides new evidence that the CD38-/- mouse could be a relevant model to study pathophysiological brain mechanisms of mental disorders such as ASD.

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Section: Resultsmentioning

confidence: 99%

Section: Slice Preparation and Electrophysiological Recordingsmentioning

confidence: 99%

A multiscale analysis in CD38 ^−/− mice unveils major prefrontal cortex dysfunctions

et al. 2019

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“…Synaptic response analysis and decomposition of synaptic conductance changes used in these studies were similar to those extensively described in previous papers [ 17 , 36 – 39 ]. Single stimuli applied at low frequency (0.05 Hz) did not induce plasticity.…”

Section: Methodsmentioning

confidence: 99%

“…After a HFS protocol, responses displayed LTP, LTD or no plasticity. These effects were due to the activation of NMDARs and their blockade with D-L-AP5 prevent the induction of plasticity in L5PyNs [ 17 , 36 ]. In order to sort L5PyNs displaying LTP or LTD, we retained an enhancement or a depression of IntgT higher or lower than 20% of the control IntgT before the HFS protocol as already described elsewhere [ 40 , 41 ].…”

Section: Methodsmentioning

confidence: 99%

“…5-HT1ARs are generally known for their inhibitory effect on LTP at perforant pathway-dentate synapses in hippocampus in vitro [ 16 ]. In a previous study, we demonstrated that postsynaptic 5-HT1ARs activation, through a modulation of NMDARs, facilitate LTD in the PFC [ 17 ]. In the case of DA, the effects are mediated by the D1-class receptors (D1 and D5) and by the D2-class receptors (D2, D3, D4) [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Dopaminergic D1 Receptors on Plasticity Is Dependent of Serotoninergic 5-HT1A Receptors in L5-Pyramidal Neurons of the Prefrontal Cortex

et al. 2015

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Major depression and schizophrenia are associated with dysfunctions of serotoninergic and dopaminergic systems mainly in the prefrontal cortex (PFC). Both serotonin and dopamine are known to modulate synaptic plasticity. 5-HT1A receptors (5-HT1ARs) and dopaminergic type D1 receptors are highly represented on dendritic spines of layer 5 pyramidal neurons (L5PyNs) in PFC. How these receptors interact to tune plasticity is poorly understood. Here we show that D1-like receptors (D1Rs) activation requires functional 5HT1ARs to facilitate LTP induction at the expense of LTD. Using 129/Sv and 5-HT1AR-KO mice, we recorded post-synaptic currents evoked by electrical stimulation in layer 2/3 after activation or inhibition of D1Rs. High frequency stimulation resulted in the induction of LTP, LTD or no plasticity. The D1 agonist markedly enhanced the NMDA current in 129/Sv mice and the percentage of L5PyNs displaying LTP was enhanced whereas LTD was reduced. In 5-HT1AR-KO mice, the D1 agonist failed to increase the NMDA current and orientated the plasticity towards L5PyNs displaying LTD, thus revealing a prominent role of 5-HT1ARs in dopamine-induced modulation of plasticity. Our data suggest that in pathological situation where 5-HT1ARs expression varies, dopaminergic treatment used for its ability to increase LTP could turn to be less and less effective.

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Inhibition of Serotonin Reuptake in the Medial Prefrontal Cortex during Acquisition of a Condition Reflex Fear Reaction Promotes Formation of Generalized Fear

Saul’skaya

Marchuk

2020

Neurosci Behav Physi

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5-HT1A receptors direct the orientation of plasticity in layer 5 pyramidal neurons of the mouse prefrontal cortex

Cited by 22 publications

References 57 publications

A multiscale analysis in CD38 ^−/− mice unveils major prefrontal cortex dysfunctions

A multiscale analysis in CD38 ^−/− mice unveils major prefrontal cortex dysfunctions

Effect of Dopaminergic D1 Receptors on Plasticity Is Dependent of Serotoninergic 5-HT1A Receptors in L5-Pyramidal Neurons of the Prefrontal Cortex

Inhibition of Serotonin Reuptake in the Medial Prefrontal Cortex during Acquisition of a Condition Reflex Fear Reaction Promotes Formation of Generalized Fear

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5-HT1A receptors direct the orientation of plasticity in layer 5 pyramidal neurons of the mouse prefrontal cortex

Cited by 22 publications

References 57 publications

A multiscale analysis in CD38 −/− mice unveils major prefrontal cortex dysfunctions

A multiscale analysis in CD38 −/− mice unveils major prefrontal cortex dysfunctions

Effect of Dopaminergic D1 Receptors on Plasticity Is Dependent of Serotoninergic 5-HT1A Receptors in L5-Pyramidal Neurons of the Prefrontal Cortex

Inhibition of Serotonin Reuptake in the Medial Prefrontal Cortex during Acquisition of a Condition Reflex Fear Reaction Promotes Formation of Generalized Fear

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A multiscale analysis in CD38 ^−/− mice unveils major prefrontal cortex dysfunctions

A multiscale analysis in CD38 ^−/− mice unveils major prefrontal cortex dysfunctions