[Generic characteristics and specific characteristics of the ponto-geniculo-occipital spike activity (PGO) in 2 baboons, Papio hamadryas and Papio papio].
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Averaged evoked responses (AER) to light flashes were recorded in baboons (Papio papio) during wakefulness, slow-wave sleep and rapid eye movement (REM) periods, at the visual cortex, retrocalcarine sulcus, optic tract (OT), lateral geniculate (LG) and pulvinar. Waking AERs were composed: in the OT, of a negative, low amplitude wave at 13.3 msec (I), a high amplitude wave at 34.8 msec (II), a negative wave at 72 msec (III) and a late component at 151 msec; in the LG, a small positive wave (II) with a peak latency of 40 msec, a high amplitude negative wave (III) with a latency of 70 msec and a late component; in the pulvinar of two low amplitude short latency waves (I and II), respectively negative and positive at 25 msec and 40 msec, then a high amplitude negative wave (III) at 75 msec and a late component; in the retrocalcarine sulcus 3 positive waves (I, II and III) were recorded at 25, 45 and 100 msec and a late component; in the visual cortex, 3 low amplitude negative waves (II, III and IV at 40, 50 and 54 msec, then a positive wave at 80 msec and some late components. In slow-wave sleep, AERs did not change in the OT, but in the LG and pulvinar, they showed an increase in the amplitude of wave II from stage 1 to stage 3. At the cortical level, early waves (II for the retrocalcarine sulcus, II and IV for the visual cortex) presented a marked increase in amplitude during stages 2 and 3, but only a slight increase for stage 1. Peak latency increase of each wave in cortical and subcortical AERs was seen during slow-wave sleep. REM AERs resembled, in amplitude and peak latency, those recorded in the LG and pulvinar during wakefulness; in the visual cortex and retrocalcarine sulcus, they were similar to those obtained during wakefulness and stage 1. In conclusion, a different evoked response was found between visual cortex and deep structures (except for the OT): firstly, during slow-wave sleep (the AERs showed a difference for stage 1 between the visual cortex or the retrocalcarine sulcus and the LG or the pulvinar), secondly, in REM (on the cortex, REM AERs looked like wakefulness and stage 1 responses); on the contrary, in the LG and pulvinar, REM AERs were similar only to those recorded during waking. Finally, it can be said that for Papio papio the differentiation and structural responses between the various stages of sleep (particularly light sleep and REM) were greater in the cortex than in the thalamic structures.
The ability of cortisone to modify EEG and seizure activity was investigated in the baboon, Papio papio. Acute intramuscular doses (0.5-4 mg/kg) caused a dose-dependent increase in seizure response to a flashing light stimulus. This increase in seizure response was apparent in both seizure duration and the spread of convulsive activity. Along with enhancement of seizures, cortisone was found to cause marked changes in the EEG, ranging from the appearance of interictal paroxysmal activity to alterations in spectral characteristics of the wave forms. Increases in slow waves appeared concomitant with a decrease in fast activity in the 18-25 c/sec range. Since previous studies have indicated that seizure proclivity in the Papio papio is maximal at the time of the day when cortisol excretion rates peak, these findings lend further evidence to the idea that corticosteroids may be involved in the thythmic variation of seizure activity in the baboon.
The karyotypes of two species of baboons, Papio papio and P. anubis, and of two species of Macaca, M. mulatta and M. fascicularis, are compared after the use of numerous banding techniques. No difference was detected between the karyotype of the two Papio species. However, a minor change in the T-staining of a short segment, probably heterochromatic, could be detected between the Papio species and M. mulatta. A paracentric inversion exists between these three and M. fascicularis. These karyotypes are briefly compared with those of the Pongidae and man. The value of the karyotypic criteria and of the methods used for taxonomy is discussed.
Daily electrical stimulation of the amygdala in Senegalese baboons (Papio papio) resulted in the development of generalized convulsive seizures focal onset through five distinct clinical stages in an average of 72 days. The chronologic pattern of electroclinical features suggested that vertical intrahemispheric ictal dissemination was of primary importance in the progressive seizure development. Some animals developed spontaneous recurrence of both partial complex and primary generalized seizures. The kindling preparation in P. papio represents a unique model of human epilepsy with its secondary generalized convulsive seizure development, spontaneously recurrent partial and primary generalized seizures in the background of predisposed epileptogenic susceptibility.
The sheath of the bipolar perikarya of the vestibular ganglion (Scarpa) in Papio papio is made up of several Schwann cells which concur to form loose myelin, and at most five layers of compact myelin. Most of the Schwann cytoplasmic layers stop at the emergence of both neurites, forming at the point an incomplete Ranvier half-node. The constitution of the vestibular perikaryal sheath in Papio is intermediate between those previously described in the Rat and in the Human.
The status of Papio papio as a model of clinical epilepsy has been reviewed. The anticonvulsant effects of single doses of various classic and experimental agents have been compared against seizures induced in the P. papio by intermittent light stimulation. Long-acting but not short-acting barbiturates have been shown fully to control seizures with minor sedative effects. Diphenylhydantoin (in chronic doses only) and trimethadione are often effective but not consistently so. Diazepam and clonazepam block seizures at very low doses both acutely and chronically. However, an initial dose well above threshold seems essential if anticonvulsant effects are to be maintained under chronic administration of these compounds. Carbamazepine and SC 13504 (1-benzhydryl-4(6 methyl-2-pyridylmethyleneimino)piperazine), as well as two nonstimulant analogues of amphetamine, were shown to be promising anticonvulsants in this model. A biphasic action of tetrahydrocannabinol, anticonvulsant at a few micrograms per kilogram but not at higher doses, was also demonstrated. Finally, the anticonvulsant action of intraventricular epinephrine and norepinephrine was reported.
Two new 1,5 benzodiazepines have been evaluated acutely as anticonvulsants in baboons, Papio papio, with photosensitive epilepsy. BAU 426 (8-Chlor-6-[2-chlorphenyl]-4H-s-triazolo-[4,3-a] [1,5-benzodiazepin-5-[6-H]on) and BAU 500 (analogue of BAU 426 with [2-trifluor methylphenyl] substituted for [2-chlorphenyl]), 0.1--5.0 mg/kg, were administered i.v. to baboons with and without priming with D,L allylglycine. BAU 426 or BAU 500, 0.1--0.2 mg/kg, produced partial or transient protection against photically induced myoclonus or epileptic responses. Complete protection, in the absence of signs of sedation or acute neurological toxicity, was seen 1--4 h after 0.5--2 mg/kg. EEG changes typical of benzodiazepines were seen for 1--3 h and clinical signs of sedation with some muscular hypotonia were evident for 1 h after either drug, 5 mg/kg. Clinical trials are required to determine if these compounds are superior to 1,4 benzodiazepines as anticonvulsants.
Report of a case of candidiasis of the digestive tract associated to an obstructive epithelial tumor, with great invasive ability, in a captive Baboon, Papio papio (Desm.). Included is a discussion of the incidence of some intestinal disturbances involving candidiasis of subhuman Primates.
Modifications of the latero-dorsal (L.D.) nucleus of the thalamus have been observed earlier in man in relation to limbic lesion of various etiologies. Our proposal was to determine the role of L.D. in memory disturbances. We attempted to study the connections of L.D. in Papio papio baboon after surgical lesion using silver impregnations as well as traditional techniques. We found three afferent pathways: from the fornix, the posterior cingulate and the parietal cortex (area 7). The most important is the afferent system from the fornix, it terminates in the antero-dorso-medial part of L.D.; the other two afferent pathways have a postero-lateral projection in L.D. The three efferent systems to parietal cortex, cingulate and fornix were not delineated in this study. It was concluded that the antero-dorso-medial portion of L.D. is connected to the limbic system and the ventro-postero-lateral portion integrated into a large parieto-cingulo-parahippocampal circuit to which it is joined by direct and indirect projections with several relays. These connections have important implications, perhaps, in our understanding of memory disturbances.
The effects of intracerebroventricular (i.c.v.) or systemic injections of Met- or Leu-enkephalin, beta-endorphin, FK 33.824 (D-Ala2, MePhe4, Met(O5)-ol-enkephalin) and of morphine and naloxone have been studied in baboons, Papio papio, which spontaneously show photically induced epileptic responses. Animals were chronically implanted with epidural or deep recording electrodes and a cannula in one lateral ventricle, and tested whilst seated in a primate chair. In some animals the natural syndrome was enhanced by the prior administration of DL-allylglycine, 100--200 mg/kg, i.v. Met- or Leu-enkephalin, 1--10 mg, i.c.v., did not lead to any manifest focal or generalized seizure discharges. Nor did it lead to any consistent enhancement or reduction of photically induced myoclonic responses (as tested 5--10 min after injection). beta-Endorphin, 0.1--0.5 mg, i.c.v., did not enhance or impair photically induced myoclonic responses. FK 33.824, 0.1--0.5 mg, i.c.v., depressed respiration and slowed EEG background rhythms for 9--15 h. This was associated with a loss of myoclonic responses to photic stimulation. These effects were reversed for 20--40 min following the injection of naloxone, 1 mg/kg i.m. A depression of respiration and a slowing of EEG rhythms was seen beginning 5--20 min after FK 33.824, 2 or 4 mg/kg, i.v. The higher dose also abolished photically induced myoclonic responses. Naloxone, 1 mg/kg, definitively reversed these effects. Morphine, 5--10 mg i.c.v., tended to increase the latency to onset of generalized myoclonus during photic stimulation. Myoclonic responses were delayed or diminished after morphine, 5 mg/kg, i.m. Naloxone, 1--2 mg/kg i.m., reversed this effect. Naloxone, 0.2--5.0 mg/kg i.m., alone, did not significantly modify photically induced myoclonus, either in animals of low or high initial responsiveness, or in those pretreated with allylglycine.
The sleep pattern of sixteen baboons (Papio papio) was studied under two very different conditions: (1) in a laboratory at Marseilles, the monkey being immobilized in a restraining chair in a soundproof cubicle; (2) in an African reserve, the monkey being housed in a large cage placed in its natural environment. Some very marked differences emerged. Sleep in the laboratory was longer (by 24 min) and richer in stage 3 and paradoxical sleep. In Africa, however, the sleep showed much more stage 1, was more fragmented and stages 2 and 3 and paradoxical sleep episodes were of shorter duration. Records made in Africa indicate that sleep is independent of slight environmental changes (day length, brightness of the moon, variations in temperature, calls of predators). But the comparison of the two series of results reveals the reorganization which occurs when the monkey is exposed to such different conditions. This adaptation to the environment affects, unequally, the various slow sleep stages and paradoxical sleep. In fact, the major modifications occur in stages 1 and 3 of slow sleep and in paradoxical sleep, while stage 2 appears to constitute the stable, unmodifiable nucleus of sleep.
1. Evoked responses to single visual stimuli (VEP) and driving by intermittent light stimulation (ILS) were recorded with macroelectrodes from the central white matter (centrum semiovale) of 12 Papio papio baboons. 2. Two types of VEP were identified: VEPs with constant morphology, localized in the long associative bundles connecting the occipital, temporal and frontal lobes; VEPs with variable morphology and without any preferential localization; these probably originate from other types of fibres also belonging to the centrum semi-ovale. 3. Concerning the long associative bundles which have been individualized, they might be the equivalent of the occipito-frontal and the superior and inferior longitudinal bundles well known in man. The fusion frequency observed in these bundles during ILS increases from the frontal to the occipital lobe, because of their involvement (particularly in the parieto-temporal region) with other fibres of the centrum semi-ovale also likely to be driven by ILS. The existence of driving by ILS in these bundles demonstrates an activation of the frontal lobe by visual impulses.
Ketamine was administered to 18 baboons (Papio papio) to disrupt epileptic discharges elicited through intracarotid air injection. Discharge suppression was obtained in all animals but could be preceded by a phase of enhancement of the epileptic patterns, which rendered necessary the injection of a supplementary dose. The mechanisms of Ketamine action are discussed, in connection with data from the literature. Some of the latter suggest that its use in proved epileptics facilitates paroxystic patterns or even convulsions while others emphasize its antiepileptic action. Present data corroborate the ambivalent action of this drug. However, its dominant depressant effect obtained with increasing doses is somewhat favourable to its administration to epileptic patients.
The acute pharmacological effects of melatonin (5-methoxy-N-acetyl-tryptamine) were evaluated on behaviour and electrographic signs in the photosensitive baboon (Papio papio), including visually evoked potentials VEPs). Doses of 5 and 10 mg/kg i.v. had little effect, contrasting with the enhancement of spontaneous paroxysmal activity and latency of clinical signs elicited by intermittent light stimulation (ILS) produced by the 20 and 50 mg/kg doses. Moreover, a modification of the electrographic pattern of discharge during ILS-induced myoclonic responses was observed. These observations indicate a slight decrease of light sensitivity after melatonin. Only frontal VEPs were modified, with increase in amplitude of their late components for all doses tested. These effects lasted for 2-4 h. The participation of serotoninergic mechanisms involved in melatonin effect and in this model of experimental epilepsy are discussed.
The effects of the intravenous or intracerebroventricular injection of the stereoisomers, and the racemic mixture, of allylglycine (2-amino-pent-4-enoic acid) have been studied in baboons, Papio papio, with photosensitive epilepsy. Enhancement of the natural syndrome of photosensitivy epilepsy is seen 1-12 h (maximally at 3-8 h) after L-allyglycine, 100 mg/kg, intravenously, or D,L-allyglycine, 200 mg/kg, intravenously. Such enhancement is seen with a slower onset, and to a lesser, and more variable, extent after D-allyglycine, 500-750 mg/kg, intravenously. Brief focal or generalised seizures occurred (in the absence of intermittent photic stimulation) after L-allyglycine, 150-200 mg/kg, intravenously. This effect is similar to that previously observed after D,L-allyglycine, 300-400 mg/kg. D-Allyglycine, 780 mg/kg, intravenously produced episodes of vertical nystagmus with increased extensor motor tone, but no 'spontaneous' seizures. Intracerebroventricular injection of L-allylglycine, D-allyglycine or D,L-allyglycine, 100 mg in 1 ml saline, did not modify the natural syndrome of photosensitive epilepsy. D-Allylglycine, or D,L-allyglycine, 100 mg intracerebroventricularly, after 1-2 h gave rise to a syndrome with vomiting, sustained vertical nystagmus, and intermittent extensor spasms. The results are interpreted in terms of regional differences in the metabolism of the two isomers to active compounds that can inhibit glutamic acid decarboxylase. D-Allylglycine is active only at the brain stem and cerebellum because D-amino acid oxidase is largely confined to these brain areas.
Acute changes in spontaneous motor activity, the EEG and photically induced epileptic responses have been observed in baboons (Papio papio) following the i.v. injection of drugs acting on dopaminergic transmission. Apomorphine hydrochloride, 0.5-1.0 mg/kg, produced a phase of acute excitement with accentuated vigilance and abnormal buccal motor activity lasting 30-40 min; during this phase myoclonic responses to intermittent photic stimulation were absent. After piribedil (ET 495, 1,2'' -pyrimidyl-4-piperonylpiperazine), 2-10 mg/kg, acute excitement was not seen. Intermittent delta activity was prominent in the EEG for 1-3 hr, and was associated with a slight reduction in photically induced epileptic responses. Haloperidol 0.6-1.2 mg/kg, produced a long-lasting reduction in spontaneous motor activity with an increased incidence of spontaneous EEG spikes and waves and a great enhancement of paroxysmal EEG activity during photic stimulation. Pimozide, 0.5-2.5 mg/kg, normally produced mild sedation and some EEG slowing. 2 animals responded idiosyncratically to both haloperidol and pimozide, displaying intermittent dystonic episodes with bucco-facial dyskinesia. These findings suggest that activation of dopaminergic receptors can lead to a reduction in myoclonic responses to photic stimulation.
After several trains of intermittent photic stimulation (IPS) each lasting 10 seconds and sometimes inducing paroxysmal electrical activity, isolated flashes or salves of 2 or 3 light flashes are capable of inducing bifrontal paroxysmal discharges in photosensitive Papio papio, an effect which is augmented by allylglycine or the use of highly photosensitive animals. Use of these salves repeated every second enabled the authors to demonstrate two types of changes in cortical excitability after intermittent photic stimulation: 1. responses which were more frequent and of greater amplitude appearing in the first 3 or 4 seconds after IPS; after paralysis of the animal amplitude and frequency of the responses are augmented. 2. if trains of intermittent photic stimulation are repeated regularly a seizure occurs after 5 to 15 trains. In the paralysed animal, more trains are required although large responses are seen after each train whereas in the non-paralysed animal the seizure occurs rapidly but the responses are on average weaker and less frequent than in 1. The relationship between photosensitive epilepsy and these responses is discussed as well as that of somatic afferents.