ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
Long-term depression (LTD) is an activity-dependent form of synaptic plasticity, the counterpart to LONG-TERM POTENTIATION (LTP). LTD can be HOMOSYNAPTIC (in which the activated synapses themselves are depressed) or HETEROSYNAPTIC (in which depression in one set of synapses is induced by activity in a neighbouring set). There are persuasive theoretical reasons for postulating the existence of a mechanism for reversing LTP, in order to avoid the loss of plasticity which would occur if LTP were to become saturated. On the other hand, this argument does not demand the existence of LTD, since LTP itself decays naturally over a period of days. Be that as it may, while there were sporadic reports of both homosynaptic and heterosynaptic LTD in the hippocampal (see HIPPOCAMPUS) literature following the first description of LTP in 1973, it was not until the publication of a reliable protocol for the experimental induction of homosynaptic LTD by Dudek & Bear (1992) that the phenomenon became accessible to routine experimental investigation. The induction protocol for producing LTP in young animals requires a long train of low-frequency stimuli, typically 900 stimuli at 1 Hz; in the adult animal, a modification of this protocol consisting of repetitive pairs of pulses, is more effective. Like LTP, LTD is input-specific; whether it is also associative has not been established, although in most (but not all) studies, its induction has been found to be dependent on NMDA RECEPTORS. Induction of LTD is also blocked by protein phosphatase inhibitors.
Pathophysiology of Complex Regional Pain Syndrome
Gary W. Jay in Practical Guide to Chronic Pain Syndromes, 2016
Experimental evidence suggests that central sensitization is similar to long-term potentiation (LTP) that occurs in the CA1 region of the hippocampus that is induced by enhanced synaptic currents. Long-term depression (LTD) is the opposite in which synaptic currents are diminished (50). A perceptual correlate of LTP and LTD has been shown in patients (51). A sustained nociceptive barrage in PTNs activates voltage-gated calcium and nonspecific ion channels. This is correlated with the “wind-up” phenomenon in which nociceptive input causes repetitive firing of PTNs and enhances pain (48). Partial nerve or distal axonal injury is clearly present in CRPS type II, and Oaklander’s recent studies suggest that CRPS I may be secondary to small-fiber degeneration associated with minimal nerve injury to terminal twigs of C and A-delta fibers (52) in soft tissue. The mechanisms that cause damage to axonal pain afferents in soft tissue are not clear but (i) crossed after-discharge in which potassium from actively conducting fibers diffuses and depolarizes contiguous axons and (ii) abnormalities from the “inflammatory soup” (such as reactive oxygen species or products of Wallerian degeneration) have been suggested (53, 54). Another important physiological correlate of nerve injury is instability of the axon membrane that causes potential oscillations that initiate ectopic firing near the DRG (55, 56).
Memory
Mohamed Ahmed Abd El-Hay in Understanding Psychology for Medicine and Nursing, 2019
Long-term potentiation (LTP) is operationally defined as a long-lasting increase in synaptic efficacy following high-frequency stimulation of the afferent fibers (Shors & Matzel, 1997). Changes in synaptic efficacy are thought to play a key role in the formation of long-lasting memories. LTP has a number of properties that make it suitable as a physiological substrate of memory: (1) synapse specificity: it occurs only at potentiated synapses that are activated by the tetanic stimulation; (2) cooperativity: multiple inputs must be activated simultaneously to produce sufficient postsynaptic depolarization to induce LTP; and (3) it is associative: when a weak input that is normally insufficient to induce LTP is paired with a strong input, the weak input will become potentiated (Mayford, Siegelbaum, & Kandel, 2012). LTP occurs prominently in the hippocampus, a structure important for memory. Long-term depression (LTD) of synaptic transmission is the opposite of LTP, i.e., a decrease in the strength of synaptic connections. The encoding of long-term memories is suggested to involve modification of synaptic connections through LTP and LTD.
Behavior and electrophysiological effects on striatum-nigra circuit after high frequency stimulation. Relevance to Parkinson and epilepsy
Published in International Journal of Neuroscience, 2023
Igor Tchaikovsky, Marilia Marinho Lucena, Belmira-Lara da Silveira Andrade da Costa, Norberto Garcia-Cairasco, Pedro V. Carelli, Marcelo Cairrao
The longterm potentiation (LTP) and longterm depression (LTD) are plasticity events related to an increase or decrease of strengthening of synaptic connections, respectively [1]. In the striatum, it is possible to induce LTP or LTD, depending on the stimulation parameters [2, 3]. While LTD was reported to be the major form of corticostriatal plasticity, it has been shown that LTP and LTD can be induced by the high frequency stimulation (HFS) of corticostriatal fibers [4]. Notably, the substantia nigra is a key determinant of striatum excitability [3]. The medium-sized spiny projection neurons (95% of all striatum neurons [5]) of the neostriatum are a site at which dopamine inputs from the substantia nigra converge with excitatory inputs from the cerebral cortex [3, 6]. In vivo findings show that LTD may occur in the corticostriatal pathway after HFS, and this depression can be prevented or reversed by concomitant stimulation of the substantia nigra in controls, not on dopamine depleted rats [3]. This suggests that stimulation of the substantia nigra would increase the firing rate in dorsomedial striatum. But the effect on the firing rate of dorsomedial striatum after nigra excitation or inhibition has never been measured directly. This information is important for the understanding of Parkinson’s disease, a condition where functional relationship between striatum and substantia nigra is impaired.
An update on potential pharmacotherapies for cognitive impairment in bipolar disorder
Published in Expert Opinion on Pharmacotherapy, 2023
Danica E. Johnson, Roger S. McIntyre, Rodrigo B. Mansur, Joshua D. Rosenblat
Ketamine is a dissociative anesthetic emerging as a potential treatment for the affective symptoms of treatment-resistant MDD and BD [124]. Ketamine is a racemic mixture consisting of the R-enantiomer (R(-)-ketamine) and the S-enantiomer (S(+)-ketamine). The S-enantiomer of ketamine, esketamine, was recently approved for treatment-resistant depression and has demonstrated efficacy in bipolar depression [125]. There is also a significant amount of evidence supporting the racemic mixture for treatment-resistant unipolar and bipolar depression [125]. Furthermore, ketamine’s mechanism of action may make it a candidate for treating cognitive impairment in MDD and BD [126]. Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist [126]. These receptors play an essential role in the neuroplastic processes of long-term potentiation (LTP) and long-term depression (LTD), which are crucial for learning and memory [126].
Comparison of ELF-EMFs stimulation with current stimulation on the regulation of LTP of SC-CA1 synapses in young rat hippocampus
Published in International Journal of Radiation Biology, 2021
Yu Zheng, Wenjun Zhao, Xiaoxu Ma, Lei Dong, Lei Tian, Mei Zhou
Modern neuroscience research believes that synaptic plasticity is closely related to the learning and memory of higher animals. According to Hebb’s theory, synaptic plasticity is the basis of the mechanisms regulating learning and memory at the cellular level (Hebb 1949). Long-term potentiation (LTP) is one of the important manifestations of synaptic plasticity, and it is involved in the formation of brain learning and memory (Teyler and DiScenna 1987; Bliss and Collingridge 1993; Cooke and Bliss 2006), while stable long-term potentiation or long-term depression (LTD) can be induced on the Schaffer collateral branches in the hippocampal slices, representing the best model for studying the efficiency of synaptic transmission (Malenka and Bear 2004). Rahman et al. (2013) believed that the study of isolated brain slices may represent a bottom-up research method, and it has the advantage to precisely control the external stimulation, regulate neuron morphology and synaptic activity, and clarify the acute effects on pyramidal neuron cell bodies and axon ends. Therefore, isolated hippocampal slices have become a powerful tool to explore the effects of magnetic fields on the brain. However, LTP induction is clearly reduced with advancing age. Indeed, long-term potentiation was inducted by a stronger stimulation in the hippocampal CA1 region of aged rats (Pereda et al. 2019). The brain slices of SD rats at the age of 3 weeks show more evident CA1 region, they are more sensitive to external stimuli, and they show a better LTP induction effect.
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