Featured
-
-
Article
| Open AccessInterneuron-specific plasticity at parvalbumin and somatostatin inhibitory synapses onto CA1 pyramidal neurons shapes hippocampal output
Inhibitory interneuron subtypes differentially control place cell representations in CA1. Here, the authors show that parvalbumin and somatostatin interneuron synapses onto CA1 pyramidal neurons exhibit distinct plasticity mechanisms and incorporating this insight into circuit-level modeling leads to stable place cell representations.
- Matt Udakis
- , Victor Pedrosa
- & Jack R. Mellor
-
Article
| Open AccessAstrocyte-mediated switch in spike timing-dependent plasticity during hippocampal development
Presynaptic spike timing-dependent long-term depression at hippocampal CA3-CA1 synapses is evident until the third postnatal week in mice. The authors show that maturation beyond four weeks is associated with a switch to long-term potentiation in which astrocytes play a central role.
- Rafael Falcón-Moya
- , Mikel Pérez-Rodríguez
- & Antonio Rodríguez-Moreno
-
Article
| Open AccessNeuroinspired unsupervised learning and pruning with subquantum CBRAM arrays
To realize the potential of resistive RAM crossbar arrays as platforms for neuromorphic computing, reduced network-level energy consumption must be achieved. Here, the authors use a hardware/software co-design approach to realize reduced energy consumption during network training for the network.
- Yuhan Shi
- , Leon Nguyen
- & Duygu Kuzum
-
Article
| Open AccessDopamine–endocannabinoid interactions mediate spike-timing-dependent potentiation in the striatum
Dopamine tightly regulates plasticity at corticostriatal synapses. Here, the authors report that endocannabinoid dependent LTP induced with few spikes in the striatum is impaired in a rodent model of Parkinson’s disease, requires dopamine through presynaptic D2 receptors located on corticostriatal inputs.
- Hao Xu
- , Sylvie Perez
- & Laurent Venance
-
Article
| Open AccessReinforcement determines the timing dependence of corticostriatal synaptic plasticity in vivo
Spike timing dependent plasticity (STDP) has been studied extensively in slices but whether such pairings can induce plasticity in vivo is not known. Here the authors report an experimental paradigm that achieves bidirectional corticostriatal STDP in vivo through modulation by behaviourally relevant reinforcement signals, mediated by dopamine and adenosine signaling.
- Simon D. Fisher
- , Paul B. Robertson
- & John N.J. Reynolds
-
Article
| Open AccessAstrocytes gate Hebbian synaptic plasticity in the striatum
Astrocytes regulate synaptic signalling via EAAT glutamate uptake, though whether they play a role in Hebbian plasticity is unknown. Here, the authors find targeting EAAT2 disrupts the emergence of spike timing-dependent plasticity, which highlights the role of astrocytes as gatekeepers for Hebbian plasticity.
- Silvana Valtcheva
- & Laurent Venance
-
Article
| Open AccessLayer-specific cholinergic control of human and mouse cortical synaptic plasticity
Nicotinic acetylcholine receptors (nAChRs) are differentially expressed across cortical layers, yet it is unclear whether they show layer-specific effects on synaptic plasticity in the prefrontal cortex. Here, the authors compare nAChRs across L6 and L2/3 in human and mouse cortex and find they mediate opposite effects on synaptic plasticity.
- Matthijs B. Verhoog
- , Joshua Obermayer
- & Huibert D. Mansvelder
-
Article
| Open AccessUpward synaptic scaling is dependent on neurotransmission rather than spiking
Synaptic upscaling is characterized by an increase in the strength of excitatory inputs to a neuron as a compensatory response to chronic reductions in spiking activity. Here, the authors demonstrate that reduced glutamatergic transmission, rather than reduced spiking activity, directly triggers upscaling.
- Ming-fai Fong
- , Jonathan P. Newman
- & Peter Wenner
-
Article |
Formation and maintenance of neuronal assemblies through synaptic plasticity
Connectivity patterns between neurons in the brain store recent sensory experiences, but how these patterns form is unclear. Here, the authors provide a model describing the process through which synaptic plasticity combined with homeostatic mechanisms allow stable neuronal assemblies to form.
- Ashok Litwin-Kumar
- & Brent Doiron