Disease relevance of Axotomy

• Thus, decreases in muscarinic binding activity which occur in the superior cervical ganglion after axotomy or 6-hydroxydopamine treatment may be explained by a loss of nerve growth factor supplied to the ganglion [1].
• Flunarizine has been shown to protect neurons against death induced by serum deprivation, nerve growth factor deprivation, oxidative stress, axotomy and ischemia [2].
• Streptozotocin-induced diabetes mellitus causes changes in primary sensory neuronal cytoskeletal mRNA levels that mimic those caused by axotomy [3].
• In investigating the effect of spinal injury on cord-projection central neurons, we found that rat rubrospinal neurons retained glutamatergic afferents and, in general, ionotropic glutamate receptor expression following spinal axotomy [4].
• A significant increased survival of motoneurons was observed in animals pretreated with adenovirus encoding BDNF (34.5%, P < 0.05) ou GDNF (41.9%, P < 0.05) 1 week after axotomy [5].

High impact information on Axotomy

• Local application of GDNF to the transected facial nerve prevents the massive motor neuron cell death and atrophy that normally follows axotomy in the neonatal period [6].
• Ciliary neurotrophic factor prevents the degeneration of motor neurons after axotomy [7].
• Flunarizine protects neurons from death after axotomy or NGF deprivation [8].
• Cholinergic neuronal degeneration after axotomy has been proposed to be due to the loss of a retrogradely transported neurotrophic factor, possibly nerve growth factor (NGF) [9].
• Hopefully, similar functional consequences will soon be found for other peptides induced in these neurons after axotomy, such as vasoactive intestinal peptide and pituitary adenylate cyclase-activating peptide [10].

Chemical compound and disease context of Axotomy

• The persistence of limited substance P-like immunoreactive ganglion cells 10 days after surgery indicates that these cells have a relatively protracted response to axotomy [11].
• Glial cell death was reduced (mean number TUNEL positive cells 2 months after axotomy: no treatment 51/ganglion pair, NAC 16/ganglion pair), and mitochondrial architecture was preserved [12].
• No overlap of sensitivity to capsaicin and expression of galanin in rat dorsal root ganglion neurons after axotomy [13].
• The cells which are resistant to axotomy are destroyed by intraocular injection of kainic acid, whereas ganglion cells are not killed [14].
• The NF-kappaB inhibitor, sulfasalazine, was used to block the activation of NF-kappaB in the axotomized retina, and the number of ganglion cells was quantified using retrograde in the presence or absence of sulfasalazine after axotomy [15].

Biological context of Axotomy

• Downregulation of Na(v)1.9, which results from a lack of peripheral glial cell-derived neurotrophic factor following peripheral axotomy, might retune DRG neurons and contribute to their hyperexcitability after nerve injury [16].
• Apoptosis resulting from normal development or from axotomy can be inhibited markedly by exogenous neuregulin [17].
• Because these results raised the possibility that axonal loss may influence neurotrophin expression only in SCs that have differentiated toward a myelinating phenotype, we measured BDNF mRNA after axotomy in the cervical sympathetic trunk (CST), a predominantly unmyelinated autonomic nerve [18].
• Changes in the synthesis and axonal transport of neurofilament (NF) proteins and tubulin were examined after various selective axotomies of adult rat DRG cells [19].
• Removal of NT-3 4-5 weeks after beginning treatment resulted in a decline of conduction velocity and EPSP amplitude within 1 week to values characteristic of axotomy [20].

Anatomical context of Axotomy

• Motor neurons in CCS-/- mice showed increased rate of death after facial nerve axotomy, a response documented for SOD1-/- mice [21].
• Northern blot analysis revealed LIF expression in peripheral nerve that was increased in distal segments after axotomy [22].
• Using differential screening strategies, we identified a novel protein, termed ninjurin (for nerve injury-induced protein), that is up-regulated after axotomy in neurons and in Schwann cells surrounding the distal nerve segment [23].
• In vivo, IL-3 was infused into the lateral ventricles of rats after unilateral axotomy of the septohippocampal pathways [24].
• Thus, LIF plays a role in transmitter changes induced by axotomy but not by developmental interactions with sweat glands [25].

Associations of Axotomy with chemical compounds

• These results suggest that transient activation of PKC, PKA, and/or serine phosphatase inhibition by axotomy triggers persistent intracellular changes that may be related to polarity loss in these neurons [26].
• Taken together, these findings suggest that activation of c-Jun mediates the loss of dopamine neurons after axotomy injury [27].
• Axotomy induces the expression of vasopressin receptors in cranial and spinal motor nuclei in the adult rat [28].
• M-35 potentiated the facilitation of the flexor reflex by conditioning stimulation of cutaneous unmyelinated afferents in rats with intact nerves and the potentiating effect of M-35 on the conditioning-stimulation-induced reflex facilitation of the cutaneous unmyelinated afferents was strongly enhanced after axotomy [29].
• Administration of testosterone attenuates neuronal loss following axotomy in the brain-stem motor nuclei of female rats [30].

Gene context of Axotomy

• In vivo, CT-1 protected neonatal sciatic motoneurons against the effects of axotomy [31].
• BDNF and NT-4/5 prevent atrophy of rat rubrospinal neurons after cervical axotomy, stimulate GAP-43 and Talpha1-tubulin mRNA expression, and promote axonal regeneration [32].
• In newborn animals in which CNTF is not yet expressed, exogenous CNTF that is locally administered very effectively protects motoneurons from degeneration by axotomy [33].
• In a sciatic axotomy model of neuronal injury in the neonate, death of DRG neurons was also reduced by JNK3 deficiency [34].
• Administration of nerve growth factor (NGF) rescued the immunoreactivity of substance P, which is known to disappear after peripheral axotomy, but not influence that of both E-cadherin or alpha N-catenin [35].

Analytical, diagnostic and therapeutic context of Axotomy

• To determine the source of the anterogradely transported BDNF, we performed in situ hybridization in a variety of tissues before and after axotomy [36].
• Unilateral preganglionic denervation or postganglionic axotomy causes declines in alpha3, beta4, and alpha5 transcript levels, ranging from twofold to 3 [37].
• Electron microscopy analysis reveals that the ultrastructural alterations associated with axotomy and ionomycin-induced growth cone formation are practically identical [38].
• 2. Immunocytochemistry was used to study the distribution and density of tyrosine hydroxylase-immunoreactive (TH-IR) fibres within the lumbar dorsal root ganglia and lumbar spinal nerves 14 days following continuous intrathecal infusion of LIF (0.33 mg ml-1), or 14 days following unilateral peripheral nerve axotomy [39].
• However, mGluR6 was expressed in adult RGCs after axotomy. mGluR1 and -7 were also found more frequently in axotomized RGCs than in the adult control group [40].

References