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Biomedical subjects

J C Hackman

Publications and source records attributed to J C Hackman.

41 records · Page 3Linked to original sources
PubMed1980

Hyperpolarization of frog primary afferent fibres caused by activation of a sodium pump.

1. In the isolated frog spinal cord repetitive stimulation of a lumbar dorsal root produced a sustained negative potential recorded from an adjacent inactive dorsal root by sucrose gap techniques. This negative potential was followed by a positive potential, an indication that the dorsal root terminals were hyperpolarized. Increasing the duration of the tetanus applied to the active root increased the amplitude and duration of the after-hyperpolarization which could be up to 6 mV and 3 min respectively. 2. The hyperpolarization presumably reflected an increased rate of active sodium pumping. Since it was reversibly reduced by metabolic inhibitors (dinitrophenol, NaCN) and cooling (Q10, 2 . 6) it was clearly dependent upon intact metabolic activity. In addition, a variety of procedures used to inhibit sodium pumps (including application of ouabain, elimination of potassium from the superfusate, and partial substitution of lithium for sodium ions) significantly and reversibly decreased the potential. 3. The hyperpolarization was not dependent upon intact chemical synaptic transmission since it could survive prolonged immersion of the cord in Ringer solution containing manganese or magnesium ions. 4. It is suggested that the hyperpolarization of inactive fibres resulted from a decreased extracellular potassium concentration in the dorsal horn produced as a result of a pumping mechanism which extruded sodium and transported potassium inwards by dorsal root fibres directly activated by the tetanus.

Animals↗
PubMed1978

Some actions of catechol on synaptic transmission in the isolated spinal cord of the frog.

The isolated frog spinal cord was used to investigate the synaptic effects of the convulsant agent catechol. Addition of the compound to the superfusate consistently enhanced orthodromic reflex activity recorded from ventral roots and augmented primary afferent depolarization. Concomitantly catechol altered the polarization changes produced in ventral and dorsal roots by putative neurotransmitter amino acids when these compounds were applied in Mg2+-containing Ringer. Catechol reduced the hyperpolarizations induced in motoneurons by the neutral amino acids, GABA, beta-alanine, taurine and glycine, but did not affect the depolarizations produced by the dicarboxylic amino acids, L-glutamate and L-aspartate. In contrast, catechol increased the dorsal root depolarizations elicited by both neutral and dicarboxylic amino acids and also the depolarizations produced by elevated potassium concentrations. Catechol did not bring about significant changes in the passive electrical properties of motoneurons or dorsal root fibers. In addition, it did not alter either the high affinity uptake or the depolarization-evoked release of tritiated GABA, glycine, L-glutamate and L-aspartate. It appears that the postsynaptic actions of catechol explain its ability to enhance spinal reflexes.

Action Potentials↗
PubMed1978

Pentylenetetrazol and reflex activity of isolated frog spinal cord.

The superfused in vitro frog spinal cord preparation was used to investigate the effects of pentylenetetrazol (PTZ) on the spinal cord. PTZ depressed monosynaptic, but augmented polysynaptic reflexes, and decreased primary afferent deplorization. Concurrently, in Ringer's solution containing sufficient magnesium or cobalt ions to block synaptic transmission, PTZ antagonized the hyperpolarizing effects on motoneurons and the depolarizing effects on primary afferent fibers of the inhibitory amino acids GABA, beta-alanine, taurine, and glycine. PTZ did not affect responses to the excitatory amino acids glutamic acid and aspartic acid. Furthermore, PTZ did not alter high affinity uptake by cord slices, K+ -evoked release of [3H]GABA from them, or the spinal concentration of GABA. These data suggest that PTZ may produce its excitatory effects by postsynaptic blockade of inhibitory processes mediated by GABA (and possibly by other amino acids).

Amino Acids↗