Sensitivity and selectivity for continuous perception values--a comment.

Droperidol is used in anesthesia as an antiemetic and as a component in neuroleptanalgesia. Its mechanism of action is thought to involve dopamine receptor blockade in the brain. The electrophysiological consequences associated with this action however, have not been elucidated. In this study we demonstrate a dose-dependent electrophysiological response to droperidol in central nervous system (CNS) neurons that express dopamine receptors that is absent in CNS neurons that do not express dopamine receptors. Primary dissociated cell (PDC) cultures were prepared from embryonal tissue dissected from ventral mesencephalon (VM) and spinal cord (SC). VM neurons were used to investigate the electrophysiological action of droperidol, a dopamine receptor antagonist, since these cultures contain neurons having dopamine receptors on their surface. SC neurons were used as a control as they do not express dopamine receptors. Some dopamine receptors are on dopaminergic neurons and therefore are called autoreceptors, while others are on nondopaminergic neurons, such as GABA producing (GABAergic) neurons. All neurons in both PDC cultures were spontaneously active. The percentage of neurons which spontaneously generated action potentials was reduced in a dose-dependent manner by droperidol (1 nM-10 microM) only in PDC cultures of VM. Exposure to droperidol had no effect on neurons from PDC cultures of SC which lack dopamine receptors. Our results suggest that droperidol modulates the electrophysiological properties of VM neurons with dopamine receptors possibly through facilitation of inhibitory interneurons. The reduced activity of VM neurons might contribute to the antiemetic and/or anesthetic activity of droperidol, since the concentrations of droperidol used in this study are at clinically relevant concentrations.

Action Potentials↗

PubMed2000

Electrophysiological evidence for reciprocal insulo-insular connectivity of baroreceptor-related neurons.

The recent indications of specialized lateralization of cardiovascular regulation within the right and left posterior insular cortex of the rat, suggest the possibility of transcallosal connectivity between these regions. This has not been previously demonstrated using physiological techniques. Extracellular neural recordings in 34 urethane anesthetized male Sprague-Dawley rats demonstrated reciprocal interinsular antidromic and orthodromic activation, elicited with similar median onset latencies (18 ms). The corresponding conduction velocity of these fibers (0.6 m/s) suggests that they may be unmyelinated. Many of the cells showing interhemispheric connectivity also responded to baroreceptor activation, further emphasizing the connectivity pattern in baroreceptor-related units. Both 1 and 25 Hz microstimulation of the contralateral insula indicated that the most frequent orthodromic response was inhibitory, either alone or as part of a biphasic pattern including activation. Chemical stimulation of the insula using L-glutamate was associated with both excitatory and inhibitory orthodromic activation of the contralateral posterior insula, confirming that the orthodromic electrical stimulation was not solely due to activation of fibers of passage. These data suggest that the two insulae may communicate with each other to integrate and balance cardiovascular function between hemispheres.

Action Potentials↗

PubMed2000

Electrical responses in hippocampal slices after prolonged global ischemia: effects of neuroprotectors.

A simple and reproducible animal model of global ischemia, induced by decapitation in 30-day-old Wistar rats, has been developed. It allows to perform electrophysiological analysis of the postischemic reperfusion period in the brain slices. Periods of ischemia up to 40 min increase population spikes measured in the CA1 area of the hippocampus during 2-5 h of reperfusion. Thus after 30-min decapitation-induced ischemia (at t(ischem)=25 degrees C), the mean amplitude of the recorded maximum orthodromic population spikes was 159% of the control obtained in the non-ischemic animals. Longer ischemic episodes result in the depression of the population spikes. After 2 h of ischemia, the amplitude of population spikes was about 89% of control. After 3 h of decapitation ischemia, the neurons could not be reactivated. The duration of ischemic episode needed for the irreversible depression of the electrical activity of the brain neurons drastically depends on the temperature at which the ischemic brain is maintained. Thus, only 2 h were needed at 30 degrees C as compared to nearly 3 h at 25 degrees C. We have found that intraperitoneal injection of neuroprotectors which precedes decapitation enables reactivation of the post-ischemic neurons even after very long periods of global ischemia. Thus, MK-801, a non-competitive NMDA receptors antagonist, or NBQX, a blocker of AMPA receptors, administrated 15 min before the long-term (90 min) decapitation ischemia (30 degrees C), induced dose-dependent recovery of population spike with ED(50) values 0.2 mg/kg and 3 mg/kg respectively. Our results demonstrate that, in spite of the high vulnerability of hippocampal neurons to hypoxia and ischemia, their electrical activity can be restored after prolonged (more then 1 h) decapitation ischemia. Administration of NMDA or AMPA antagonists enhances recovery.

Action Potentials↗