[Student evaluation of university instruction].
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Biomedical subjects
Publications and source records attributed to J Mares.
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The development of cortical penicillin foci in the occipital region was studied in rats whose ages ranged from five days up to the adult age. The local application of penicillin induced the formation of an epileptogenic focus for the first time at the age of seven days. With advancing age, the amplitude of focal discharges increased, the duration of the individual components of the discharge shortened, its originally negative-positive configuration changed to a triphasic form and in the third week of life initial positivity, for a time, become the dominant component of the discharge. Projection of the discharges to the contralateral hemisphere was found to be inconstant in the second postnatal week, but appeared regularly from the age of 14 days. Synchronization of the discharges of two symmetrical foci was very poor in 7-day-old young, but improved noticeably by the 14th day; it was never complete, however, even in adulthood. The activity of symmetrical foci changed spontaneously to ECoG seizures, which were most common in 7-day-old young (in which ictal activity was usually not generalized, however) and were least frequent in 14-day-old animals. Focal discharges could not be reliably triggered by electrical stimulation of the contralateral cortex until the age of 18 days and later. The occipital part of the cortex develops somewhat later than the sensorimotor, frontal region, and during its development there also appeared phenomena which are not present in the frontal cortex.
Infant rats, together with the female, were exposed to a simulated altitude of 7,000 m every day from birth to the age of 17 days, excepting the 6th, 7th, 13th and 14th day. Animals were studied on the 18th day, 20 hours after the last exposure to hypoxia. Rats aged 12, 15 and 18 days acted as the controls. The number of myelinated axones of the corpus callosum rose from the 12th to the 18th day; the number in animals exposed to hypoxia did not differ significantly from the number in the 15-day-old controls. Axonal section area likewise increased from the 12th to the 18th day and again the value in animals exposed to hypoxia was no different from section area in 15-day-old animals. The number of myelin lamellae rose from the 12th to the 18th day, but in animals exposed to hypoxia it did not differ significantly from the value found in 12-day-old animals. The thickness of the myelin layer increased from the 12th to the 18th day; in the experimental animals it was the same as in the 12-day-old controls. The myelin lamellae likewise became thicker, between the 12th and the 15th day; in animals exposed to hypoxia this parameter was the same as the value in 12-day-old rats. In the electrophysiological part of the study, the development of the interhemispheric response was analysed. In animals exposed to hypoxia, the individual waves of the IHR had the same shape and latent periods as in 15-day-old animals. The results demonstrate that hypoxia has a profound effect on morphological and functional maturation of the corpus callosum in infant rats.
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The sensorimotor area of rat cerebral cortex was subjected to repeated electrical stimulation at 10-min intervals, with resultant formation and progressive lengthening of self-sustained after-discharges (SSAD). One and 60 min after the third SSAD ended, we carried out an electron microscopy morphometric analysis of the agranular synaptic vesicles in type I synapses (after Gray) in the second cortical layer of the homotopic area of the unstimulated hemisphere. One minute after the seizure ended, 5.8% enlargement of the synaptic vesicles compared with the control was demonstrated in zone II of the synapse (0.1-0.2 micron from the active zone of the synapse). Neither the size nor the shape of the synaptic vesicles in the other parts of the synaptic apparatus altered. Sixty min after the seizure ended, a 5.5% enlargement of the synaptic vesicles in zone I (0.0-0.1 micron) and a 5.4% enlargement of those in zone II was found. The synaptic vesicles in zone I in the experimental animals were more oval than in the controls. Our findings support the vesicular theory and testify that hyperfunction, up to temporary exhaustion of the synaptic apparatuses, produces a change in the transmitter content of the synaptic vesicles. A raised amount of transmitter in the synaptic vesicles near the active zone could be one of the factors responsible for continued hyperexcitability of the tissue one hour after the seizure had ended. The results likewise support the concept of two mechanisms of synaptic vesicle formation, and hence of the existence of two different vesicle populations.
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Repeated electrical stimulation of the sensorimotor area in the rat cerebral cortex at 10-min intervals led to the formation and progressive lengthening of self-sustained after-discharges [SSAD]. One hour after the third SSAD ended, we evaluated the number of synaptic vesicles in type I synapses according to Gray in the second cortical layer of the homotopical part of the unstimulated hemisphere in the vicinity of the active synaptic zone and the total number of vesicles in sections of the presynaptic bag. We also made a semiquantitative evaluation of exocytotic and endocytotic activity on the presynaptic membrane. No statistically significant differences between the experimental and the control animals were demonstrated in any of the ultrastructural parameters studied. Persistent hyperexcitability of the tissues one hour after the SSAD ended was evidently due to other synaptic transmission mechanisms, which cannot be detected by morphological methods.
Repeated electrical stimulation of the sensorimotor region of rat cerebral cortex at 10 min intervals led to the development and progressive prolongation of self-sustained after-discharges (SSAD). One minute after the third SSAD ended, an electronoptic morphological analysis of type I synapses after Gray from the second cortical layer of the homotopic area of the unstimulated hemisphere was carried out. In the experimental animals, an 11.7% increase in the area of the presynaptic bag and a 5.5% increase in its perimeter were demonstrated. The number of agranular synaptic vesicles per constant unit area fell by 70.8%. The area of the mitochondria in the presynaptic ending increased by 49.8% and their perimeter by 16.1%. The area of the postsynaptic element increased by 34.1% and its perimeter by 15.7%. Changes in the synapses are evaluated as manifestations of exhaustion and primarily as a manifestation of ion shifts during the epileptic seizure. The findings nevertheless also testify to incipient activation of restitution mechanisms in the structures of the synaptic apparatus within a very short time after termination of the seizure.
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The sensorimotor area of rat cerebral cortex was subjected to repetitive electrical stimulation at 10-min intervals; this led to progressive lengthening of self-sustained afterdischarges (SSADs). At 50-60 s after cessation of the third SSAD the brains of the animals were perfused transaortally with fixing fluid, and a quantitative electron microscopic analysis of type I synapses in the second cortical layer of the sensorimotor area of the contralateral hemisphere was carried out. In a zone 0.1 micron wide adjacent to the presynaptic membrane in the active zone, the number of synaptic vesicles (converted to the number per 0.01 micron2 area) in the experimental animals fell by 64.6%. In a zone of the same width 0.1 micron distant from the presynaptic membrane, it fell by 67.6%. The mean absolute synaptic vesicle count per presynaptic bag section fell by 66.6%. The number of synapses showing signs of exocytosis rose in the experimental animals from 3.8 to 5.9%, while the number with clearly demonstrable exocytosis rose from 0.7 to 11.4%. The proportion of synapses with signs of (clearly demonstrable) endocytosis rose from 2.8% (2.1%) in the controls to 7.1% (3.7%) in the experimental rats. In the experimental and control animals we demonstrated complex vesicle formation in 4.3 and 3.8%, respectively, of the synapses and dense-cored vesicles in 7.7 and 2.8%, respectively, of the synapses. We consider changes in the number and formation of synaptic vesicles to be signs of exhaustion of the synapses caused by the previous epileptic seizure, which simultaneously activates mechanisms of vesicle formation.
The disinfection of a farm with Dikonit (active substance: sodium dichlorocyanuran) exerted no significant influence on the course of the spreading of cryptosporidiosis infections in newborn calves. The oocysts of Cryptosporidium sp., isolated from the faeces of a spontaneously infected calf and left in a 2.5% disinfecting solution of Dikonit under laboratory conditions for four hours, did not lose their viability. Laboratory mice experimentally infected with these "disinfected" oocysts, began to produce oocysts of Cryptosporidium sp. the sixth day from infection. The findings of different developmental stages of this protozoan obtained during the histological examination of the intestinal tissue of test mice are also considered as evidence of successful experimental infection. The cryptosporidium-free period which lasted only 14 days from disinfection was mainly due to thorough mechanical cleaning of the area where the calves were kept after birth. This is also proved by the results of the examination of old residues of calf faeces scraped from the floors: only individual individual oocysts of Cryptosporidium sp. were found in these samples.
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The ECoG pattern of self-sustained after-discharges (SSADs) evoked by rhythmic electrical stimulation of the cerebral cortex is far from uniform. In acute experiments on male rats the authors studied the significance of the frequency, intensity and length of stimulation for the character of the resultant SSAD. In the first group (11 rats), a stimulation frequency of 8 Hz was used; the stimulation series, which lasted 10 and 20 s, always led to the formation of a SSAD composed of spike-and-wave rhythm right from the outset. Shortening the time of stimulation markedly reduced its effectiveness. In the second group (10 animals), stimulation with 50 Hz frequency often evoked a complex SSAD starting with desynchronization, which was followed by fast spike activity of increasing amplitude and only later by spike-and-wave rhythm or by polyspike-and-wave rhythm. Towards the end, serrated waves--i.e. graphoelements typical of SSADs evoked by electrical stimulation of limbic structures--often appeared in the SSAD. A higher stimulation intensity increased the incidence of this complex SSAD. In this group a minimum duration of stimulation was also essential (series of less than 2 s were not reliably effective). When this second type of SSAD ended, depression of ECoG activity was followed in 27% of the cases by a spontaneous recurrent seizure (RS). The ECoG character of these RS can be very variable. The two types of seizures evoked by slow and fast stimulation differ from each other not only in respect of their ECoG pattern (where the difference is probably due to more pronounced propagation to subcortical structures after faster stimulation), but also as regards the presumed mechanism of their onset.