Changes in the dendritic geometry of mouse superior cervical ganglion cells following postganglionic axotomy

Yawo, Hiromu

doi:10.1523/jneurosci.07-11-03703.1987

Cited by 96 publications

(73 citation statements)

References 43 publications

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“…Furthermore, the number of presynaptic axons innervating each sympathetic neuron is proportional to the number of primary dendrites [39]. It was reported that axotomy of sympathetic neurons causes significant dendritic atrophy [57].…”

Section: Discussionmentioning

confidence: 99%

Differences in Morphology and Neuropeptide Immunoreactivity of Superior Cervical Ganglion Neurons that Innervate the Major Salivary Glands in Rats.

Miyauchi

Asamoto

Nojyo

et al. 2001

Acta Histochem. Cytochem

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A neuronal tracer, WGA-HRP, was injected into the rat parotid gland (PG), submandibular gland (SMG), and sublingual gland (SLG) to label the superior cervical ganglion (SCG) neurons, and the number, size of soma, dendritic arborization and immunoreactivities (IR) of vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY) were investigated. The number and size of neurons projecting into SMG were greater than those of neurons projecting into the PG or SLG. The PG and SLG projecting neurons did not show significant differences in their number and size of soma, even the weight of the SLG was much smaller than the other two glands. The total length of dendrites of the SMG projecting neurons was greater than those of the PG or SLG projecting neurons. PG and SLG projecting neurons showed no significant difference in the total length of their dendrites. PG and SLG projecting neurons with NPY-IR were larger in number than SMG projecting neurons. SLG projecting neurons with VIP-IR were greater in number than neurons projecting into the other two glands. Our results indicate the differences in morphology and neuropeptide immunoreactivities among the SCG neurons which may be due to the differences in the neuronal functions and the participation of neurotrophic factors.

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Section: Discussionmentioning

confidence: 99%

Differences in Morphology and Neuropeptide Immunoreactivity of Superior Cervical Ganglion Neurons that Innervate the Major Salivary Glands in Rats.

Miyauchi

Asamoto

Nojyo

et al. 2001

Acta Histochem. Cytochem

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“…In mammalian neurons in vivo, dendrite simplification has been documented after axon injury (18)(19)(20). We monitored dendrite shape in ddaC neurons after distal axotomy and found that fine dendrite branches were trimmed back after distal axon severing (Fig.…”

Section: Increased Microtubule Dynamics and Dendrite Stabilization Afmentioning

confidence: 94%

Axon injury and stress trigger a microtubule-based neuroprotective pathway

Chen

Stone

Tao

et al. 2012

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

102

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Axon injury elicits profound cellular changes, including axon regeneration. However, the full range of neuronal injury responses remains to be elucidated. Surprisingly, after axons of Drosophila dendritic arborization neurons were severed, dendrites were more resistant to injury-induced degeneration. Concomitant with stabilization, microtubule dynamics in dendrites increased. Moreover, dendrite stabilization was suppressed when microtubule dynamics was dampened, which was achieved by lowering levels of the microtubule nucleation protein γ-tubulin. Increased microtubule dynamics and global neuronal stabilization were also activated by expression of expanded polyglutamine (poly-Q) proteins SCA1, SCA3, and huntingtin. In all cases, dynamics were increased through microtubule nucleation and depended on JNK signaling, indicating that acute axon injury and long-term neuronal stress activate a common cytoskeleton-based stabilization program. Reducing levels of γ-tubulin exacerbated long-term degeneration induced by SCA3 in branched sensory neurons and in a well established Drosophila eye model of poly-Q-induced neurodegeneration. Thus, increased microtubule dynamics can delay short-term injury-induced degeneration, and, in the case of poly-Q proteins, can counteract progressive longer-term degeneration. We conclude that axon injury or stress triggers a microtubulebased neuroprotective pathway that stabilizes neurons against degeneration.M any animals generate a single set of neurons that must function for the entire life of the individual. Each neuron typically has a single axon that transmits signals to other neurons or output cells such as muscle. As axons can extend long distances, they are at risk for injury, and, if the single axon is damaged, the cell can no longer function. Many neurons thus mount major responses to axon injury. The best characterized of these responses is axon regeneration, the process in which a neuron extends the stump of the existing axon or grows a new axon from a dendrite (1-3).In addition to the regenerative response, axon injury can cause other less well-understood changes. For example, in mammalian dorsal root ganglion cells, injury of the peripheral axon causes a transcriptional response that increases the capacity of the central axon to regenerate if it is subsequently injured (4, 5). In Drosophila sensory neurons, axon injury causes cytoskeletal changes in the entire dendrite arbor, specifically the number of growing microtubules is up-regulated (6). In this study, we investigated the functional significance of the cytoskeletal changes in the dendrite arbor. We present results that suggest the altered microtubule dynamics in dendrites acts to stabilize them, and thus axon injury seems to trigger a neuroprotective pathway that acts on the rest of the cell. However, this neuroprotective pathway is turned on only transiently after axon injury and subsides as axon regeneration initiates.Axon injury is a very acute neuronal stress. Neurons are also subject to a variety of long-term stress...

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“…These findings indicate that normal cells with more marked ADPs have simpler dendritic trees. Axotomy of sympathetic neurones produces a striking dendritic retraction (Yawo, 1987) and, in the rat, the Chloride current in sympathetic neurones Values are given as means + S.E.M. * P < 0'001, different from control (t test).…”

Section: Iadp Is a Chloride Currentmentioning

confidence: 96%

“…However, another possibility is that the channels are present in the non-axotomized sympathetic neurone but are located in the distal dendrites, where the effect of their activation on the membrane potential recorded at the cell body would be too small to detect. The dendritic retraction produced by axotomy (Yawo, 1987) would make the ADP visible from the cell body in rat sympathetic neurones, but not in guinea-pig ganglion cells that have longer dendrites (Purves & Lichtman, 1985). Considering the above, a membrane potential change produced by the activation of the chloride conductance would be too small to be recorded from the cell body of normal rat and guinea-pig ganglion cells, but could be seen in mouse sympathetic neurones which have very short dendrites (Purves & Lichtman, 1985).…”

mentioning

confidence: 96%

Calcium‐activated chloride current in normal mouse sympathetic ganglion cells.

Castro

Geijo-Barrientos

Gallego

1997

The Journal of Physiology

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1. In rat sympathetic ganglion cells, axotomy induces the appearance of a depolarizing afterpotential (ADP) produced by a calcium-activated chloride current. Here we report that this current is also present in normal sympathetic neurones from the mouse. 2. In an in vitro preparation of the superior cervical ganglion, an ADP was observed after spike firing in 50% of the cells studied with single-electrode current-and voltage-clamp techniques. 3. When the cells were voltage clamped at -50 mV in the presence of tetrodotoxin (ITX) and tetraethylammonium chloride (TEA), depolarizing jumps evoked inward calcium currents which were contaminated by outward chloride currents, followed by slowly decaying inward chloride tail currents. 4. The ADP and the inward tail currents disappeared when calcium was removed from the extracellular solution or when cadmium was added. 5. The reversal potential for the inward tail current was approximately -24 mV and was displaced in agreement with the Nernst equation for chloride when the extracellular NaCl was replaced by sucrose or sodium isethionate. The chloride channel blocker anthracene-9-carboxylic acid (9AC) inhibited both the ADP and the tail current. 6. Using intracellular injection of neurobiotin, we found that cells with shorter dendrites had larger ADPs. In axotomized ganglia practically all cells showed very pronounced ADPs. 7. We conclude that normal mouse sympathetic ganglion cells have a calcium-activated chloride current that generates an ADP. The channels responsible for this current are probably located in the dendrites.

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Changes in the dendritic geometry of mouse superior cervical ganglion cells following postganglionic axotomy

Cited by 96 publications

References 43 publications

Differences in Morphology and Neuropeptide Immunoreactivity of Superior Cervical Ganglion Neurons that Innervate the Major Salivary Glands in Rats.

Differences in Morphology and Neuropeptide Immunoreactivity of Superior Cervical Ganglion Neurons that Innervate the Major Salivary Glands in Rats.

Axon injury and stress trigger a microtubule-based neuroprotective pathway

Calcium‐activated chloride current in normal mouse sympathetic ganglion cells.

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