Abstract
Inhibitory neurons play a fundamental role in the normal operation of neuronal networks. Diverse types of inhibitory neurons serve vital functions in cortical networks, such as balancing excitation and taming excessive activity, organizing neuronal activity in spatial and temporal patterns, and shaping response selectivity. Serving these, and a multitude of other functions effectively requires fine-tuning of inhibition, mediated by synaptic plasticity. Plasticity of inhibitory systems can be mediated by changes at inhibitory synapses and/or by changes at excitatory synapses at inhibitory neurons. In this review, we consider that latter locus: plasticity at excitatory synapses to inhibitory neurons. Despite the fact that plasticity of excitatory synaptic transmission to interneurons has been studied in much less detail than in pyramids and other excitatory cells, an abundance of forms and mechanisms of plasticity have been observed in interneurons. Specific requirements and rules for induction, while exhibiting a broad diversity, could correlate with distinct sources of excitatory inputs and distinct types of inhibitory neurons. One common requirement for the induction of plasticity is the rise of intracellular calcium, which could be mediated by a variety of ligand-gated, voltage-dependent, and intrinsic mechanisms. The majority of the investigated forms of plasticity can be classified as Hebbian-type associative plasticity. Hebbian-type learning rules mediate adaptive changes of synaptic transmission. However, these rules also introduce intrinsic positive feedback on synaptic weight changes, making plastic synapses and learning networks prone to runaway dynamics. Because real inhibitory neurons do not express runaway dynamics, additional plasticity mechanisms that counteract imbalances introduced by Hebbian-type rules must exist. We argue that weight-dependent heterosynaptic plasticity has a number of characteristics that make it an ideal candidate mechanism to achieve homeostatic regulation of synaptic weight changes at excitatory synapses to inhibitory neurons.
Highlights
We argue that such homeostatic regulation of synaptic weight changes can be achieved by heterosynaptic plasticity at excitatory synapses to inhibitory neurons
Blockade of NMDA receptor channels (NMDAR) prevented induction of both long-term potentiation (LTP) and long-term depression (LTD) (Laezza and Dingledine, 2004). These results indicate that, at P9-P12, the bulk of calcium influx occurs via NMDARs and, when combined with the influx via CP-AMPARs, could provide [Ca2+]i rise sufficient for triggering LTP
One important consequence of the diversity of rules and mechanisms of plasticity is that the same pattern of activity may lead to different outcomes and even opposite-sign changes; e.g., in CA3 str. lacumosum/moleculare interneurons, tetanization of mossy fibers paired with postsynaptic depolarization leads to LTP at synapses equipped with CI-AMPARs but to no changes or LTD at CP-AMPAR synapses (Galván et al, 2008)
Summary
One common requirement for the induction of plasticity is the rise of intracellular calcium, which could be mediated by a variety of ligand-gated, voltage-dependent, and intrinsic mechanisms. Hebbian-type learning rules mediate adaptive changes of synaptic transmission. These rules introduce intrinsic positive feedback on synaptic weight changes, making plastic synapses and learning networks prone to runaway dynamics. Because real inhibitory neurons do not express runaway dynamics, additional plasticity mechanisms that counteract imbalances introduced by Hebbian-type rules must exist. We argue that weight-dependent heterosynaptic plasticity has a number of characteristics that make it an ideal candidate mechanism to achieve homeostatic regulation of synaptic weight changes at excitatory synapses to inhibitory neurons
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