FRAP: histochemistry of the primary nociceptive neuron

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Abstract

Primary nociceptive neurons of small rodents are genuinely labelled by an extralysosomal, fluoride-resistant acid phosphatase (FRAP) activity. FRAP is present in the perikarya (in dorsal root ganglia), in peripheral terminals (skin, cornea, mucous membranes, etc.) and in central terminals (in the spinal cord or brain stem) of primary nociceptive neurons. In the spinal cord, FRAP-positive central endings establish either DSA (dense sinusoid axon) or LDCV terminals (containing large dense core vesicles). DSA terminals are present in the substantia gelatinosa Rolandi and in the spinal trigeminal nucleus, while LDCV terminals characterize Lissauer's tract, faisceau de la corne postererieure, noyaux basilaire externe, the paratrigeminal nucleus and nucleus tractus solitarii. Circumstantial evidence suggest that FRAP in DSA and LDCV terminals is associated with the metabolism of somatostatin and/or substance P, respectively. Dorsal rhizotomy, resulting in Wallerian degeneration of DSA and LDCV terminals, is followed by a rapid disappearance of FRAP from the ipsilateral, ipsisegmental dorsal horn. On the other hand, transection of a peripheral nerve, resulting in transganglionic degenerative atrophy of impaired DSA and LDCV terminals, is followed by a slowly proceeding diminution of ipsilateral, ipsisegmental FRAP reaction, cluminating in a complete loss of enzyme activity 10-14 days after surgery. The enzyme drop-out in the Rolando substance, following transganglionic degenerative atrophy, enables identification of central somatotopic representation of peripheral nerves and body surfaces in the dorsal horn. Essentially a synaptic uncoupling between first and second-order nociceptive neurons, transganglionic atrophy can also be evoked by perineural application of very small amounts of microtubule inhibitors around peripheral nerves. Such an approach might be useful in therapeutic efforts aimed at alleviating intractable pain in human subjects. Once the transected peripheral nerve regenerates, synaptic coupling between first and second-order nociceptive neurons in the spinal cord or brain stem, which has been disorganized by transganglionic degenerative atrophy, is reestablished by regenerative proliferation, i.e. sprouting of central terminals followed by synaptoneogenesis.

Original languageEnglish
JournalProgress in Histochemistry and Cytochemistry
Volume14
Issue number1
Publication statusPublished - 1981

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Nociceptors
Acid Phosphatase
Fluorides
Neurons
Presynaptic Terminals
Peripheral Nerves
Atrophy
Spinal Cord
Brain Stem
Brain
Substantia Gelatinosa
Spinal Trigeminal Nucleus
Rhizotomy
Wallerian Degeneration
Intractable Pain
Solitary Nucleus
Secretory Vesicles
Spinal Ganglia
Enzyme activity
Enzymes

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry

Cite this

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title = "FRAP: histochemistry of the primary nociceptive neuron",
abstract = "Primary nociceptive neurons of small rodents are genuinely labelled by an extralysosomal, fluoride-resistant acid phosphatase (FRAP) activity. FRAP is present in the perikarya (in dorsal root ganglia), in peripheral terminals (skin, cornea, mucous membranes, etc.) and in central terminals (in the spinal cord or brain stem) of primary nociceptive neurons. In the spinal cord, FRAP-positive central endings establish either DSA (dense sinusoid axon) or LDCV terminals (containing large dense core vesicles). DSA terminals are present in the substantia gelatinosa Rolandi and in the spinal trigeminal nucleus, while LDCV terminals characterize Lissauer's tract, faisceau de la corne postererieure, noyaux basilaire externe, the paratrigeminal nucleus and nucleus tractus solitarii. Circumstantial evidence suggest that FRAP in DSA and LDCV terminals is associated with the metabolism of somatostatin and/or substance P, respectively. Dorsal rhizotomy, resulting in Wallerian degeneration of DSA and LDCV terminals, is followed by a rapid disappearance of FRAP from the ipsilateral, ipsisegmental dorsal horn. On the other hand, transection of a peripheral nerve, resulting in transganglionic degenerative atrophy of impaired DSA and LDCV terminals, is followed by a slowly proceeding diminution of ipsilateral, ipsisegmental FRAP reaction, cluminating in a complete loss of enzyme activity 10-14 days after surgery. The enzyme drop-out in the Rolando substance, following transganglionic degenerative atrophy, enables identification of central somatotopic representation of peripheral nerves and body surfaces in the dorsal horn. Essentially a synaptic uncoupling between first and second-order nociceptive neurons, transganglionic atrophy can also be evoked by perineural application of very small amounts of microtubule inhibitors around peripheral nerves. Such an approach might be useful in therapeutic efforts aimed at alleviating intractable pain in human subjects. Once the transected peripheral nerve regenerates, synaptic coupling between first and second-order nociceptive neurons in the spinal cord or brain stem, which has been disorganized by transganglionic degenerative atrophy, is reestablished by regenerative proliferation, i.e. sprouting of central terminals followed by synaptoneogenesis.",
author = "E. Knyih{\'a}r-Csillik and B. Csillik",
year = "1981",
language = "English",
volume = "14",
journal = "Progress in Histochemistry and Cytochemistry",
issn = "0079-6336",
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T2 - histochemistry of the primary nociceptive neuron

AU - Knyihár-Csillik, E.

AU - Csillik, B.

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N2 - Primary nociceptive neurons of small rodents are genuinely labelled by an extralysosomal, fluoride-resistant acid phosphatase (FRAP) activity. FRAP is present in the perikarya (in dorsal root ganglia), in peripheral terminals (skin, cornea, mucous membranes, etc.) and in central terminals (in the spinal cord or brain stem) of primary nociceptive neurons. In the spinal cord, FRAP-positive central endings establish either DSA (dense sinusoid axon) or LDCV terminals (containing large dense core vesicles). DSA terminals are present in the substantia gelatinosa Rolandi and in the spinal trigeminal nucleus, while LDCV terminals characterize Lissauer's tract, faisceau de la corne postererieure, noyaux basilaire externe, the paratrigeminal nucleus and nucleus tractus solitarii. Circumstantial evidence suggest that FRAP in DSA and LDCV terminals is associated with the metabolism of somatostatin and/or substance P, respectively. Dorsal rhizotomy, resulting in Wallerian degeneration of DSA and LDCV terminals, is followed by a rapid disappearance of FRAP from the ipsilateral, ipsisegmental dorsal horn. On the other hand, transection of a peripheral nerve, resulting in transganglionic degenerative atrophy of impaired DSA and LDCV terminals, is followed by a slowly proceeding diminution of ipsilateral, ipsisegmental FRAP reaction, cluminating in a complete loss of enzyme activity 10-14 days after surgery. The enzyme drop-out in the Rolando substance, following transganglionic degenerative atrophy, enables identification of central somatotopic representation of peripheral nerves and body surfaces in the dorsal horn. Essentially a synaptic uncoupling between first and second-order nociceptive neurons, transganglionic atrophy can also be evoked by perineural application of very small amounts of microtubule inhibitors around peripheral nerves. Such an approach might be useful in therapeutic efforts aimed at alleviating intractable pain in human subjects. Once the transected peripheral nerve regenerates, synaptic coupling between first and second-order nociceptive neurons in the spinal cord or brain stem, which has been disorganized by transganglionic degenerative atrophy, is reestablished by regenerative proliferation, i.e. sprouting of central terminals followed by synaptoneogenesis.

AB - Primary nociceptive neurons of small rodents are genuinely labelled by an extralysosomal, fluoride-resistant acid phosphatase (FRAP) activity. FRAP is present in the perikarya (in dorsal root ganglia), in peripheral terminals (skin, cornea, mucous membranes, etc.) and in central terminals (in the spinal cord or brain stem) of primary nociceptive neurons. In the spinal cord, FRAP-positive central endings establish either DSA (dense sinusoid axon) or LDCV terminals (containing large dense core vesicles). DSA terminals are present in the substantia gelatinosa Rolandi and in the spinal trigeminal nucleus, while LDCV terminals characterize Lissauer's tract, faisceau de la corne postererieure, noyaux basilaire externe, the paratrigeminal nucleus and nucleus tractus solitarii. Circumstantial evidence suggest that FRAP in DSA and LDCV terminals is associated with the metabolism of somatostatin and/or substance P, respectively. Dorsal rhizotomy, resulting in Wallerian degeneration of DSA and LDCV terminals, is followed by a rapid disappearance of FRAP from the ipsilateral, ipsisegmental dorsal horn. On the other hand, transection of a peripheral nerve, resulting in transganglionic degenerative atrophy of impaired DSA and LDCV terminals, is followed by a slowly proceeding diminution of ipsilateral, ipsisegmental FRAP reaction, cluminating in a complete loss of enzyme activity 10-14 days after surgery. The enzyme drop-out in the Rolando substance, following transganglionic degenerative atrophy, enables identification of central somatotopic representation of peripheral nerves and body surfaces in the dorsal horn. Essentially a synaptic uncoupling between first and second-order nociceptive neurons, transganglionic atrophy can also be evoked by perineural application of very small amounts of microtubule inhibitors around peripheral nerves. Such an approach might be useful in therapeutic efforts aimed at alleviating intractable pain in human subjects. Once the transected peripheral nerve regenerates, synaptic coupling between first and second-order nociceptive neurons in the spinal cord or brain stem, which has been disorganized by transganglionic degenerative atrophy, is reestablished by regenerative proliferation, i.e. sprouting of central terminals followed by synaptoneogenesis.

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