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Peripheral target contact regulates Ca2+channels in the cell bodies of bullfrog sympathetic ganglion B-neurons

Autonomic Neuroscience
Publication Date
DOI: 10.1016/s1566-0702(01)00259-4
  • Nerve Growth Factor
  • Neurotrophin
  • Sympathectomy
  • Nerve Injury
  • Neuropathic Pain
  • Axotomy
  • Chemistry


Abstract Tyrosine-hydroxylase immunohistochemistry demonstrated that a single injection of 120 mg/kg 6-hydroxydopamine (6-OHDA) reversibly disconnected bullfrog sympathetic ganglia from their peripheral targets. This was correlated with a decrease in sympathetic outflow to the eyes and a reversible decrease in pupil diameter. 6-OHDA did not damage the cell bodies of ganglionic neurons. Calcium channel current in ganglionic B-neurons, (measured at −10 mV; holding potential −60 mV; Ba 2+ as charge carrier; I Ba) was reduced. It reached a minimum of about 40% of control amplitude 7–14 days after 6-OHDA injection and recovered to 73% of control amplitude after 63 days. 6-OHDA induced loss and recovery of functional sympathetic innervation of peripheral target tissues, as determined by measurement of pupil diameter, occurred at a similar rate. Thus, pupil diameter attained minimum values 7–14 days after 6-OHDA treatment and recovered to 81% of control after 63 days. The properties of Ca 2+ channels in sympathetic neurons are, therefore, determined by continuity of contact with peripheral target. 6-OHDA also decreased the peak amplitude and duration of the afterhyperpolarization (a.h.p) that follows the action potential (a.p.). The rate of recovery of a.h.p duration was more rapid than the rate of recovery of peak a.h.p. amplitude. This may reflect known differences in properties of two types of Ca 2+-sensitive K + currents, I C and I AHP. I C, which is responsible for the peak amplitude of the a.h.p has a low affinity for Ca 2+, whereas I AHP, which determines a.h.p. duration, has higher Ca 2+ affinity.

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