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Órgano Oficial del Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz

2002, Number 3

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Salud Mental 2002; 25 (3)

Efecto de la naloxona sobre un foco epiléptico inducido por penicilina en la amígdala del lóbulo temporal de gatos. EEG y registros polisomnográficos de 23 horas

Martínez A, Fernández-Mas R, Valdés-Cruz A, Magdaleno-Madrigal V, Fernández-Guardiola A

Language: Spanish
References: 41
Page: 56-63
PDF size: 491.27 Kb.


ABSTRACT

It is known that epileptic activity modifies the system of the endogenous opioids, increasing its concentration at the end of the ictal and post-ictal phases. It is also known that μ opioid receptors stimulation in the pontine reticular formation inhibits rapid eye movement (REM) sleep.
Besides, opioid peptides induce an excitatory effect generating a desynchronization on the electroencephalogram (EEG) and, a reduction of slow-wave sleep and REM sleep. Based on clinical and experimental observation carried out in animal models, there seems to be an intimate relationship between epilepsy and sleep, because epileptic activity is facilitated during slow-wave sleep while it is inhibited during the REM sleep. Based on these data, we analyzed the effect of naloxone on the epileptic activity induced by penicillin sodium g (Pn) in the amygdala of the temporal lobe, and also EEG and polysomnographic 23-h recordings in cats.
The considered variables were the following: a) latency, amplitude and duration of the interictal spikes in the EEG, and b) the changes in the organization of sleep caused by the epileptic activity.
Two effects were observed by the naloxone injection: the first was upon epilepsy progression and sleep, and the second on the sleep-wake cycle, under control conditions. Recordings were obtained in different situations. Group I received microinjections of saline solution in amygdala (control n=28), group II received microinjections of Pn in amygdala (n=40), group III received microinjections of Pn in amygdala plus naloxone IP (n=20), and group IV only received naloxone via IP (n=8). The recordings were qualified manually and were captured by means of the computational program Winsleep (Windows platform), to obtain the descriptive statistic of each stage (total number, total time, average duration in minutes, percentage, and latency). Numeric data were analyzed with the t-Student’s test for two independent groups.
The effects of the Pn plus the naloxone injection produced a facilitation of the afterdischarge (an increase on amplitude and frequency), which stabilizes between 10-15 minutes; occasionally, this afterdischarge leads to focal seizures. In the organization of the sleep-wake cycle we observed a decrease in the total time of the wakefulness, a decrease in the total time of the slow-wave sleep I (SWS-I), an increase in the total time of the slow-wave sleep (SWS-II), and a decrease in the latency of the first REM sleep (in comparison with Pn alone).
Dosages of 1 mg/kg of naloxone alone produced a prolonged desynchronization of the EEG characterized by an increase in the wakefulness, a decrease in the SWS-I, SWS-II, and in the REM sleep.
The data obtained on the present study showed the facilitator effect of naloxone on the epileptic activity of the amplitude and frequency of the afterdischarge. Besides, we observed an increase of the SWS-II and a decrease of the latency of the REM sleep; in the sleep-wake cycle under control conditions, we observed a decrease of the SWS-I and II joined to an increase in the wakefulness.
Our results demonstrate naloxone administration blocks the inhibitory effect of the opioids (liberated in the amygdala by the application of Pn) on the onset of the REM sleep and an activation of the mechanisms of induction of the SWS-II. This points out to the possibility that enkephalinergic inhibitory processes control the appearance of the REM sleep, but it has not been elucidated so far.


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