Olfactory coding: tagging and tuning odor-activated synapses for memory

A recent study in the locust olfactory system shows how neuromodulators can alter the rules of synaptic plasticity to form associative memories through the use of 'tagged' synapses.     

Perforated synapses and plasticity

Against a background of existing models relating perforated synapses to synaptic plasticity, the numerical density and frequency of perforated synapses in rat neocortex have been assessed from 1 d to 22 mo of age using the disector procedure, and changes in their morphology were assessed using 3-D computer reconstructions. The data point toward perforated and nonperforated synapses being separate synaptic populations from early in development, and with perforated synapses playing a part in the maintenance of neuronal postsynaptic density surface area from mid-adulthood onwards. This suggests that they play a crucial role in synaptic plasticity, although its nature may be different from that postulated by most recent workers.     

Structural plasticity at crustacean neuromuscular synapses

Crustacean motor axons innervate muscle fibers via a multiplicity of synaptic terminals which release small but variable amounts of transmitter. Differences in release performance appear to be correlated with the size of synaptic contacts and presynaptic dense bars (active zones). These structural parameters proliferate via sprouting from existing synaptic terminals and relocate to ever more distal sites during development and growth of an identified axon. Moreover, alterations in number of synaptic contacts and active zones occur in adults following stimulation or decentralization, demonstrating structural plasticity of crustacean neuromuscular synapses.     

Fly photoreceptor synapses: their development, evolution, and plasticity

Recent studies are reviewed on the synapses of photoreceptor terminals in the first optic neuropile of the flies, Musca and Drosophila. Afferent synaptic contacts are of uniform dimensions; they have a postsynaptic tetrad with a membrane organization of P-face particles, resembling other inhibitory synapses. A distributed population of such contact sites forms progressively during synaptogenesis by the selective, sequential accretion of identified postsynaptic elements at the receptor terminal. The comparative anatomy of this synapse indicates that elements have also been added during its phylogeny from an ancestral dyad. All cells are homologs of those in other species of Diptera. The number of synaptic sites is regulated by both pre- and postsynaptic cells, in proportion to their cell surfaces; an independent size increase in the receptor terminals (procured in the Drosophila mutant gigas) produces an increase in their synaptic population. The number of sites declines with age, however, accompanied by an increase in size of those synaptic sites remaining; this occurs for both afferent and feedback photoreceptor synapses. Lastly, the number of sites changes with visual experience; the frequency of feedback synapses is larger following dark rearing during early adult life than following visual experience.     

Interactions between neural networks: a mechanism for tuning chaos and oscillations

We show that chaos and oscillations in a higher-order binary neural network can be tuned effectively using interactions between neural networks. Our results suggest that network interactions may be useful as a means of adjusting the level of dynamic activities in systems that employ chaos and oscillations for information processing, or as a means of suppressing oscillatory behaviors in systems that require stability. URL: http:// www.ntu.edu.sg/home/elpwang     

Synaptic plasticity at hippocampal mossy fibre synapses

The dentate gyrus provides the main input to the hippocampus. Information reaches the CA3 region through mossy fibre synapses made by dentate granule cell axons. Synaptic plasticity at the mossy fibre-pyramidal cell synapse is unusual for several reasons, including low basal release probability, pronounced frequency facilitation and a lack of N-methyl-D-aspartate receptor involvement in long-term potentiation. In the past few years, some of the mechanisms underlying the peculiar features of mossy fibre synapses have been elucidated. Here we describe recent work from several laboratories on the various forms of synaptic plasticity at hippocampal mossy fibre synapses. We conclude that these contacts have just begun to reveal their many secrets.     

GABAA receptor trafficking-mediated plasticity of inhibitory synapses

Proper developmental, neural cell-type-specific, and activity-dependent regulation of GABAergic transmission is essential for virtually all aspects of CNS function. The number of GABA(A) receptors in the postsynaptic membrane directly controls the efficacy of GABAergic synaptic transmission. Thus, regulated trafficking of GABA(A) receptors is essential for understanding brain function in both health and disease. Here we summarize recent progress in the understanding of mechanisms that allow dynamic adaptation of cell surface expression and postsynaptic accumulation and function of GABA(A) receptors. This includes activity-dependent and cell-type-specific changes in subunit gene expression, assembly of subunits into receptors, as well as exocytosis, endocytic recycling, diffusion dynamics, and degradation of GABA(A) receptors. In particular, we focus on the roles of receptor-interacting proteins, scaffold proteins, synaptic adhesion proteins, and enzymes that regulate the trafficking and function of receptors and associated proteins. In addition, we review neuropeptide signaling pathways that affect neural excitability through changes in GABA(A)R trafficking.     

Structural plasticity of synapses in Alzheimer's disease

Plasticity of the synaptic contact zone was previously observed following loss of synapses in the cerebral cortex of normal aging humans. The present study was undertaken to determine if there was quantitative evidence of synapse loss and synapse plasticity in the inferior temporal, superior parietal, parieto-occipital, and superior frontal cortical regions in Alzheimer's disease (AD), and how such changes related to the neurofibrillary tangles and amyloid plaques. The results showed that age at autopsy did not correlate with the numbers of synapses, plaques, or tangles. However, the numbers of synapses strongly reflected the pathology of AD; in all four brain regions, there were fewer synapses as the numbers of plaques and tangles increased. In the inferior temporal and superior parietal cortices, the loss of synapses was accompanied by an increase in the synaptic contact length. The results suggest that, in some cerebral cortical brain regions, synapses are capable of plasticity changes, even when the pathology of AD and loss of synapses are severe.     

Endocannabinoids mediate synaptic plasticity at mixed synapses

Endocannabinoids are generally known to suppress excitatory or inhibitory synaptic transmission. Now, in an elegant series of experiments, Cachope et al. reveal a novel signaling pathway whereby endocannabinoids indirectly potentiate mixed chemical and electrical synapses. Gap junction-mediated transmission can thus be potentiated via distinct frequency-dependent mechanisms.     

Homeostatic synaptic plasticity: from single synapses to neural circuits

Homeostatic synaptic plasticity remains an enigmatic form of synaptic plasticity. Increasing interest on the topic has fuelled a surge of recent studies that have identified key molecular players and the signaling pathways involved. However, the new findings also highlight our lack of knowledge concerning some of the basic properties of homeostatic synaptic plasticity. In this review we address how homeostatic mechanisms balance synaptic strengths between the presynaptic and the postsynaptic terminals and across synapses that share the same postsynaptic neuron.     

Beyond spike timing: the role of nonlinear plasticity and unreliable synapses

 Spike-timing-dependent plasticity (STDP) strengthens synapses that are activated immediately before a postsynaptic spike, and weakens those that are activated after a spike. To prevent an uncontrolled growth of the synaptic strengths, weakening must dominate strengthening for uncorrelated spike times. However, this weight-normalization property would preclude Hebbian potentiation when the pre- and postsynaptic neurons are strongly active without specific spike-time correlations. We show that nonlinear STDP as inherent in the data of Markram et al. [(1997) Science 275:213–215] can preserve the benefits of both weight normalization and Hebbian plasticity, and hence can account for learning based on spike-time correlations and on mean firing rates. As examples we consider the moving-threshold property of the Bienenstock–Cooper–Munro rule, the development of direction-selective simple cells by changing short-term synaptic depression, and the joint adaptation of axonal and dendritic delays. Without threshold nonlinearity at low frequencies, the development of direction selectivity does not stabilize in a natural stimulation environment. Without synaptic unreliability there is no causal development of axonal and dendritic delays. Received: 22 April 2002 / Accepted: 23 May 2002 Acknowledgements. This study was supported by the Swiss National Science Foundation (grant 3152-065234.01) and the Silva-Casa foundation. The author thanks Stefano Fusi, Henry Markram, and Misha Tsodyks for helpful discussions, Nissim Buchs and Martin Schneider for their simulations, and Jan Reutimann for proof reading. Correspondence to: e-mail: wsenn@cns.unibe.ch, Tel.: +41-31-6318721, Fax: 41-31-6314611     

Mechanisms of long-term plasticity of hippocampal GABAergic synapses

Long-term potentiation and depression of synaptic transmission have been considered as cellular mechanisms of memory in studies conducted in recent decades. These studies were predominantly focused on mechanisms underlying plasticity at excitatory synapses. Nevertheless, normal central nervous system functioning requires maintenance of a balance between inhibition and excitation, suggesting existence of similar modulation of glutamatergic and GABAergic synapses. Here we review the involvement of G-protein-coupled receptors in the generation of long-term changes in synaptic transmission of inhibitory synapses. We considered the role of endocannabinoid and glutamate systems, GABA_B and opioid receptors in the induction of long-term potentiation and long-term depression in inhibitory synapses. The preand postsynaptic effects of activation of these receptors are also discussed.     

mRNA at synapses,synaptic plasticity,and memory consolidation

Miller et al. (this issue of Neuron) report that deletion of the 3'UTR of alpha-CaMKII mRNA prevents dendritic delivery of the mRNA in transgenic mice and thus local synthesis of alpha-CaMKII protein in dendrites. 3'UTR mutant mice exhibit decreases in alpha-CaMKII protein in postsynaptic densities, and deficits in late phase LTP and in memory consolidation.     

Brain-derived neurotrophic factor in arterial baroreceptor pathways: implications for activity-dependent plasticity at baroafferent synapses

Functional characteristics of the arterial baroreceptor reflex change throughout ontogenesis, including perinatal adjustments of the reflex gain and adult resetting during hypertension. However, the cellular mechanisms that underlie these functional changes are not completely understood. Here, we provide evidence that brain-derived neurotrophic factor (BDNF), a neurotrophin with a well-established role in activity-dependent neuronal plasticity, is abundantly expressed in vivo by a large subset of developing and adult rat baroreceptor afferents. Immunoreactivity to BDNF is present in the cell bodies of baroafferent neurons in the nodose ganglion, their central projections in the solitary tract, and terminal-like structures in the lower brainstem nucleus tractus solitarius . Using ELISA in situ combined with electrical field stimulation, we show that native BDNF is released from cultured newborn nodose ganglion neurons in response to patterns that mimic the in vivo activity of baroreceptor afferents. In particular, high-frequency bursting patterns of baroreceptor firing, which are known to evoke plastic changes at baroreceptor synapses, are significantly more effective at releasing BDNF than tonic patterns of the same average frequency. Together, our study indicates that BDNF expressed by first-order baroreceptor neurons is a likely mediator of both developmental and post-developmental modifications at first-order synapses in arterial baroreceptor pathways.