NESH Regulates Dendritic Spine Morphology and Synapse Formation

Bae, Jeomil; Sung, Bong Hwan; Cho, In Ha; Kim, Seon-Myung; Song, Woo Keun

doi:10.1371/journal.pone.0034677

Cited by 26 publications

(24 citation statements)

References 53 publications

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“…Dendritic spines are the primary site for excitatory synapses, and, as such, aberrant changes in spine morphology would be expected to lead to pathological changes through alterations in synaptic connections and their strength (Bae et al, 2012;Kuwajima et al, 2012;Murakoshi and Yasuda, 2012). Plasticity of spines is associated with changes in shape and size.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Restoration of Spines and their Synapses in L-DOPA-Induced Dyskinesia: Involvement of Corticostriatal but Not Thalamostriatal Synapses

Zhang

Meredith²,

Mendoza-Elias

et al. 2013

Journal of Neuroscience

109

149

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We examined the structural plasticity of excitatory synapses from corticostriatal and thalamostriatal pathways and their postsynaptic targets in adult Sprague-Dawley rats to understand how these striatal circuits change in L-DOPA-induced dyskinesias (LIDs). We present here detailed electron and light microscopic analyses that provide new insight into the nature of the structural and synaptic remodeling of medium spiny neurons in response to LIDs. Numerous studies have implicated enhanced glutamate signaling and persistent long-term potentiation as central to the behavioral sensitization phenomenon of LIDs. Moreover, experience-dependent alterations in behavior are thought to involve structural modifications, specifically alterations in patterns of synaptic connectivity. Thus, we hypothesized that in the striatum of rats with LIDs, one of two major glutamatergic pathways would form new or altered contacts, especially onto the spines of medium spiny neuron (MSNs). Our data provide compelling evidence for a dramatic rewiring of the striatum of dyskinetic rats and that this rewiring involves corticostriatal but not thalamostriatal contacts onto MSNs. There is a dramatic increase in corticostriatal contacts onto spines and dendrites that appear to be directly linked to dyskinetic behaviors, since they were not seen in the striatum of animals that did not develop dyskinesia. There is also an aberrant increase in spines receiving more than one excitatory contact(i.e., multisynaptic spines) in the dyskinetic animals compared with the 6-hydroxydopamine-treated and control rats. Such alterations could substantially impair the ability of striatal neurons to gate cortically driven signals and contribute to the loss of bidirectional synaptic plasticity.

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Section: Discussionmentioning

confidence: 99%

Aberrant Restoration of Spines and their Synapses in L-DOPA-Induced Dyskinesia: Involvement of Corticostriatal but Not Thalamostriatal Synapses

Zhang

Meredith²,

Mendoza-Elias

et al. 2013

Journal of Neuroscience

109

149

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“…Spine volume parameters were defined as those measures between 0.02 and 0.2 μm 3 (Merino-Serrais et al 2013). Spine head diameters were defined as those measures between 0.3 and 1.2 μm (Bae et al 2012). …”

Section: Methodsmentioning

confidence: 99%

HIV-1 Transgenic Female Rat: Synaptodendritic Alterations of Medium Spiny Neurons in the Nucleus Accumbens

Roscoe

Mactutus

Booze

2014

J Neuroimmune Pharmacol

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HIV-1 associated neurocognitive deficits are increasing in prevalence, although the neuronal basis for these deficits is unclear. HIV-1 Tg rats constitutively express 7 of 9 HIV-associated proteins, and may be useful for studying the neuropathological substrates of HIV-1 associated neurocognitive disorders (HAND). In this study, adult female HIV-1 Tg rats and F344 control rats had similar growth rates, estrous cyclicity and startle reflex inhibition to a visual prepulse stimulus. Medium spiny neurons (MSNs) in the nucleus accumbens (NAcc) were ballistically-labeled utilizing the indocarbocyanine dye DiI. The branching complexity of MSNs in the NAcc was significantly decreased in HIV-1 Tg rats, relative to controls; moreover, the shorter length and decreased volume of dendritic spines, but unchanged head diameter, in HIV-1 Tg rats suggested a reduction of longer spines and an increase in shorter, less projected spines, indicating a population shift to a more immature spine phenotype. Collectively, these results from HIV-1 Tg female rats indicated significant synaptodendritic alterations of MSNs in the NAcc occur as a consequence of chronic, low-level, exposure to HIV-1 associated proteins.

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“…These morphological alterations correlate with negatively altered both short-and long-term memory formation (155). The manipulation of NESH/Abi-3 expression has multiple effects: overexpression of NESH/Abi-3 in cultured neurons reduces the amount of mushroom-type spines and synapse density but increases the thin filopodia, while siRNA knockdown also reduces mushroom spine numbers but increases spine density (26). Whether NESH/Abi-3 activity is regulated by synaptic stimulation was not determined as yet.…”

Section: A Actin Binding and Cytoskeletal Proteinsmentioning

confidence: 99%

Dendritic Spines: The Locus of Structural and Functional Plasticity

Sala

Segal

2014

Physiological Reviews

404

376

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The introduction of high-resolution time lapse imaging and molecular biological tools has changed dramatically the rate of progress towards the understanding of the complex structure-function relations in synapses of central spiny neurons. Standing issues, including the sequence of molecular and structural processes leading to formation, morphological change, and longevity of dendritic spines, as well as the functions of dendritic spines in neurological/psychiatric diseases are being addressed in a growing number of recent studies. There are still unsettled issues with respect to spine formation and plasticity: Are spines formed first, followed by synapse formation, or are synapses formed first, followed by emergence of a spine? What are the immediate and long-lasting changes in spine properties following exposure to plasticity-producing stimulation? Is spine volume/shape indicative of its function? These and other issues are addressed in this review, which highlights the complexity of molecular pathways involved in regulation of spine structure and function, and which contributes to the understanding of central synaptic interactions in health and disease.

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NESH Regulates Dendritic Spine Morphology and Synapse Formation

Cited by 26 publications

References 53 publications

Aberrant Restoration of Spines and their Synapses in L-DOPA-Induced Dyskinesia: Involvement of Corticostriatal but Not Thalamostriatal Synapses

Aberrant Restoration of Spines and their Synapses in L-DOPA-Induced Dyskinesia: Involvement of Corticostriatal but Not Thalamostriatal Synapses

HIV-1 Transgenic Female Rat: Synaptodendritic Alterations of Medium Spiny Neurons in the Nucleus Accumbens

Dendritic Spines: The Locus of Structural and Functional Plasticity

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