A voltammetric technique was used (differential pulse voltammetry with a carbon fibre microelectrode) to investigate dynamics of the changes of catecholamine overflow in the corpus striatum following electroconvulsive stimulation (ECS) of chloral hydrate-anaesthetized rats. Application of "maximal" ECS (50 Hz, AC, sine wave, approximately 150 mA, 0.2 s) caused large enhancement of catechol-oxidative current (CA.OC): In the first minute after its arrest, the CA.OC peak raised to 1032±405% (n=5, mean±S.D.) of the controls (P<0.001, Student's t-test). This large elevation of the extracellular catecholamine content ceased rapidly - the baseline level was attained in the second minute. CA.OC changes evoked by a "minimal" ECS (50 Hz, AC, sine wave, approximately 30 mA, 0.2 s) were equivocal in the first minute (increase, decrease: 145 ±56 %, P>0.05, n=6). Possible mechanisms of the ECS therapeutic effect are discussed.
Differential pulse voltammetry with a carbon fibre microelectrode (ME) was used in pentobarbital- anaesthetized rats for monitoring the stobadine current (STB.C) on both sides of the blood-brain barrier (BBB) in the arterial bloodstream (BS) and in the corpus striatum (CS). The STB.C exhibited a distinct peak at a polarization voltage 540±30 mV (n=4). The maximum of STB.C in BS attained 2-3 min after the STB administration (2.8 mg/100 g in 1.0 ml saline solution i.a.) was followed by a rapid decrease to about 20 % within next 3 min. The STB readily passed across the BBB: the STB.C peak appeared in the CS in the 3rd minute and continued to rise up to the 30th min. The administration of STB did not prevent a large increase (1347±326 %, n=3) of the catechol-oxidative current (CA.OC) occurring in the CS between the 4th and 5th minute after cardiac arrest. However, a decrease of ME sensitivity to CA.OC in the presence of STB was observed. This fact leads to the speculation whether a similar "quenching" of dopamine by STB could not participate in the protective effects of STB observed in the brain exposed to hypoxia-reoxygenation.
Using a microelectrode with carbon filaments and the voltammctric technique, changes evoked in the catechol oxidation current (CA.OC) and multiple unit activity (MUA) by microinjection of 3-5 ¿ri 03 mol.I'1 KC1 were studied in the reticular formation (RF) of the medulla oblongata of anaesthetized rats; the effect of KC1 stimulation of the RF and corpus striatum (S) on the CA.OC in these structures was compared. The microinjection of KC1 in the vicinity of the working electrode in the RF caused depression of MUA which began 2-3 s after administration, persisted for up to 6 min after and then diminished, reaching control values within 9 min. The voltammctric signal was first recorded in the 1st min after microinjection, when there was an evident decrease in the CA.OC value (59 % of the control value); this effect reached its maximum 7 min after administration (a mean drop to 23 % of the control), while at the end of the experiment (i.e. after 24 min) CA.OC values had risen to 45-80 % of the control value. The response in the S had a biphasic character, however. Immediately after the microinjection (1st min), the mean CA.OC value rose to 626 % of the control, while in the second phase (3-10 min) it was seen to fall below the control values (means 21-63 % of the control). The differences in the changes evoked by K+ depolarization in the concentration of catecholamines in the RF and S microenvironment are discussed from the aspect of the existence of different pools of the transmitter and
other regional differences. The possibility of a relationship between considered.