ABSTRACT
Neuroplasticity is often referred to as the ability of the nervous system to undergo adaptive functional and morphological modifications in response to internal and/or external environmental changes. Neuroplasticity can occur in all species and may be expressed in a variety of forms depending upon the systems studied. Synaptic plas ticity (i.e., changes in the strength or efficacy of synaptic transmission), one of many forms of neuroplasticity, has attracted a great deal of attention because of its poten tial role in the development of neural circuitry, learning, and memory, as well as a number of neuropathologies (Chen & Tonegawa, 1997; Klintsova & Greenough, 1999; Nicoll & Malenka, 1995). While several different forms of synaptic plasticity have been found throughout the mammalian central nervous system (CNS) during the past several decades (Chen & Tonegawa, 1997; Frey & Morris, 1998; Klintsova & Greenough, 1999; McBain & Maccaferri, 1997), the most extensively studied examples are the long-term changes in synaptic efficacy observed at the glutamatergic synapses of the CA1 region of the hippocampus (Malinow & Mainen 1996; Zhuo & Hawkins 1995). Within these synapses high-frequency stimulation has been shown to induce a long-term potentia tion (LTP) of synaptic transmission, while a prolonged low-frequency-stimulation (LFS) often causes a long-term depression (LTD). As both LTP and LTD are considered prime candidates for cellular mechanisms for learning and memory (Bliss & Collingridge 1993; Fujii et al. 1996; Lisman, 1997), understanding mechanisms mediating these forms of synaptic plasticity has been one of the most intensively studied topics in the field of neuroscience (Bliss & Collingridge, 1993; Malenka & Nicoll, 1999; McBain & Maccaferri, 1997).
