Serotonergic control of developmental plasticity
- Mind Brain Institute and Department of Neurosciences, The Johns Hopkins University, 3400 North Charles Street, Baltimore, MD 21218
Synapses in the brain are more than just coupling devices between neurons. Their efficiency in relaying neural activity can change according to their use. This plastic characteristic of synapses is considered essential for learning and memory storage and for the refinement of connections during development. A model of choice for studying synaptic modifications is the visual cortex, which shortly after birth is in a state of enhanced plasticity. During this time the cortical circuitry can be altered with simple manipulations of visual experience. For example, deprivation of vision in one eye (monocular deprivation) shifts the response of cortical neurons toward the nondeprived eye (1). It was recognized early on that in addition to the activity patterns imposed by retinal inputs, visual cortical plasticity depends on the integrity of three diffusely projecting neurotransmitter systems, using noradrenaline (NE), acetylcholine (ACh), and serotonin (5HT), respectively. These neuromodulatory systems convey information on the behavioral state of the animal, and their disruption prevents ocular dominance shifts caused by monocular deprivation (2–5). Hence, these neuromodulators have been regarded as “enabling factors” that perform the important function of gating experience-induced plasticity under certain behavioral states (6). This idea may have to be revised and expanded in view of new results recently published in PNAS (7). This study provides evidence that activation of serotonergic receptors might control not only when plasticity occurs, but also where a given input will be strengthened or weakened.
Our understanding of the mechanism by which neuromodulators affect experience-induced plasticity derives primarily from studies conducted in vitro, in the brain slice preparation. There is now ample evidence that ACh, NE, and 5HT can affect the induction of two forms of activity-dependent synaptic modification: long-term potentiation (LTP) and long-term depression (LTD). LTP and LTD are the …
