Related Experiment Video
Updated: Mar 25, 2026

Presynaptically Silent Synapses Studied with Light Microscopy
Published on: January 4, 2010
Presynaptic serotonin 2A receptors modulate thalamocortical plasticity and associative learning
Alexander Barre1, Coralie Berthoux1, Dimitri De Bundel1
1Département de Neurosciences, Centre National de la Recherche Scientifique, UMR-5203, Institut de Génomique Fonctionnelle, F-34094 Montpellier, France; Département de Neurosciences, Institut National de la Santé et de la Recherche Médicale, U1191, F-34094 Montpellier, France; Université de Montpellier, F-34094 Montpellier, France.
Abstract:
Higher-level cognitive processes strongly depend on a complex interplay between mediodorsal thalamus nuclei and the prefrontal cortex (PFC). Alteration of thalamofrontal connectivity has been involved in cognitive deficits of schizophrenia. Prefrontal serotonin (5-HT)2A receptors play an essential role in cortical network activity, but the mechanism underlying their modulation of glutamatergic transmission and plasticity at thalamocortical synapses remains largely unexplored. Here, we show that 5-HT2A receptor activation enhances NMDA transmission and gates the induction of temporal-dependent plasticity mediated by NMDA receptors at thalamocortical synapses in acute PFC slices. Expressing 5-HT2A receptors in the mediodorsal thalamus (presynaptic site) of 5-HT2A receptor-deficient mice, but not in the PFC (postsynaptic site), using a viral gene-delivery approach, rescued the otherwise absent potentiation of NMDA transmission, induction of temporal plasticity, and deficit in associative memory. These results provide, to our knowledge, the first physiological evidence of a role of presynaptic 5-HT2A receptors located at thalamocortical synapses in the control of thalamofrontal connectivity and the associated cognitive functions.
More Related Videos
Related Concept Videos
Role of Neurotransmitters in Memory
Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
Long-term Depression
Calcium Ion Concentration Mechanism
If over...
Long-term Depression
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Synaptic Signaling
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...

