PubMed Health⌕ Search

PubMed · 8013594

Decrease of extracellular catecholamine content in the vicinity of cortical penicillin-induced epileptogenic focus: voltammetric study in the rat.

Abstract

Differential pulse voltammetry with carbon-fibre microelectrodes was used in chloralhydrate-anaesthetized rats to test the influence of the penicillin-G-Na (PNC)-induced (topical application, approximately 2000 IU) epileptic activity on the catecholamine content (catechol-oxidative current, CA.OC) in the parietal cortex. In the experimental group (n = 4) after PNC a nonlinear CA.OC lowering was observed; this decrease during the first 10 min was faster than in the control group (n = 4). Significantly different values were observed from the 4th min after application. The best fit for this experimental curve gave the logarithmic function (f(t) = a+b.ln(t), a = 105.8, b = -10.6) with regression coefficient r = 0.98. From the 12th min after PNC application until the end of the experiments (54th min) CA.OC values ranged from 78% to 84% of the control group.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Pavlásek, P Mares, M Haburcák, C Masánová. 1994. Decrease of extracellular catecholamine content in the vicinity of cortical penicillin-induced epileptogenic focus: voltammetric study in the rat.. https://doi.org/10.1007/bf00229113

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Comparative effects of methamphetamine and nicotine on the striatal [(11)C]raclopride binding in unanesthetized monkeys.

Although a very large literature exists on the in vitro, ex vivo, and in vivo effects of nicotine on dopamine release in rodents, similar data in primates are scant. This study was initiated to compare methamphetamine to nicotine given i.v. to normal unanesthetized monkeys using positron emission tomography (PET) techniques. Release of dopamine in the striatum using [(11)C]raclopride was determined indirectly in four nicotine-naïve adult Macaca mulatta monkeys under conscious and isoflurane-anesthetized conditions using high-resolution PET. [(11)C]Raclopride was given i.v. as a bolus injection followed by continuous infusion with steady state over 30-45 min. Nicotine bitartrate was then given as a bolus plus infusion for 30 min in doses of 32 microg/kg + 0.8 microg/kg/min or 100 microg/kg + 2.53 microg/kg/min as base. The larger doses of nicotine caused significant cardiovascular effects; these doses did not displace [(11)C]raclopride binding in either dorsal or ventral striatum under the anesthetized conscious condition. In contrast, isoflurane-anesthesia induced a slight but significant dose-dependent reduction of [(11)C]raclopride binding by nicotine even at the same doses used in the anesthetized condition. Methamphetamine in bolus doses of 0.1, 0.3, and 1.0 mg/kg i.v. under conscious condition caused a significant displacement of [(11)C]raclopride and isoflurane-anesthesia facilitated the displacement induced by nicotine. These results indicate that nicotine, in high tobacco-smoking-related doses, does not release sufficient brain dopamine to displace [(11)C]raclopride in the striatum in the awake and fully conscious state, in contrast to small doses of methamphetamine.

Anesthesia↗

Disruption of the two-state membrane potential of striatal neurones during cortical desynchronisation in anaesthetised rats.

In anaesthetised animals, the very negative resting membrane potential of striatal spiny neurones (down state) is interrupted periodically by depolarising plateaux (up states) which are probably driven by excitatory input. In the absence of active synaptic input, as occurs in vitro, potassium currents hold the membrane potential of striatal spiny neurones in the down state. Because striatal spiny neurones fire action potentials only during the up state, these plateau depolarisations have been perceived as enabling events that allow information processing through cerebral cortex-basal ganglia circuits. Recent studies have demonstrated that the robust membrane potential fluctuation of spiny neurones is strongly correlated to the slow electroencephalographic rhythms that are typical of slow wave sleep and anaesthesia. To further understand the impact of cortical activity states on striatal function, we studied the membrane potential of striatal neurones during cortical desynchronised states. Simultaneous in vivo recordings of striatal neurones and the electrocorticogram in urethane-anaesthetised rats revealed that rhythmic alternation between up and down states was disrupted during episodes of spontaneous or induced cortical desynchronisation. Instead of showing robust two-state fluctuations, the membrane potential of striatal neurones displayed a persisting depolarised state with fast, low-amplitude modulations. Spiny neurones remained in this persistent up state until the cortex resumed ~1 Hz synchronous activity. Most of the recorded neurones exhibited a low firing probability, irrespective of the cortical activity state. Time series analysis failed to reveal significant correlations between the membrane potential of striatal neurones and the desynchronised electrocorticogram. Our results suggest that during cortical desynchronisation continuous uncorrelated excitatory input sustains the membrane potential of striatal neurones in a persisting depolarised state, but that substantial additional input is necessary to impel the neurones to threshold. Our data support that the prevailing cortical activity state determines the duration of the enabling depolarising events that take place in striatal spiny neurones.

Anesthesia↗

Tonic sympathoinhibition arising from the hypothalamic PVN in the conscious rabbit.

In the conscious rabbit muscimol (1-10 nmol/side) was microinjected into the hypothalamic paraventricular nucleus to inhibit neuronal function and the acute changes in mean arterial pressure (MAP), heart rate and renal sympathetic nerve activity (RSNA) were monitored. Muscimol (1 nmol) had no effect on the cardiovascular variables, as was the case with vehicle. However, muscimol (10 nmol) elicited a significant increase in RSNA of 184+/-40% and a reduction in heart rate of 49+/-12 beats/min but no change in MAP. The effect of blocking endogenous glutamatergic inputs with the glutamate antagonist, kynurenate (25 nmol), into the PVN was also examined. Kynurenate elicited an increase in RSNA of 35+/-9% with no significant change in MAP or HR. The results suggest that muscimol inhibits a tonically active inhibitory influence on RSNA arising from the PVN in the conscious rabbit. A glutamatergic input into the PVN appears to contribute to the tonic activation of this inhibitory influence.

Anesthesia↗