Abstract
The numbers and strengths of synapses in the brain change throughout development, and even into adulthood, as synaptic inputs are added, eliminated, and refined in response to ongoing neural activity. A number of experimental techniques can assess these changes, including single-cell electrophysiological recording which offers measurements of synaptic inputs with high temporal resolution. Coupled with electrical stimulation, photoactivatable opsins, and caged compounds, to facilitate fine spatiotemporal control over release of neurotransmitters, electrophysiological recordings allow for precise dissection of presynaptic and postsynaptic mechanisms of action. Here, we discuss the strengths and pitfalls of various techniques commonly used to analyze synapses, including miniature excitatory/inhibitory (E/I) postsynaptic currents, evoked release, and optogenetic stimulation. Together, these techniques can provide multiple lines of convergent evidence to generate meaningful insight into the emergence of circuit connectivity and maturation. A full understanding of potential caveats and alternative explanations for findings is essential to avoid data misinterpretation.
Highlights
A fundamental basis of information transfer in the nervous system is the release of neurotransmitter from the presynaptic terminal into the synaptic cleft to activate receptors on the postsynaptic neuron
While much work has focused on the recruitment of amino-3-hydroxy-5-methyl-4isoxazolepropionic acid receptors (AMPAR) to existing synapses, long-term potentiation (LTP) may reflect the addition of new AMPAR-containing synapses (Kerchner and Nicoll, 2008; Araki et al, 2015)
Assuming that AMPARs and N-methyl-D-aspartate receptors (NMDAR) are localized to all synapses, 1/CV2 should be equal for both receptor subtypes due to trial-by-trial variability of Q released from the presynaptic terminal
Summary
A fundamental basis of information transfer in the nervous system is the release of neurotransmitter from the presynaptic terminal into the synaptic cleft to activate receptors on the postsynaptic neuron. These receptors can activate downstream signaling processes and initiate ionic flux through receptor pores. This in turn can alter the transmembrane electrical potential, which propagates to the cell body and axon hillock to evoke an action potential (AP) in the postsynaptic neuron. Through dynamic recruitment of postsynaptic receptor complexes and modulation of presynaptic vesicular release, these changes contribute to the cellular basis of learning and memory in the brain
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