[Depression of penicillin-evoked seizure discharges of cerebrospinal neurons by magnesium ions]. / Ugnetenie ionami magniia vyzvannykh penitsillinom sudorozhnykh razriadov spinnomozgovykh neironov.

In experiments on narcotized spinal cats perfusion of the lumbosacral segments of the spinal cord with penicillin (50 mmol/l) containing artificial cerebrospinal fluid led to the appearance of spontaneous negative small potentials in the dorsal roots and spontaneous repetitive bursts of impulses in the ventral roots of the perfused segments. The epileptogenic activity of penicillin was reduced or completely blocked if administration of the penicillin containing cerebrospinal fluid was preceded by 20-30 minute perfusion of the central canal of the lumbosacral segments with cerebrospinal fluid containing a high concentration of magnesium ions.

[Effect of temperature on the spontaneous rhythmic activity of the neurons in the spinal centers of the frog lymphatic hearts]. / Vliianie temperatury na spontannuiu ritmicheskuiu aktivnost' neironov spinal'nykh tsentrov limfaticheskikh serdets liagushki.

Spontaneous rhythmic bursts of impulses were recorded from motoneurons related to posterior lymphatic hearts in 10th and/or 11th ventral roots of isolated frog spinal cord in vitro at the temperature of 1 degree C to 28 degrees C. The burst frequency varied from 10-12/min (at 1-3 degrees C) to 50-70/min (at 26-28 degrees C). The mean burst frequency for the 5-15 degrees C range was 2.5 +/- 0.22. High temperature sensitivity of neurons in spinal centers for lymphatic hearts of frogs may be an efficient mechanism for temperature adaptation of these poikilothermic animals.

[Suppression of the dorsal root potentials of the cat spinal cord by manganese and cobalt ions]. / Ugnetenie potentsialov dorsal'nykh koreshkov spinnogo kozga koshki ionami margantsa i kobal'ta.

In anesthetized spinal cats, perfusion of lumbosacral spinal cord with artificial CSF containing manganese (1.5-3.0 Mm/l) or cobalt (6.0 mM/l) ions, led to reversible suppression of negative dorsal root potentials (DRP), induced by stimulation of ipsilateral hindlimbs' afferent nerves. The depression of the DRP proceeded in connection with the depression of presynaptic inhibition of extensor monosynaptic reflexes induced with impulse volleys in the group I flexor muscle afferents. The depression of inhibition was not associated with changes in amplitudes of testing monosynaptic reflexes. The DRP is concluded to have a synaptic origin.

[Furosemide depression of the dorsal root potentials and of the presynaptic inhibition of monosynaptic reflexes in the cat spinal cord]. / Ugnetenie furosemidom potentsialov dorsal'nykh koreshkov i presinapticheskogo tormozheniia monosinapticheskikh refleksov v spinnom mozge koshki.

In experiments on spinal narcotized cats perfusion of the lumbosacral cord through the central canal with artificial cerebrospinal fluid containing furosemide (15-48 mmol/l) led to the reversible selective depression of negative DRP and to the depression of prolonged "presynaptic" inhibition of extensor monosynaptic reflexes produced by volleys in flexor muscle afferents of group 1.

[Method of prolonged perfusion of the spinal cord central canal in the adult cat in vivo in neurophysiological studies]. / Metod dlitel'noi perfuzii tsentral'nogo kanala spinnogo mozga vzrosloi koshki in vivo dlia neirofiziologicheskikh issledovanii.

A method for in-vivo long-lasting perfusion of the central canal of the cat lumbosacral spinal cord with artificial cerebrospinal fluid is described. The method provides for a stable continuous flow of perfusion fluid for many hours. The perfusion adjustment does not entail any injuries to the inferior lumbar and sacral segments of the spinal cord or their roots.

[Primary afferent depolarization induced by gamma-aminobutyric acid injected into the central canal of the spinal cord in the cat]. / Depoliarizatsiia pervichnykh afferentov, vyzvannaia gamma-aminomaslianoi kislotoi, vvedennoi v tsentral'nyi kanal spinnogo mozga koshki.

The method of perfusion of the central canal of the cat spinal cord in vivo was used to study the effects of GABA on membrane potential changes in primary afferent terminals. It was shown with the use of the sucrose gap technique for recording the spinal dorsal root potentials that addition of GABA (5-50 mM/l) to the perfusate produced dose-dependent depolarization of the primary afferents. The depolarizing effect of GABA was abolished by bicuculline (2 mg/kg i. v.). The GABA-induced depolarization of the primary afferents was fully preserved after the synaptically induced depolarization of the primary afferents was reversed by addition of 20 mM/l Mg2 to the perfusate.

[Effect of magnesium ions on presynaptic inhibition of monosynaptic reflexes]. / Deistvie ionov magniia na presinapticheskoe tormozhenie monosinapticheskikh refleksov.

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.

[Depolarization of primary afferents and presynaptic inhibition of monosynaptic reflexes]. / Depoliarizatsiia pervichnykh afferentov i presinapticheskoe tormozhenie monosinapticheskikh refleksov.

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.

[New evidence of depression of depolarization of primary afferents with ammonium ions]. / Novye dokazatel'stva ugneteniia depoliarizatsii pervichnykh afferentov ionami ammoniia.

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.

[Block of presynaptic inhibition of spinal cord reflexes by ammonium acetate]. / Ugnetenie presinapticheskogo tormozheniia spinnomozgovykh refleksov atsetatom ammoniia.

In experiments on cats ammonium acetate (AA) injected intravenously (2--4 mM/kg body weight) depressed the process of primary afferent depolarization (PAD) which were thought to be responsible for presynaptic inhibition of spinal reflexes. PAD depression is reversible and proceeds in parallel to depression of postsynaptic inhibition of monosynaptic reflexes. The ammonium depression of PAD is not connected with the block of the negative postsynaptic potential recorded from the dorsal surface of the spinal cord or with the block of the reflex electrical discharges from the ventral roots. A conclusion was drawn that one of the possible mechanisms for convulsive action of AA consists in depression of presynaptic inhibition. It is supposed that the depression of PAD by AA results from the block of the chloride ion pump existing in primary afferent terminals. The block of the pump leads to abolition of the EMF for the outwardly directed transmembrane chloride current producing PAD.

[Effect of ammonium acetate on depolarization processes in the central terminals of primary afferents]. / Deistvie atsetata ammoniia na protsessy depoliarizatsii tsentral'nykh okonchanii pervichnykh afferentov

Experiments on cats determined that ammonium acetate injected intravenously (2-4 mM/kg) supressed the processes of primary afferent depolarization (PAD) which are thought to be responsible for the presynaptic inhibition of spinal reflexes. The supression was transient and proceeded in paralle to depression of postsynaptic inhibition of monosynaptic reflexes. Ammonium acetate slightly decreased the amplitude of the negative postsynaptic potentials recorded form the dorsal surface of lumbar cord in response to stimulation of hind limb afferent nerves and increased polysynaptic reflex discharges in appropriate ventral roots. These findings make it unlikely that the ammonium depression of PAD is a result of impairment of interneuronal activity. A suggestion is made that ammonium depression of PAD results from diminition of the EMF for synaptic currents producing PAD.

[Organization of the rhythmic activity of the spinal center motoneurons of the lymphatic hearts of Rana temporaria frogs]. / Organizatsiia ritmicheskoi aktivnosti motoneironov spinal'nykh tsentrov limfaticheskikh serdets liagushki Rana temporaria

Spontaneous rhythmic impulse discharges of motoneurons of spinal centers of the posterior lymphatic hearts have been recorded from the ventral roots of isolated spinal cord perfused by oxygenated Ringer's solution. Inhibition of the transmission in interneuronal synapses evoked by abolition of Ca ions from the external solution and by the addition to the latter of 1--4 mM EDTA was accompanied by the block of the spontaneous impulse activity. Blocking of rhythmic efferent discharges in the anterior roots was also observed after the addition to normal Ringer's solution of 10--30 mM MgCl2. Inhibition of the spontaneous activity by high Mg content in the perfusion fluid could be alleviated by the addition of 5--15 mM CaCl2 to this solution. Antidromic impulses in the ventral roots of the XI and X segments, evoked by rhythmic electrical stimulation of these roots, did not affect the intrinsic rhythm of motor discharges.

[Electrotonic potentials of spinal cord dorsal roots in frogs with experimental tetanus]. / Elektrotonicheskie potentsialy dorzal'nykh koreshkov spinnogo mozga u liagushek s éksperimental'nym stolbniakom

Tetanus toxin administered to frogs in doses which produced general tetanus depressed the reciprocal inhibition of spinal reflexes. This depression was not associated with the block of the processes which led to depolarization fo the central terminals of the primary afferent fibers.