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Synaptic transmission is the basis of neuronal communication and is thus the most important element in brain functions, ranging from sensory input to information processing. Changes in synaptic transmission can result in the formation or dissolution of memories, and can equally lead to neurological and psychiatric disorders. The proteins composing the synapse, and their respective functions, are getting increasingly known. One aspect that has become evident in the last years is that most synaptic functions are performed not by single proteins, but by highly organized multi-protein machineries, which interact dynamically to provide responses optimally suited to the needs of the neuronal network. To decipher synaptic and neuronal function, it is essential to understand the organisational, morphological and functional aspects of the molecular nanomachines that operate at the synapse. We discuss these aspects in 11 different chapters, focusing on the structure and function of the active zone, on the functional anatomy of the synaptic vesicle, and on some of the best known soluble protein complexes from the synapse, including those involved in endocytosis and vesicle recycling.
The cytoplasmic free Ca2+ concentration ([Ca2+]i) is a key determinant of neuronal information transfer and processing. It controls a plethora of fundamental processes, including transmitter release and the induction of synaptic plasticity. This enigmatic second messenger conveys its wide variety of actions by binding to a subgroup of Ca2+ binding proteins (CaBPs) known as “Ca2+ sensors”. Well known examples of Ca2+ sensors are Troponin-C in skeletal muscle, Synaptotagmin in presynaptic terminals, and Calmodulin (CaM) in all eukaryotic cells. Since the levels of [Ca2+]i directly influence the potency of Ca2+ sensors, the Ca2+ concentration is tightly controlled by several mechanisms incl...
Activity within neural circuits shapes the synaptic properties of component neurons in a manner that maintains stable excitatory drive, a process referred to as homeostatic plasticity. These potent and adaptive mechanisms have been demonstrated to modulate activity at the level of an individual neuron, synapse, circuit, or entire network, and dysregulation at some or all of these levels may contribute to neuropsychiatric disorders, intellectual disability, and epilepsy. Greater mechanistic understanding of homeostatic plasticity will provide key insights into the etiology of these disorders, which may result from network instability and synaptic dysfunction. Over the past 15 years, the molec...
No. 2, pt. 2 of November issue each year from v. 19 (1963)-47 (1970) and v. 55 (1972)- contain the Abstracts of papers presented at the Annual Meeting of the American Society for Cell Biology, 3d (1963)-10th (1970) and 12th (1972)-