5/28/2023 0 Comments Spinal tap still has the taggerMany synapses exhibit paired-pulse facilitation at longer interstimulus intervals (20–500 ms). Paired-pulse depression is commonly observed at all synapses at short (less than 20 ms) interstimulus intervals, and most probably results from inactivation of voltage-dependent sodium or calcium channels or from a transient depletion of the release-ready pool of vesicles docked at the presynaptic terminal. When two stimuli are delivered within a short interval, the response to the second stimulus can be either enhanced or depressed relative to the response to the first stimulus ( Katz and Miledi, 1968 Zucker and Regehr, 2002). This increase in presynaptic calcium in turn causes changes in the probability of neurotransmitter release by directly modifying the biochemical processes that underlie the exocytosis of synaptic vesicles. Most forms of short-term synaptic plasticity are triggered by short bursts of activity causing a transient accumulation of calcium in presynaptic nerve terminals. These are thought to play important roles in short-term adaptations to sensory inputs, transient changes in behavioral states, and short-lasting forms of memory. Numerous forms of short-term synaptic plasticity, lasting on the order of milliseconds to several minutes, have been observed at virtually every synapse examined in organisms ranging from simple invertebrates to mammals ( Zucker and Regehr, 2002). After briefly reviewing short-lasting forms of synaptic plasticity, we will emphasize current understanding of the cellular mechanisms and possible functions of the class of phenomena commonly termed long-term potentiation (LTP) and long-term depression (LTD). Here, we attempt to provide a broad overview of the mechanisms of the most prominent forms of plasticity observed at excitatory synapses in the mammalian brain. Furthermore, virtually all excitatory synapses in the mammalian brain simultaneously express a number of different forms of synaptic plasticity. Synaptic transmission can be either enhanced or depressed by activity, and these changes span temporal domains ranging from milliseconds to hours, days, and presumably even longer. Given the diversity of the functions ascribed to synaptic plasticity, it is not surprising that many forms and mechanisms of synaptic plasticity have been described. Thus, elucidating the detailed molecular mechanisms underlying synaptic plasticity in any number of different brain regions is critical for understanding the neural basis of many aspects of normal and pathological brain function. Synaptic plasticity is also thought to play key roles in the early development of neural circuitry and evidence is accumulating that impairments in synaptic plasticity mechanisms contribute to several prominent neuropsychiatric disorders. Synaptic plasticity specifically refers to the activity-dependent modification of the strength or efficacy of synaptic transmission at preexisting synapses, and for over a century has been proposed to play a central role in the capacity of the brain to incorporate transient experiences into persistent memory traces. One of the most important and fascinating properties of the mammalian brain is its plasticity the capacity of the neural activity generated by an experience to modify neural circuit function and thereby modify subsequent thoughts, feelings, and behavior.
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