1 In this study, LTP was induced using a stimulating electrode to induce a brief high-frequency train of action potentials in the afferent pathway, thereby ensuring coincident pre- and post-synaptic depolarization. Recordings of the synaptic response evoked in the population of activated granule cells revealed a lasting enhancement of synaptic strength following tetanic stimulation. 18 In vitro preparations, however, have provided most of the insights relating to the cellular mechanisms of synaptic plasticity. This approach has revealed that repeated pairing of single presynaptic stimuli with post-synaptic depolarization is sufficient to induce LTP, bypassing the requirement for high frequency stimulation.
20 Furthermore, the concept of spike timing-dependent plasticity has been developed following the important observation in other in vitro preparations that the timing of pre- and post-synaptic action potentials determines the polarity of synaptic change. Repeated activation of a presynaptic spike followed by post-synaptic spike, within a brief time window of approximately 50 ms, leads to LTP, while the reverse order leads to LTD. These three characteristics of longevity, input-specificity and associativity are important, not just because they fulfill criteria predicted of an efficient memory mechanism, but because they provide clues as to the molecular mechanisms underlying LTP and LTD, mechanisms that could potentially be addressed to rectify synaptic malfunction.
The most fascinating and important property of the mammalian brain is its remarkable plasticity, which can be thought of as the ability of experience to modify neural circuitry and thereby to modify future thought, behavior, and feeling. Thinking simplistically, neural activity can modify the behavior of neural circuits by one of three mechanisms: by modifying the strength or efficacy of synaptic transmission at preexisting synapses, by eliciting the growth of new synaptic connections or the pruning away of existing ones, or by modulating the excitability properties of individual neurons. Because of its fundamental importance, there has been an enormous amount of work describing the many forms of synaptic plasticity and their underlying mechanisms.
Synaptic transmission can either be enhanced or depressed by activity, and these alterations span temporal domains ranging from milliseconds to enduring modifications that may persist for days or weeks and perhaps even longer.
More lasting changes are thought to play important roles in the construction of neural circuits during development and with long-term forms of memory in the mature nervous system. Given these diverse functions, it is not surprising that many forms and mechanisms of synaptic plasticity have been described.
There are two main types of neuroplasticity: Functional plasticity: the brain's ability to move functions from a damaged area of the brain to other undamaged areas. Structural plasticity: the brain's ability to actually change its physical structure as a result of learning.
1. Long-term potentiation (LTP) is a form of activity-dependent plasticity which results in a persistent enhancement of synaptic transmission.
2.The NMDA-type receptor is critical for some forms of LTP, in particular LTP at the CA3-CA1 synapse in the hippocampus. The postsynaptic spines of CA1 neurons have two types of glutamate receptors; NMDA-type glutamate receptors and the AMPA-type glutamate receptors
3. Long-term potentiation, or LTP, is a process by which synaptic connections between neurons become stronger with frequent activation. LTP is thought to be a way in which the brain changes in response to experience, and thus may be an mechanism underlying learning and memory.
Trending now
This is a popular solution!
Step by step
Solved in 2 steps with 2 images
