Academic journal article Canadian Journal of Experimental Psychology

Neuromodulation, Development and Synaptic Plasticity

Academic journal article Canadian Journal of Experimental Psychology

Neuromodulation, Development and Synaptic Plasticity

Article excerpt

Abstract We discuss parallels in the mechanisms underlying use-dependent synaptic plasticity during development and long-term potentiation (LTP) and long-term depression (LTD) in neocortical synapses. Neuromodulators, such as norepinephrine, serotonin, and acetylcholine have also been implicated in regulating both developmental plasticity and LTP/LTD. There are many potential levels of interaction between neuromodulators and plasticity. Ion channels are substrates for modulation in many cell types. We discuss examples of modulation of voltage-gated Ca^sup 2+^ channels and Ca^sup 2+^-dependent K+ channels and the consequences for neocortical pyramidal cell firing behaviour. At the time when developmental plasticity is most evident in rat cortex, the substrate for modulation is changing as the densities and relative proportions of various ion channels types are altered during ontogeny. We discuss examples of changes in K+ and Ca^sup 2+^ channels and the consequence for modulation of neuronal activity.

Current models for the regulation of synaptic strength are derived from concepts first proposed in the work of Donald Hebb (c.f. Bear et al., 1987; Gruel et al., 1987). In particular, Hebb proposed that correlated activity between pre- and post-synaptic neurons increases the strength of the intervening synapse, while temporally disjunct activity leads to a weakening of synaptic strength (frequently referred to as Hebb's Postulate; Hebb, 1949). In this chapter, we will first summarize recent theories concerning (i) the mechanisms for developmental synaptic plasticity in neocortex and (ii) long-term potentiation (LTP) and long-term depression (LTD) in neocortex and hippocampus. We will then outline possible interactions between the neuromodulatory effects of transmitters and changes in synaptic strength in cortical regions. Finally, we will review developmental changes in the electrical properties of neocortical pyramidal neurons in the context of synaptic plasticity and neuromodulation.

In this chapter, plasticity is defined as changes in synaptic strength, including the formation of new connections, change in the strength of existing synapses, or elimination of synapses. Several forms of plasticity have been described in cortical regions of the mammalian brain, including: developmental changes in synaptic connectivity (e.g., ocular dominance shifts in cat visual cortex: Wiesel, 1982), responses to injury (e.g. response of rodent barrel cortex to injury to whiskers [Van der Loos & Woolsey, 1973] or peripheral nerves [Donoghue & Sanes, 1987), and changes due to learning and memory. LTP and LTD are thought to be our best cellular models of these latter phenomena (Collingridge & Singer, 1991; Malenka & Nicoll, 1993).

THEORIES OF SYNAPTIC PLASTICITY

Developmental plasticity. Singer and colleagues (Artola, Brocher, & Singer, 1990; Collingridge & Singer, 1991; Gruhel, Luhmann, & Singer, 1987) have suggested a Hebbian gating mechanism for developmental changes in synaptic strength in which presynaptic activity must be paired with attainment of a postsynaptic voltage threshold in order for changes in synaptic efficacy to occur. The proposed threshold would be a level of depolarization greater than that required for initiation of Na+ action potentials and would correspond to Ca^sup 2+^ influx due to either (i) the removal of the Mg^sup 2+^ blockade of current through N-methyl-D-aspartate (NMDA)-type excitatory amino acid receptors, or (ii) opening of voltage-gated Ca^sup 2+^ channels (Figure lA,B). The channels act as molecular detectors of coincidence between synaptic transmission and postsynaptic depolarization. Intracellular free Ca^sup 2+^ would then act as a second messenger inducing changes in the postsynaptic membrane and, thus, changes in synaptic efficacy. Bear and colleagues have proposed a similar model, with the additional feature that the modification threshold may vary, dependent upon the activation history of the neurons (Bear et al. …

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