Nerve Terminal Remodeling Visualized in Living Mice by Repeated Examination of the Same Neuron

Purves, Dale; Voyvodic, James T.; Magrassi, Lorenzo; Yawo, Hiromu

doi:10.1126/science.3685967

Cited by 120 publications

(39 citation statements)

References 19 publications

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“…The clear implication of this result is that in the adult brain maintenance of dendritic arborization patterns depends on the activity profile of local afferents. It has been known for some time that neurons in peripheral nervous system ganglia demonstrate a turnover of dendrites (53)(54)(55). The advent of multiphoton microscopy has allowed confirmation, both in vitro (56) and in vivo (57), that the dendritic protrusions (spines and filipodia) of immature central neurons can alter over tens of minutes in response to manipulations of afferent activation.…”

Section: Discussionmentioning

confidence: 99%

Activity-dependent maintenance and growth of dendrites in adult cortex

Tailby

Wright

Metha

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Whereas it is widely accepted that the adult cortex is capable of a remarkable degree of functional plasticity, demonstrations of accompanying structural changes have been limited. We examined the basal dendritic field morphology of dye-filled neurons in layers III and IV of the mature barrel cortex after vibrissal-deafferentation in adult rats. Eight weeks later, the tendency for these neurons to orient their dendritic arbors toward the center of their home barrel was found to be disrupted by the resultant reduced activity of thalamocortical innervation. Measures of spine density and total dendritic length were normal, indicating that the loss of dendritic bias was accompanied by growth of dendrites directed away from the barrel center. This finding suggests that in the mature cortex, the apparently static structural attributes of the normal adult cortex depend on maintenance of patterns of afferent activity; with the corollary that changes in these patterns can induce structural plasticity.barrel field ͉ plasticity ͉ pyramidal cell ͉ spines ͉ vibrissae

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Section: Discussionmentioning

confidence: 99%

Activity-dependent maintenance and growth of dendrites in adult cortex

Tailby

Wright

Metha

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…The postsynaptic ciliary cell was distinguished from the choroidal cell on the basis of its location and large size. After recordings, some ganglia were perfused for 3 min by a saline solution containing 10SMm 4-(4-dimethylaminostyryl)-N-methylpyridinium iodide (Molecular Probes Inc., Eugene, OR, USA) which selectively labelled presynaptic terminals of the mouse submandibular ganglion (Purves, Voyvodic, Magrassi & Yawo, 1987) as well as chick ciliary ganglion (H. Yawo, unpublished observation). The calyx-type nerve terminal was identified from each cell tested (n = 8).…”

Section: Epsc Recordingsmentioning

confidence: 99%

Omega‐conotoxin‐sensitive and ‐resistant transmitter release from the chick ciliary presynaptic terminal.

Yawo

Chuhma

1994

The Journal of Physiology

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7. Similarly, the EPSC was smaller in the 10 mm Ca2+-l mm K+ solution containing 5 /uM La3+ than in the 2 mm Ca2+-16 mM Mg2+ solution, whereas the A[Ca2+]pre was larger in the 10 mM Ca2+-1 mm K+ solution containing 5/M Li3+ than in the 2 mm Ca2'-16 mM Mg2+ solution. 8. It is concluded that the w-CgTX-sensitive Ca21 conductance of the presynaptic terminal is the principal source of Ca2" involved in transmitter release. Although the w0-CgTXresistant conductance which is inactivated at depolarized membrane potentials also participated in the transmitter release, the ability of releasing transmitters relative to A[Ca2+]pre was reduced after treating with w-CgTX. It is suggested that the W-CgTXsensitive Ca2+ channels may cluster near the release sites. Since the w-CgTX-sensitive channels are outnumbered, it should be rare for the w-CgTX-resistant Ca21 channels to be adjacent to each other.

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“…Such an approach has revealed fundamental insights into the plasticity of synapses in the peripheral nervous system and their sculpting over development. [14][15][16] Technical advances have recently made it feasible to image individual synapses over extended periods of time in the CNS. In particular, the advent of Green Flourescent Protein (GFP) and its spectral variants and the ability to generate transgenic mice or viral vectors to drive the expression of such proteins in specific cell types in the nervous system [17][18][19] are allowing for long-term imaging of individual synaptic structures at high resolution in living animals.…”

Section: Introductionmentioning

confidence: 99%

Two-photon imaging of synaptic plasticity and pathology in the living mouse brain

Grutzendler

Gan

2006

NeuroRX

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Summary: Two-photon microscopy (TPM) has become an increasingly important tool for imaging the structure and function of brain cells in living animals. TPM imaging studies of neuronal structures over intervals ranging from seconds to years have begun to provide important insights into the structural plasticity of synapses and the modulating effects of experience in the intact brain. TPM has also started to reveal how neuronal connections are altered in animal models of neurodegeneration, acute brain injury, and cerebrovascular disease.Here, we review some of these studies with special emphasis on the degree of structural dynamism of postsynaptic dendritic spines in the adult mouse brain as well as synaptic pathology in mouse models of Alzheimer's disease and cerebral ischemia. We also discuss technical considerations that are critical for the acquisition and interpretation of data from TPM in vivo.

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Nerve Terminal Remodeling Visualized in Living Mice by Repeated Examination of the Same Neuron

Cited by 120 publications

References 19 publications

Activity-dependent maintenance and growth of dendrites in adult cortex

Activity-dependent maintenance and growth of dendrites in adult cortex

Omega‐conotoxin‐sensitive and ‐resistant transmitter release from the chick ciliary presynaptic terminal.

Two-photon imaging of synaptic plasticity and pathology in the living mouse brain

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