PubMed Health⌕ Search

Biomedical subjects

G A Erzina

Publications and source records attributed to G A Erzina.

6 recordsLinked to original sources
PubMed1981

[Effect of magnesium ions on presynaptic inhibition of monosynaptic reflexes].

In experiments on spinal narcotized cats perfusion of lumbosacral spinal cord through central canal with artificial cerebrospinal fluid containing high concentration (20-46 mM) of magnesium ions led to reversible depression of negative DRP as well as to depression of prolonged "presynaptic" inhibition of extensor monosynaptic reflexes produced by repetitive impulse volleys in group I flexor muscle afferents. Magnesium did not cause a depression of monosynaptic reflex discharges in spinal ventral roots.

Animals↗
PubMed1980

[Depolarization of primary afferents and presynaptic inhibition of monosynaptic reflexes].

In experiments on anesthetized spinal cats, perfusion of the lumbosacral spinal cord through the central canal with artificial cerebrospinal fluid containing ammonium ions led to reversible suppression of slow negative dorsal root potentials (DRP). The suppression of DRP proceeded in parallel to suppression of postsynaptic inhibition of motoneurons but was not related to a marked weakening of prolonged "presynaptic" inhibition of extensor monosynaptic reflexes produced by repetitive impulse volleys in group I flexor muscle afferents. It is concluded that primary afferent depolarization alone does not lead to presynaptic inhibition of synaptic transmission. A decisive factor for the inhibition might be the GABA-induced increase in chloride conductance of the presynaptic membrane, which, however, does not result in the terminal depolarizing current flow after the blockade of chloride pump with ammonium ions.

Ammonium Chloride↗
PubMed1979

[New evidence of depression of depolarization of primary afferents with ammonium ions].

Perfusion of the central canal of the lumbar segment of the spinal cord with artificial cerebrospinal fluid (CSF) supplemented with ammonium ions induced in cats depression of slow negative electrotonic potentials of dorsal roots (PDR). PDR depression developed simultaneously with postsynaptic depression of the inhibition of monosynaptic reflexes, however it was not related to the depression of mono- or polysynaptic reflex discharges. Further perfusion of the central canal with normal CSF resulted in a complete restoration of the PDR as well as inhibition of control reflexes. It is suggested that PDR depression with ammonium ions could be the result of the blocking of the chloric pump acting the afferent terminals and creating electromotive power for outward transmembranous chloric current producing depolarization of the afferent fibres.

Action Potentials↗