Memory, cellular

Lisman, J.E. and Fallon, J.R. (1999). What maintains memories Science, 283, 339-340 McGaugh, J.L. (2000). Memory - a century of consolidation. Science, 287, 248-251 Miyashita, Y. (2004). Cognitive memory cellular and network machineries and their top-down control. Science, 306, 435-440... 

CaM plays a key role in many cellular processes. In the CNS, it is involved in synaptic transmission and neuronal plasticity associated with short-term and longterm potentiation, and learning and memory processes. 

Alzheimer s disease (AD) 2. In the hippocampus of p-amylo id-treated rats, an animal model of AD, 2-AG levels are elevated and exert neuroprotection but also participate in memory retention loss 2. Inhibitors of cellular re-uptake or CB-, antagonists, possibly depending on the phase of the disorder... 

PKC is a family of enzymes whose members play central roles in transducing information from external stimuli to cellular responses. Members of this family of serine/ threonine kinases respond to signals that cause lipid hydrolysis. PKC isozymes phosphorylate an abundance of substrates, leading to both short-term cellular responses such as regulation of membrane transport and long-term responses such as memory and learning. 

PKC isozymes are involved in a wide array of diverse cellular functions [5]. Most isozymes (e.g., PKC (3) are involved in proliferative responses, and hyperactivation with phorbol esters most typically results in cell growth and differentiation. However, isozymes can have opposing functions. PKC 8 is well-characterized as an apoptotic kinase, whereas the closely related PKC e is antiapoptotic. PKC also plays a key role in learning and memory. 

Turner BM (2002) Cellular memory and the histone code. Cell 111 285-291... 

Goldman-Rakic P. S. (1995). Cellular basis of working memory. Neuron 14(3), 477-85. 

Adenylyl cyclase in learning and memory. The cAMP-signal transduction cascade has been demonstrated to play a role critical to the formation of long-term memory in both cellular models and in animals. The specific adenylyl cyclases involved are being identified by current research. In AC1 mutant mice there is a partial disruption of long-term potentiation (LTP), a cellular model of... 

Synaptic re-entry reinforcement (SRR) is a candidate cellular process for consolidating and storing memory traces 869... 

By definition, learning is the acquisition of new information, whereas memory is the retention of acquired information. Driven by knowledge obtained by scientists before them, various disciples of neuroscience over the course of the past 100 years have learned more about various components of learning and memory, whether at the molecular level of synapses or at the systems level of brain circuitry. The concept of memory of mind has existed since the time of Aristotle. It is only during the past 50 years or so that scientists have begun to unravel some of the anatomical and cellular bases underlying such a complex mental process. 

Most neuroscientists regard the ideas and observations of Santiago Ramon Y Cajal at the end of 19th century as the beginning of the cellular exploration of just how memory is retained in the brain. Upon his original observation of synaptic conjunction between neurons, he immediately entertained the idea that the modification of these conjunctions could form the anatomical basis responsible for the persistence of memory. 

The foundations for exploring the molecular and cellular mechanisms of learning and memory were laid in 1949, when Canadian psychologist Donald O. Hebb came up with a simple yet profound idea to explain how memory is represented and stored in the brain. According to Hebb s postulate [6] ... 

While the conditional gene knockout experiments are supportive of a role for the NMDA receptors in memory, they are less than fully conclusive in linking the synaptic coincidence-detection feature of the NMDA receptor to memory formation. Like all loss-of-function studies, CA1-specific gene-knockout experiments could, in theory, produce memory impairment via a mechanism independent of the coincidence-detection function of the NMDA receptor. For example, one may argue that the physical absence of the NMDA receptor channels may cause subtle structural reconfiguration at the synapse, thereby altering normal synaptic transmission. Therefore, the memory impairment in CA1-specific NR1 knockout mice does not allow a firm conclusion that the coincidence-detection function of NMDA receptors controls learning and memory processes at the cellular level. 

Wittenberg, G. M. and Tsien, I. Z. An emerging molecular and cellular framework for memory processing by the hippocampus. Trends Neurosci. 25 501-505,2002. 

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