Quantitative analysis of age-related dendritic changes in medium spiny I (MSI) striatal neurons of C57BL/6N mice

McNeill, Thomas H.; Koek, Laurie L.; Brown, Sally A.; Rafols, José A.

doi:10.1016/0197-4580(90)90115-g

Cited by 24 publications

(11 citation statements)

References 44 publications

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“…Changes in neuron morphology of similar magnitude in other brain regions have been reported to affect brain function [53], [54]. Furthemore, the changes in neuron morphology that we observed are similar to reports in the literature examining the influence of age on neuron morphology [54], [55], [56], [57], [58], [59], [60]. For example, there is a 15% difference in dendritic length by sholl analysis between 2 to 18 months in rat frontal cortex [55].…”

Section: Discussionsupporting

confidence: 88%

Disease-Toxicant Interactions in Manganese Exposed Huntington Disease Mice: Early Changes in Striatal Neuron Morphology and Dopamine Metabolism

et al. 2012

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YAC128 Huntington's disease (HD) transgenic mice accumulate less manganese (Mn) in the striatum relative to wild-type (WT) littermates. We hypothesized that Mn and mutant Huntingtin (HTT) would exhibit gene-environment interactions at the level of neurochemistry and neuronal morphology. Twelve-week-old WT and YAC128 mice were exposed to MnCl2-4H2O (50 mg/kg) on days 0, 3 and 6. Striatal medium spiny neuron (MSN) morphology, as well as levels of dopamine (DA) and its metabolites (which are known to be sensitive to Mn-exposure), were analyzed at 13 weeks (7 days from initial exposure) and 16 weeks (28 days from initial exposure). No genotype-dependent differences in MSN morphology were apparent at 13 weeks. But at 16 weeks, a genotype effect was observed in YAC128 mice, manifested by an absence of the wild-type age-dependent increase in dendritic length and branching complexity. In addition, genotype-exposure interaction effects were observed for dendritic complexity measures as a function of distance from the soma, where only YAC128 mice were sensitive to Mn exposure. Furthermore, striatal DA levels were unaltered at 13 weeks by genotype or Mn exposure, but at 16 weeks, both Mn exposure and the HD genotype were associated with quantitatively similar reductions in DA and its metabolites. Interestingly, Mn exposure of YAC128 mice did not further decrease DA or its metabolites versus YAC128 vehicle exposed or Mn exposed WT mice. Taken together, these results demonstrate Mn-HD disease-toxicant interactions at the onset of striatal dendritic neuropathology in YAC128 mice. Our results identify the earliest pathological change in striatum of YAC128 mice as being between 13 to 16 weeks. Finally, we show that mutant HTT suppresses some Mn-dependent changes, such as decreased DA levels, while it exacerbates others, such as dendritic pathology.

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Section: Discussionsupporting

confidence: 88%

Disease-Toxicant Interactions in Manganese Exposed Huntington Disease Mice: Early Changes in Striatal Neuron Morphology and Dopamine Metabolism

et al. 2012

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“…2). Similarly to our studies in mice (Rafols et al, 1989;McNeill et al, 1990), the size of the dendritic arbor varied between individual MSI neurons, ranging from neurons with compact dendritic arbors and a total dendritic length of less than 1,500 m to neurons with very robust arbors and a total dendritic length more than 3,000 m. MSI neurons with dendritic arbors of various sizes were distributed randomly within the sample area and were not clustered in any particular part of the striatum. …”

Section: Resultsmentioning

confidence: 80%

“…The selection of the Golgi-Cox method was based on results from our previous studies that examined the dependability of the different Golgi methods [i.e., GolgiKopsch (Szentagothai, 1963), rapid Golgi (Valverde, 1970), and Golgi-Cox (Glaser and Van der Loos, 1981)] in both mice and rats under the same experimental paradigm. We found that in our hands the Golgi-Cox method was the most reliable method to ensure complete impregnation of striatal neurons (Cheng et al, 1997b;Rafols et al, 1989;McNeill et al, 1990). In addition, the Golgi-Cox method yields large numbers of striatal neurons with darkly impregnated cell bodies and dendrites against a relatively clear background, making cell selection for quantitative analysis relatively straightforward (Fig.…”

Section: Tissue Preparation For Golgi Impregnationmentioning

confidence: 95%

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Synapse replacement in the striatum of the adult rat following unilateral cortex ablation

McNeill

Brown

Hogg

et al. 2003

J of Comparative Neurology

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Defining the selective pattern of synapse replacement that occurs in different areas of the damaged brain is essential for predicting the limits of functional compensation that can be achieved after various types of brain injury. Here we describe the time course of dendritic reorganization, spine loss and recovery, and synapse replacement in the striatum following a unilateral cortex ablation. We found that the time course for the transient loss and recovery of dendritic spines on medium spiny I (MSI) neurons, the primary postsynaptic target for corticostriatal axons, paralleled the time course for the removal of degenerating axon terminals from the neuropil and the formation of new synapses on MSI neurons. Reinnervation of the deafferented striatum occurred chiefly by axon terminals that formed asymmetric synapses with dendritic spines of MSI neurons, and the mean density of asymmetric synapses recovered to 86% of the sham-operated rat value by 30 days postlesion. In addition, the synaptic circuitry of the reconstructed striatum was characterized by an increase in the number of multiple synaptic boutons (MSBs), i.e., presynaptic axon terminals that make contact with more than one dendritic spine. Whether the postsynaptic contacts of MSBs are formed with the dendritic spines of the same or a different parent dendrite in the striatum is unknown. Nevertheless, these data suggest that the formation of MSBs is an essential part of the compensatory response to the loss of input from the ipsilateral cortex following the aspiration lesion and may serve to modulate activity-dependent adaptive changes in the reconstructed striatum that can lead to functional recovery.

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“…Segment length is represented on the abscissa and spine density on the ordinate. McNeil1 et al, 1990), in hippocampal neurons of aged humans (Buell and Coleman, 1981;Flood et al, 1985Flood et al, , 1987, and in striatal cells in moderate grade Huntington's disease (Graveland et al, 1985;Ferrante et al, 1991). In each of these instances, however, the effects are transient and dendritic proliferation is followed by degeneration.…”

Section: Dutu Analysis: Critique and Interpretationsmentioning

confidence: 99%

Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens

1995

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Nucleus accumbens receives a dense dopaminergic innervation which is important in regulating motivated states of behavior such as goal- directed actions, stimulus-reward associations and reinforcement of addictive substances. The shell and core territories of this nucleus each receive functionally and morphologically distinct dopaminergic inputs and lesions of the ascending pathways totally deprive the core but not the shell of dopaminergic fibers. Medium spiny neurons are the principal targets of dopaminergic terminals. The present study explored whether the loss of dopamine inputs can affect these neurons and whether cells in the shell and core would be equally susceptible to such a loss. Intracellular injection in fixed slices and neuronal reconstruction were used to analyze the dendritic trees of 62 neurons in the shell and core of animals that received a unilateral, chronic 6- hydroxydopamine lesion of the medial forebrain bundle. In the dopamine- depleted core, dendrites are significantly shorter (16% decrease) than in the intact core and in both the dopamine-depleted core and lateral shell, dendrites are less spiny than in respective control regions. Dopamine loss in the medial shell is associated with significantly more tortuous dendrites that are lower in spine density. However, the number of spines is not reduced which may mean that the increase recorded for segment length, although insignificant in tests, could be responsible for the change in spine density. These data suggest that the loss of dopamine can affect accumbal neuronal morphology and, moreover, can affect neuronal structures differentially in the shell and core.

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Quantitative analysis of age-related dendritic changes in medium spiny I (MSI) striatal neurons of C57BL/6N mice

Cited by 24 publications

References 44 publications

Disease-Toxicant Interactions in Manganese Exposed Huntington Disease Mice: Early Changes in Striatal Neuron Morphology and Dopamine Metabolism

Disease-Toxicant Interactions in Manganese Exposed Huntington Disease Mice: Early Changes in Striatal Neuron Morphology and Dopamine Metabolism

Synapse replacement in the striatum of the adult rat following unilateral cortex ablation

Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens

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