Memory-Like Alterations in Aplysia Axons after Nerve Injury or Localized Depolarization
نویسندگان
چکیده
منابع مشابه
Memory-like alterations in Aplysia axons after nerve injury or localized depolarization.
Adaptive, long-term alterations of excitability have been reported in dendrites and presynaptic terminals but not along axons. Persistent enhancement of axonal excitability has been described in proximal nerve stumps at sites of nerve section in mammals, but this hyperexcitability is considered a pathological derangement important only as a cause of neuropathic pain. Identified neurons in Aplys...
متن کاملAxoplasm enriched in a protein mobilized by nerve injury induces memory-like alterations in Aplysia neurons.
Axon regeneration after injury and long-term alterations associated with learning both require protein synthesis in the neuronal cell body, but the signals that initiate these changes are largely unknown. Direct evidence that axonal injury activates molecular signals in the axon was obtained by injecting axoplasm from crushed or uncrushed nerves into somata of sensory neurons with uncrushed axo...
متن کاملAn NF-kappaB-like transcription factor in axoplasm is rapidly inactivated after nerve injury in Aplysia.
We found a protein in Aplysia neurons that has many characteristics of the transcription factor NF-kappaB. Thus, the protein recognized a radiolabeled probe containing the kappaB sequence from the human interferon-beta gene enhancer element (PRDII), and the binding was not affected by PRDIV, an ATF-2 enhancer sequence from the same gene. Binding was efficiently inhibited, however, by nonradioac...
متن کاملPeripheral regeneration and central sprouting of sensory neurone axons in Aplysia californica following nerve injury.
Morphological methods were used to examine injury-induced growth of peripheral and central axons of nociceptive mechanosensory neurones in the ventrocaudal (VC) clusters of the pleural ganglia of Aplysia californica. Pedal nerve crush transected all axons in the nerve while leaving the overlying sheath largely intact. Immunohistochemical staining was performed with an antibody to a sensory-neur...
متن کاملSerotonin induces memory-like, rapamycin-sensitive hyperexcitability in sensory axons of aplysia that contributes to injury responses.
The induction of long-term facilitation (LTF) of synapses of Aplysia sensory neurons (SNs) by serotonin (5-HT) has provided an important mechanistic model of memory, but little is known about other long-term effects of 5-HT on sensory properties. Here we show that crushing peripheral nerves results in long-term hyperexcitability (LTH) of the axons of these nociceptive SNs that requires 5-HT act...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Neuroscience
سال: 2004
ISSN: 0270-6474,1529-2401
DOI: 10.1523/jneurosci.2329-04.2004