Carbonic anhydrase activity in the peripheral nervous system of rat: the enzyme as a marker for muscle afferents

Szabolcs, Matthias; Kopp, Maximilian; Schaden, G.

doi:10.1016/0006-8993(89)90895-0

Cited by 46 publications

(14 citation statements)

References 31 publications

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“…From these data it therefore seems likely that CA-negative neurones (which have long AHPs) should have slow maximum fibre following frequencies, while CA-positive neurones could have either slow or fast fibre following frequencies (see Waddell & Lawson, 1990). Our data are therefore consistent with the suggestion by (Szabolcs et al 1989) (Kostyuk, Veselovsky, Fedulova & Tsyndrenko, 1981;Fedulova, Kostyuk & Veselovsky, 1985;Nowycky, 1992). For instance, in frog motoneurones the shorter AHP duration in the CA-positive neurones may result from a voltagedependent K+ conductance while the longer AHP may result from a Ca2+-activated K+ conductance (Barrett & Barrett, 1976).…”

Section: Ca Activity In Electrophysiologically Identified Cellssupporting

confidence: 82%

“…This was expected in view of the large myelinated CA-positive sensory fibres previously described (Szabolcs et al 1989). The percentage of positive A fibre neurones (53 %) is similar to the percentage of RT97-positive neurones with CA activity (45%).…”

Section: Ca Activity In Electrophysiologically Identified Cellsmentioning

confidence: 99%

“…As a result of CA activity, the increased H+ may be exchanged for extracellular Na+ and the increased HC03-may be exchanged with extracellular C1-. The transient rise in intracellular Na+ could stimulate the Na+-K+-ATPase (Na+ pump; Sapirstein et al 1984) and this could be important in the restitution of the normal ion balance, particularly in neurones which have the capability of firing rapid and/or prolonged bursts of APs as suggested by Szabolcs et al (1989). As well as possible effects on intracellular Na+ and K+ levels, there is evidence that CA may be important in the control of intracellular Ca2+.…”

Section: Ca Activity In Electrophysiologically Identified Cellsmentioning

confidence: 99%

“…In the CNS, CA has been described both in the glia (Trachtenberg & Sapirstein, 1980) and in the neuronal cell bodies of the cerebrum, cerebellum and medulla oblongata of the cat brain (Ridderstrale & Hansson, 1985). CA is also found in the yefferent fibres to muscle spindles (Szabolcs, Kopp & Schaden, 1989). The significance of its occurrence in high enough concentrations for clear histochemical or immunocytochemical demonstration in a subpopulation of primary afferent neurones is not yet clear.…”

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confidence: 99%

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The electrophysiological properties of rat primary afferent neurones with carbonic anhydrase activity.

Prabhakar

Lawson

1995

The Journal of Physiology

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Section: Ca Activity In Electrophysiologically Identified Cellssupporting

confidence: 82%

Section: Ca Activity In Electrophysiologically Identified Cellsmentioning

confidence: 99%

Section: Ca Activity In Electrophysiologically Identified Cellsmentioning

confidence: 99%

mentioning

confidence: 99%

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The electrophysiological properties of rat primary afferent neurones with carbonic anhydrase activity.

Prabhakar

Lawson

1995

The Journal of Physiology

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“…Carbonic anhydrase seems to be a reliable marker for muscle afferents (Szabolcs, Kopp & Schaden, 1989 (Gerebtzoff & Maeda, 1968;Schoenen, Budo, Poncelet & Gerebtzoff, 1968) synthesized by small sensory ganglion neurones (McDougal, Yuan, Dargar & Johnson, 1983). Via axonal transport the enzyme reaches the substantia gelatinosa, where it can be localized in large sinusoid axon terminals (Coimbra, Magalhaes & Sondr6-Borges, 1970;Knyihar & Csillik, 1976 (Silverman & Kruger, 1988).…”

Section: Histochemistry Of Injured Primary Sensory Neuronesmentioning

confidence: 99%

Pathobiological reactions of C‐fibre primary sensory neurones to peripheral nerve injury

Jancsó

1992

Experimental Physiology

101

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Mammalian primary sensory neurones display profound anatomical and chemical changes in response to injury of their peripheral processes. Peripheral nerve damage results in transganglionic degeneration of central terminals of A‐fibre primary afferent neurones terminating in the deeper layers of the medullary or spinal dorsal horn. The depletion of neuropeptides and other neurone‐specific macromolecules from neurones in sensory ganglia and from the superficial dorsal horn, the known central projection area of C‐fibre primary afferents, is a salient phenomenon commencing after peripheral nerve lesions. A recently devised new experimental procedure, termed the capsaicin‐gap method, permitted evaluation of the transganglionic degenerative phenomena which develop in C‐fibre primary sensory neurones after a lesion is inflicted upon their peripheral branches. The experimental findings indicated that C‐fibre primary afferent terminals underwent transganglionic degeneration following a perineural treatment with capsaicin, and that this was associated with, and probably resulted from, ganglionic cell degeneration. Studies on the effects of peripheral nerve section yielded similar results. It has therefore been suggested that the observed depletion of specific macromolecules, including sensory peptides, specific glycoconjugates and sensory neurone specific acid phosphatase, may be accounted for, at least in part, by an irreversible loss of sensory ganglion neurones. In contrast, many injured neurones express peptides, including vasoactive intestinal polypeptide, peptide histidine‐isoleucine and galanin, which can be demonstrated in only a few neurones under normal conditions. These seem to be involved in dorsal horn regenerative and/or compensatory processes following peripheral nerve damage. There is suggestive evidence that the partial deafferentation caused by the transganglionic degeneration of C‐fibre primary afferents creates favourable circumstances for an anatomical rearrangement of neuronal connections within the spinal cord dorsal horn. These changes may provide a morphological substrate of some of the functional alterations demonstrated after peripheral nerve lesions.

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Comprehensive immunofluorescence and lectin binding analysis of vibrissal follicle sinus complex innervation in the mystacial pad of the rat

et al. 1997

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The innervation of the vibrissal follicle sinus complexes (FSCs) in the mystacial pad of the rat was examined by lectin binding histofluorescence with the B subunit of Griffonia simplicifolia (GSA) and by immunofluorescence with a wide variety of antibodies for neuronal related structural proteins, enzymes, and peptides. Only anti-protein gene product 9.5 labeled all sets of innervation. Several types of mechanoreceptors were distributed to specific different targets by medium to large caliber myelinated axons. All were positive for 200 kDa neurofilament subunit, peripherin, and carbonic anhydrase. Their endings expressed synaptophysin. Labeling for the 160 kDa neurofilament subunit, calbindin, and parvalbumin varied. Anti-Schwann cell protein S100 was completely co-extensive with the axons, terminal arbors, and endings of the mechanoreceptor afferents including Merkel innervation. At least 15 different sets of unmyelinated innervation were evident based upon distribution and labeling characteristics. They consisted of four basic types: 1) peptidergic; 2) GSA binding; 3) peptidergic and GSA binding; and 4) nonpeptidergic and GSA negative (peptide-/GSA-). Previous studies had not revealed that several major sets of unmyelinated innervation were peptide-/GSA-. The unmyelinated innervation had detectable peripherin but not 160 kDa or 200 kDa neurofilament subunits. GSA-positive axons uniquely lacked anti-S100 immunoreactivity. The dense circumferentially oriented unmyelinated innervation of the inner conical body contained major sets of peptide-/GSA- and GSA innervation as well as a smaller peptidergic GSA component. A small contingent of sympathetic and possibly parasympathetic innervation was affiliated with microvasculature in the FSCs. This study confirms and refutes some previous hypotheses about biochemical and morphological relationships between peripheral innervation and sensory ganglion cells.

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Carbonic anhydrase activity in the peripheral nervous system of rat: the enzyme as a marker for muscle afferents

Cited by 46 publications

References 31 publications

The electrophysiological properties of rat primary afferent neurones with carbonic anhydrase activity.

The electrophysiological properties of rat primary afferent neurones with carbonic anhydrase activity.

Pathobiological reactions of C‐fibre primary sensory neurones to peripheral nerve injury

Comprehensive immunofluorescence and lectin binding analysis of vibrissal follicle sinus complex innervation in the mystacial pad of the rat

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