ABSTRACT
Glutamate plays central roles in neuronal functioning. Excitatory synaptic transmission in the mammalian CNS is almost exclusively glutamatergic. Long-term modulation of synaptic transmission via long-term potentiation (LTP) and long-term depression (LTD) may be the molecular basis of learning and memory (Bliss and Collingridge, 1993; Bear and Abraham, 1996), and alterations in such plasticity can be seen in transgenic models for Alzheimer’s disease (reviewed in Seabrook and Rosahl, 1999). Given the complexity of the potential glutamate receptor population in even a single neuron, it is an enormous challenge to delineate the functional responses seen following stimulation to a single receptor sub-type. Although great strides have been made in recent years towards the development of sub-type selective pharmacological agents (detailed in Chapter 4), for the majority of glutamate receptors, very few specific agonists or antagonists exist. The use of transgenic animals in which specific receptors or subunits are knocked out or mutated are a complementary tool for investigating the roles these proteins play in neuronal functioning. In this review, we shall describe transgenic mouse models for glutamate receptors, focusing principally on the role of glutamate receptor sub-types in synaptic plasticity and behaviour. The functional and behavioural responses of these mice have been summarised in Tables 15.1 and 15.2. Work describing the generation of the mice and the major findings are summarised in Figures 15.1 and 15.2.
