Neuronal plasticity

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. 

Woolf CJ, Salter MW (2000) Neuronal plasticity increasing tire gain in pain. Science 288 1765-1768... 

Turrigiano, GG and Nelson, SB (2000) Hebb and homeostasis in neuronal plasticity. Curr. Opin. 

Manji, H. K., Quiroz, J.A., Sporn, J. et al. (2003). Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for difficult-to-treat depression. Biol. Psychiatry, 53(8), 707-42. 

Dumann R. S., Malberg J., Nakawa S., D Sa C. (2004). Neuronal plasticity and survival in mood disorders. Biol. Psychiatry. 48, 732-9. 

Mattson MP, Chan SL, Leissring MA, Shepel PN, Geiger JD. Calcium signaling in the ER Its role in neuronal plasticity and neurodegenerative disorders. Trends Neurosci 2000 23 222-229. 

The NMDA receptor is an ionotropic glutamate receptor involved in fast excitatory neurotransmission. It plays a key role in a variety of CNS functions, most notably long-term potentiation (LTP) and neuronal plasticity, and is regulated by several mechanisms. One such mechanism involves the amino acid glycine (1). 

The synthesis of 5-HT can increase markedly under conditions requiring more neurotransmitter. Plasticity is an important concept in neurobiology. In general, this refers to the ability of neuronal systems to conform to either short- or long-term demands placed upon their activity or function (see Plasticity in Ch. 53). One of the processes contributing to neuronal plasticity is the ability to increase the rate of neurotransmitter synthesis and release in response to increased neuronal activity. Serotonergic neurons have this capability the synthesis of 5-HT from tryptophan is increased in a frequency-dependent manner in response to electrical stimulation of serotonergic soma [7]. The increase in synthesis results from the enhanced conversion of tryptophan to 5-HTP and is dependent on extracellular calcium ion. It is likely that the increased 5-HT synthesis results in part from alterations in the kinetic properties of tryptophan hydroxylase, perhaps due to calcium-dependent phosphorylation of the enzyme by calmodulin-dependent protein kinase II or cAMP-dependent protein kinase (PKA see Ch. 23). 

In contrast to LTP, LTD is induced by low-frequency stimulation. This causes the selective activation of PP2B (calcineurin), which maintains inhibitor-1 in its dephos-phorylated state. Several studies, including those using inhibitor-1 knockout mice and transgenic mice expressing a constitutively active form of inhibitor-1, demonstrate that the control of PP1 activity by inhibitor-1 in the hippocampus affects neuronal plasticity and learning and memory. 

Schulman, H,. Protein phosphorylation in neuronal plasticity and gene expression. Curr. Opin. Neurobiol. 5 375-381,1995. 

Both PAF [57] and COX-2 are potent mediators of the injury/inflammatory response (Fig. 33-5). PAF and COX-2 are also interrelated in neuronal plasticity. The PAF transcriptional activation of COX-2 may provide clues about novel neuronal cell-death pathways. In fact, the delayed induction of COX-2 by kainic acid precedes selective neuronal apoptosis by this agonist in the hippocampus [42,58]. 

Matsumoto, A., Arai, Y., Urano, A. and Hyodo, S. Molecular basis of neuronal plasticity to gonadal steroids. Functional Neurol 10 59-76,1995. 

ADDICTION AND NEURONAL PLASTICITY SHARE COMMON CELLULAR MECHANISMS 923... 

Addiction may result from inappropriate neuronal plasticity 923... 

Addiction may result from inappropriate neuronal plasticity. As discussed in earlier sections of this chapter, drugs of abuse activate the same neuronal pathways as natural reinforcers. However, they do so in a strong and unregulated manner that is hypothesized to lead to abnormal engagement of learning and memory mechanisms, ultimately producing abnormal plasticity in neuronal circuits involved in motivation and decision-making. As a result, the addict becomes narrowly focused on compulsive, habitual behaviors associated with the addictive... 

Neuronal plasticity is an essential component of neuronal adaptability and there is increasing evidence that this is primarily a biochemical rather than a morphological process. The neuron is not a fixed entity in terms of the quantity of transmitter it releases, and transmitters which are co-localized in a nerve terminal may be differentially secreted under different conditions. This, together with the repeated firing of some neurons that appear to have "leaky" membranes, may underlie the rhythmicity of neuronal activity within the brain. 

Experimental evidence suggests that chronic antidepressant treatments increase the formation of transcription factors within the brain which increases neuronal plasticity and leads to recovery. 

Research Group Neuronal Plasticity/Mouse Behaviour, Max-Planck-Institute of Psychiatry,... 

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