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Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Whether LTP or LTD occur at a synapse appears in some cases to be governed by the relative timing of the presynaptic and postsynaptic APs, a phenomenon referred to as spike timing-dependent plasticity (STDP). Thus, if the postsynaptic AP occurs after presynaptic AP, the resulting depolarization will relieve the Mg2+ block of NDMARs, resulting in a large Ca2+ influx, leading to LTP. On the other hand, if the postsynaptic AP occurs before presynaptic activity, then the depolarization due to the postsynaptic AP will have subsided by the time presynaptic AP occurs, thereby reducing the Ca2+ influx and leading to LTD.
Systematic Class of System Dynamics-Based and Synapse-Based Architecture Types
Published in Harald Maurer, Cognitive Science, 2021
The model is also designed with three plasticity mechanisms ("Intrinsic Plasticity (IP)", "Synaptic Normalization (SN)" and "Spike-Timing-Dependent Plasticity (STI)Pf). and with an output layer (the "readout layer"), which is trained with a supervised learning procedure.459 The network is trained in two phases. In the first phase, the recurrent layer processes the input signals with permanent plasticity. In the second phase, the permanent plasticity is switched off while the input signals are processed again, but the neuron activations serve to train the output layer. However, while the output signal in SORN is trained with a simple linear regression (see chap. 9.3), in RM-SORN, the plastic connection weights from the recurrent layer to the output layer are adjusted by the plasticity mechanism of the "reward-modulated Spike-Timing-Dependent Plasticity (rm-STDP)". The model also allows this rm-STDP mechanism to be applied to the weight adaptation in the recurrent layer, consisting of NE excitatory and NI inhibitory neurons, e.g. in the ratio 5:1. The excitatory and inhibitory neurons are fully connected, in contrast to the number of connections of the excitatory neurons to each other, whose connectivity is sparse (5-10%).457 From the output layer, whose neurons are not interconnected, a feedback connection to the recurrent layer may be necessary for certain tasks, e.g. if a sequence, such as '1234', is to be generated. A random subset of excitatory neurons of the recurrent layer receives the input (sequence).
Noradrenergic gating of long-lasting synaptic potentiation in the hippocampus: from neurobiology to translational biomedicine
Published in Journal of Neurogenetics, 2018
Peter V. Nguyen, Jennifer N. Gelinas
Note that noradrenergic receptor activation is not required for the induction of LTP by strong stimulation protocols (Murchison et al., 2004; Swanson-Park et al., 1999). However, activation of β-ARs by a beta-receptor agonist potently facilitates the induction of LTP when applied in conjunction with weaker patterns of synaptic stimulation. A seminal study by Thomas, Moody, Makhinson, & O’Dell (1996) demonstrated that β-AR activation enables the induction of LTP by theta-pulse stimulation (TPS; 150–900 stimulation pulses delivered at 5–10 Hz), a pattern of synaptic stimulation that alone, in the absence of exogenous agonists, does not potentiate synaptic transmission. This finding has been observed in several subsequent studies (see, e.g. Brown et al., 2000; Havekes et al., 2012; Katsuki, Izumi, & Zorumski, 1997; Moody, Thomas, Makhinson, & O’Dell, 1998; Qian et al., 2012; Winder et al., 1999 ). The induction of LTP by spike-timing dependent plasticity protocols, where excitatory postsynaptic potentials elicited by presynaptic fiber stimulation are paired with postsynaptic action potentials evoked by current injection through an intracellular recording electrode, was also enhanced by β-AR activation (Lin, Min, Chiu, & Yang, 2003; Makino, Johnson, Yu, Takamiya, & Huganir, 2011). Additionally, β-AR activation by pairing ISO with one 100 Hz train of HFS enables the induction of protein synthesis-dependent LTP (referred to henceforth as ‘β-LTP’) (Gelinas & Nguyen, 2005; Gelinas et al. 2007; Ma, Tzavaras, Tsokas, Landau, & Blitzer, 2011; see below for further discussion of translation-dependent β-LTP).
Improvement of gait and balance by non-invasive brain stimulation: its use in rehabilitation
Published in Expert Review of Neurotherapeutics, 2019
Brain plasticity can occur at various levels of brain organization from the ultrastructural to synaptic level. LTP and LTD are broad terms that describe the direction of long-term changes in synaptic efficacy and may be induced and maintained by varying mechanisms in different synapses and circuits [32]. The temporal order of the pre – and postsynaptic spiking determines the direction and is called spike timing-dependent plasticity. A variety of receptors and neurotransmitters are involved with LTP and LTD including NMDA and metabotropic glutamate, dopaminergic, cholinergic and adenosine receptors. Prior synaptic and cellular activity can modify the direction or degree of synaptic plasticity and is called metaplasticity.
Impaired brain plasticity as a potential therapeutic target for treatment and prevention of dementia
Published in Expert Opinion on Therapeutic Targets, 2019
LTP, a prototype of synaptic plasticity [91–93], refers to use- and time-dependent strengthening of synapses [103–108]. Paired associative stimulation (PAS) is a TMS paradigm that assesses LTP-like activity in the human cortex. Simulating spike-timing-dependent plasticity [109], PAS induces LTP-like activity through the pairing of two stimulations contemporaneously occurring in the cortex and thus activating Hebbian synapses [11,110]. PAS was developed initially for the motor cortex [11] and then adapted to the DLPFC [13]. When applied to the DLPFC, PAS consists of a stimulation of the median nerve through electrical peripheral nerve stimulation (PNS) paired with stimulation of the contralateral DLPFC through TMS (PAS = PNS + TMS). These paired stimulations are repeated over 30 min and translated into increased cortical output. Increased cortical output is manifested as an increase in TMS-induced cortical-evoked activity, as measured using TMS-electroencephalography (TMS-EEG), over the DLPFC [13]. This increase in TMS-induced cortical-evoked activity is analogous to synaptic LTP and thereafter referred to as PAS-LTP. Since PAS depends on contemporaneous arrival of the paired stimulations, PNS of the median nerve precedes TMS of the DLPFC by 25 ms. This 25 ms interstimulus interval is necessary for the PNS-induced signal to travel to the somatosensory cortex and then to the DLPFC [111–116] and activate the DLPFC neurons contemporaneously with their activation by TMS [11]. In contrast, a longer interval of 100 ms does not result in contemporaneous arrival of PNS and TMS signals in the DLPFC and, in turn, PAS-LTP. Combining PAS with EEG (PAS-EEG) to measure PAS-LTP in the DLPFC has been used in healthy [13] and disease [97,117,118] states.