scholarly journals Long vs short-term synaptic learning rules after optogenetic spike-timing-dependent plasticity

2019 ◽  
Author(s):  
Margarita Anisimova ◽  
Bas van Bommel ◽  
Marina Mikhaylova ◽  
J. Simon Wiegert ◽  
Thomas G. Oertner ◽  
...  

AbstractSpike-timing-dependent plasticity (STDP) is a candidate mechanism for information storage in the brain. However, it has been practically impossible to assess the long-term consequences of STDP because recordings from postsynaptic neurons last at most one hour. Here we introduce an optogenetic method to, with millisecond precision, independently control action potentials in two neuronal populations with light. We apply this method to study spike-timing-dependent plasticity (oSTDP) in the hippocampus and reproduce previous findings that depression or potentiation depend on the sequence of pre- and postsynaptic spiking. However, 3 days after induction, oSTDP results in potentiation regardless of the exact temporal sequence, frequency or number of pairings. Blocking activity between induction and readout prevented the synaptic potentiation, indicating that strengthened synapses have to be used to get strong. Our findings indicate that STDP potentiates synapses and that the change in synaptic strength persist to behaviorally relevant timescales.

2021 ◽  
Vol 15 ◽  
Author(s):  
Emma Louise Louth ◽  
Rasmus Langelund Jørgensen ◽  
Anders Rosendal Korshoej ◽  
Jens Christian Hedemann Sørensen ◽  
Marco Capogna

Synapses in the cerebral cortex constantly change and this dynamic property regulated by the action of neuromodulators such as dopamine (DA), is essential for reward learning and memory. DA modulates spike-timing-dependent plasticity (STDP), a cellular model of learning and memory, in juvenile rodent cortical neurons. However, it is unknown whether this neuromodulation also occurs at excitatory synapses of cortical neurons in mature adult mice or in humans. Cortical layer V pyramidal neurons were recorded with whole cell patch clamp electrophysiology and an extracellular stimulating electrode was used to induce STDP. DA was either bath-applied or optogenetically released in slices from mice. Classical STDP induction protocols triggered non-hebbian excitatory synaptic depression in the mouse or no plasticity at human cortical synapses. DA reverted long term synaptic depression to baseline in mouse via dopamine 2 type receptors or elicited long term synaptic potentiation in human cortical synapses. Furthermore, when DA was applied during an STDP protocol it depressed presynaptic inhibition in the mouse but not in the human cortex. Thus, DA modulates excitatory synaptic plasticity differently in human vs. mouse cortex. The data strengthens the importance of DA in gating cognition in humans, and may inform on therapeutic interventions to recover brain function from diseases.


2017 ◽  
Vol 88 ◽  
pp. 58-64 ◽  
Author(s):  
R.R. Borges ◽  
F.S. Borges ◽  
E.L. Lameu ◽  
A.M. Batista ◽  
K.C. Iarosz ◽  
...  

2006 ◽  
Vol 86 (3) ◽  
pp. 1033-1048 ◽  
Author(s):  
Yang Dan ◽  
Mu-Ming Poo

Information in the nervous system may be carried by both the rate and timing of neuronal spikes. Recent findings of spike timing-dependent plasticity (STDP) have fueled the interest in the potential roles of spike timing in processing and storage of information in neural circuits. Induction of long-term potentiation (LTP) and long-term depression (LTD) in a variety of in vitro and in vivo systems has been shown to depend on the temporal order of pre- and postsynaptic spiking. Spike timing-dependent modification of neuronal excitability and dendritic integration was also observed. Such STDP at the synaptic and cellular level is likely to play important roles in activity-induced functional changes in neuronal receptive fields and human perception.


2020 ◽  
Author(s):  
Emma Louise Louth ◽  
Rasmus Langelund Jørgensen ◽  
Anders Rosendal Korshøj ◽  
Jens Christian Hedemann Sørensen ◽  
Marco Capogna

AbstractSynapses in the cerebral cortex constantly change and this dynamic property regulated by the action of neuromodulators such as dopamine (DA), is essential for reward learning and memory. DA modulates spike-timing-dependent plasticity (STDP), a cellular model of learning and memory, in juvenile rodent cortical neurons. However, it is unknown whether this neuromodulation also occurs at excitatory synapses of cortical neurons in mature adult mice or in humans. Cortical layer V pyramidal neurons were recorded with whole cell patch clamp electrophysiology and an extracellular stimulating electrode was used to induce STDP. DA was either bath-applied or optogenetically released in slices from mice. Classical STDP induction protocols triggered non-Hebbian excitatory synaptic depression in the mouse or no plasticity at human cortical synapses. DA reverted long term synaptic depression to baseline in mouse or elicited long term synaptic potentiation in human cortical synapses. Furthermore, when DA was applied during a STDP protocol it depressed presynaptic inhibition in the mouse but not in the human cortex. Thus, DA modulates excitatory synaptic plasticity differently in human versus mouse cortex. The data strengthens the importance of DA in gating cognition in humans, and may inform on therapeutic interventions to recover brain function from diseases.


2019 ◽  
Vol 116 (12) ◽  
pp. 5737-5746 ◽  
Author(s):  
Karen Ka Lam Pang ◽  
Mahima Sharma ◽  
Kumar Krishna-K. ◽  
Thomas Behnisch ◽  
Sreedharan Sajikumar

In spike-timing-dependent plasticity (STDP), the direction and degree of synaptic modification are determined by the coherence of pre- and postsynaptic activities within a neuron. However, in the adult rat hippocampus, it remains unclear whether STDP-like mechanisms in a neuronal population induce synaptic potentiation of a long duration. Thus, we asked whether the magnitude and maintenance of synaptic plasticity in a population of CA1 neurons differ as a function of the temporal order and interval between pre- and postsynaptic activities. Modulation of the relative timing of Schaffer collateral fibers (presynaptic component) and CA1 axons (postsynaptic component) stimulations resulted in an asymmetric population STDP (pSTDP). The resulting potentiation in response to 20 pairings at 1 Hz was largest in magnitude and most persistent (4 h) when presynaptic activity coincided with or preceded postsynaptic activity. Interestingly, when postsynaptic activation preceded presynaptic stimulation by 20 ms, an immediate increase in field excitatory postsynaptic potentials was observed, but it eventually transformed into a synaptic depression. Furthermore, pSTDP engaged in selective forms of late-associative activity: It facilitated the maintenance of tetanization-induced early long-term potentiation (LTP) in neighboring synapses but not early long-term depression, reflecting possible mechanistic differences with classical tetanization-induced LTP. The data demonstrate that a pairing of pre- and postsynaptic activities in a neuronal population can greatly reduce the required number of synaptic plasticity-evoking events and induce a potentiation of a degree and duration similar to that with repeated tetanization. Thus, pSTDP determines synaptic efficacy in the hippocampal CA3–CA1 circuit and could bias the CA1 neuronal population toward potentiation in future events.


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