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Biomedical subjects

J Bures

Publications and source records attributed to J Bures.

At least 145 records · Page 8Linked to original sources
PubMed1989

Brain transplants enhance rather than reduce the impairment of spatial memory and olfaction in bulbectomized rats.

The possibility to compensate the loss of olfactory and non-olfactory functions due to removal of the olfactory bulb by embryonal brain grafts was investigated in adult rats. Spatial working memory was examined in an 8-arm radial water maze task 6 weeks after bulbectomy. During 15 daily trials, performance gradually improved in bulbectomized controls (n = 10) and in rats with olfactory bulb transplants (n = 9), but did not attain that of intact controls (n = 10). No improvement was observed in the rats with substantia nigra grafts (n = 8). Eleven weeks after bulbectomy, the same rats were tested in the water tank navigation task. The performance improved during ten 12-trial sessions in bulbectomized rats less than in intact controls, but more than in the transplanted rats. The olfactory food retrieval test performed 14 weeks after bulbectomy revealed almost full recovery of smell in bulbectomized rats, but not in the transplanted animals. It is concluded that the spatial memory deficit is probably due to bulbectomy-induced interference with septohippocampal function which is not alleviated, but rather enhanced by transplantation. The results suggest that the effect of brain grafting is not always beneficial.

Animals↗
PubMed1989

Activity of cortical and caudatal neurons accompanying instrumental prolongation of the extension phase of reaching in rats.

Activity of 38 cortical and 59 caudatal neurons was examined in 11 rats trained to push, with one forepaw, a hinged vertical partition accessible through a narrow horizontal tube. The rats had to overcome blockade of the operandum lasting from 0 to 130 ms. Periresponse histograms (+/- 512 ms around the onset of a series of reaching movements) showed that reach-related phasic and series-related tonic excitation prevailed in motor cortex and caudate nucleus, respectively, while inhibitory activity changes did not differ between the two structures. Perireach histograms (+/- 196 ms around onset of successful or unsuccessful displacements of locked or free operandum) showed that excitation of cortical neurons was related to amplitude and duration of the extension but no significant activity peaks corresponded to the sudden release of the movement blockage. Similar, but less expressed, changes were found in caudate neurons. It is concluded that the rats learned to prolong the extension phase of reaching but that the movement continued to be preprogrammed and independent of proprioceptive or other sensory feedback.

Animals↗
PubMed1989

Conditioned taste aversion elicited by intracerebral administration of drugs.

Conditioned taste aversion (CTA) is a vital adaptive reaction governed by highly reliable but poorly understood central mechanisms. In an attempt to elucidate the site of action of various CTA eliciting drugs, equipotent dosages were applied by the systemic (i.p.) and intracerebral (i.c.) route. Rats were offered water on days 1 and 2. On day 3 they received 0.1% sodium saccharin (CS) followed by pentobarbital anaesthesia and i.p. or i.c. injection of the drug (US). After water on day 4, the rats were allowed to choose between water and saccharin on day 5. The putative central action of amphetamine was not confirmed by this experimental arrangement, since CTA was evoked by only moderately (about 10 times) lower i.c. than i.p. dosages. Similar ratio of the i.c. to i.p. effective dosages was obtained with carbachol. On the other hand, CTA of clearly central origin was caused by harmaline and by other monoamine oxidase inhibitors, pargyline and clorgyline, which elicited comparable aversion using 500, 400 and 250 times lower i.c. than i.p. dosages, respectively. The intracerebral gradient of the effect pointed to the lower medulla (inferior olive, raphe nuclei) as the critical brain region and to serotonin as the transmitter participating in the aversive labeling of the gustatory stimulus. The CTA-forming mechanism can also be studied by analysing the action of drugs, e.g. convulsants, which do not produce CTA even when applied at highly toxic dosages (LD 50) eliciting long lasting convulsions (picrotoxin, 5 mg/kg; bicuculline, 5 mg/kg). It is concluded that comparison of brain events elicited by drugs which can or cannot serve as unconditioned stimuli in the CTA paradigm may substantially contribute to the exploration of the underlying neural mechanisms.

Animals↗
PubMed1988

Licking during forced spout alternation in rats: resetting the pacemaker or disconnecting the motor output?

Rats trained to alternate between two adjacent drinking spouts (each spout is retracted after a single lick and presented again after the animal has licked at the other spout) emit 2.5 licks instead of the optimum 1 lick per spout presentation. The question whether the pacemaker of licking is reset or continues to run during transition between spouts was addressed in three experiments performed in 10 highly overtrained rats. Videorecording analysis of oro-facial activities showed that the rat's mouth was firmly closed during the 500 ms transition between spouts. EEG was recorded from the region of hypoglossal nucleus with implanted bipolar electrodes during continued licking at one spout and during spout alternation. Averaging (n = 256, 1024 ms) centered around the onset of the first lick at the newly contacted spout showed 2-3 lick related potentials in the post-transitional interval whereas only one such wave occasionally appeared at the end of the pre-transition period. Computer plotted distributions of post-transition licks (timed with respect to the last pre-transition lick) were examined while the horizontal or vertical distance between spouts was increased. Growing spout separation changed the height but not the timing of the modes of the post-transition lick distribution. This phase-locked synchronization of pre- and post-transition licks indicates that the central timing network of the lick generator is not reset but continues to run during transition between spouts and that the cessation of tongue movements is due to inhibition of the intracycle pattern generator and motor output.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1988

Differential effect of prior paradoxical sleep deprivation on conditioned taste aversion, neophobia and attenuation of neophobia to solid food in rats.

The effect of paradoxical sleep deprivation (PSD) on subsequent acquisition of conditioned taste aversion (CTA) to liquid diets is confounded by the uncertain level of thirst when using the water tank procedure. This difficulty is eliminated when examining CTA and attenuation of neophobia (AN) to solid diets. Adult male rats (n = 100) were habituated to receive their daily ration of food during a 30-min stay in a box equipped with a row of 10 feeders baited with 2-3 g pieces of moist standard diet. 24-h PSD increased neophobic rejection of novel sweet food (with added 5% saccharose), but did not influence intensity of CTA elicited by LiCl poisoning. Addition of a bitter tasting red food dye to the sweet food caused marked neophobia which was enhanced by preceding PSD. Association of this unpalatable food with LiCl elicited strong CTA which extinguished faster in the PSD-pretreated animals. On the other hand, preacquisition PSD did not influence AN to the same stimulus. Sweet food with added blue dye elicited only mild neophobia which was enhanced by preceding 24-h PSD. Preacquisition PSD did not influence AN but significantly increased CTA to blue sweet food. It is concluded that PSD can either enhance or weaken CTA and that this complex effect on food selection learning cannot be explained by PSD-induced reduction of fear.

Animals↗
PubMed1988

Functional ablation of the olfactory bulb by spreading depression: unit activity changes and transient anosmia.

Cortical spreading depression (SD) is widely used to induce functional decortication. Development of a reliable technique for eliciting SD in the olfactory bulb (OB) of rats makes it possible to achieve functional elimination of the first relay of the olfactory pathway. In order to assess the unit activity changes accompanying OBSD, adult male hooded rats (n = 31) were anesthetized with pentobarbital and activity of OB units was recorded with carbon fiber microelectrodes. The predepression activity (12.7 +/- 0.8 Hz) increased up to 35.1 +/- 4.1 Hz during the burst which attained maximum 44 +/- 6 sec after K+ acetate injection and corresponded to the steep depolarization phase of SD slow potential. The burst lasted 20.4 +/- 2.9 sec on the average and was followed by 187 +/- 20 sec of complete silence. Gradual recovery to the predepression level lasted 229 +/- 27 sec. Activity of most units (63%) in the contralateral OB was not changed. Significant reactions of OB neurons to ipsilateral cortical SD found in 57% units were mostly inhibitory (49%). OBSD-induced anosmia was examined in a group of rats (n = 8) with unilateral bulbectomy and a guiding tube implanted into the remaining OB for microinjection of K+ acetate. One week after surgery, the animals were examined in the food-retrieval olfactory test. The microinjection of K+ acetate severely disrupted the food finding behavior in 60% rats during 3-min test. Both electrophysiological and behavioral results indicate that OBSD is a convenient tool for inducing short-lasting anosmia.

Action Potentials↗
PubMed1988

Does nondirectional signalization of target distance contribute to navigation in the Morris water maze?

The possibility that rats can navigate in the Morris water maze by reducing the difference between the memorized platform scene and the current sensory input was tested in nine blind rats. A computerized videosystem monitored the rats' movements in the pool and converted the rat-target distance into tones the frequency of which increased in 64 equal steps from 120 Hz at 128 cm to 7680 Hz at 0 cm. During 15 days of training to find a fixed platform position from different starting points (12 trials per day) average escape latencies decreased from 39.0 to 25.4 s. The performance significantly deteriorated when the acoustic distance signalization was omitted and/or when the target position was changed form trial to trial. It is concluded that blind rats solved the task by simultaneously employing search strategy based on position responses, mapping using acoustic background beacons, and distance reduction navigation. It is argued that the various strategies are additive and that their relative significance depends of the conditions of the experiment.

Acoustic Stimulation↗
PubMed1988

Changes of cortical and caudatal unit activity accompanying operant slowing of the extension phase of reaching in rats.

Activity of neurons in the motor cortex (n = 36) and caudate nucleus (n = 72) was studied in 7 rats trained to slow down reaching into a narrow horizontal tube equipped with an axially moving piston. Overtrained rats succeeded in obtaining reward by reducing extension velocity of 30 to 60% reaches below 50% of the normal value. The difficulty of the task was reflected in the amplitude of perireach histograms which showed peaks and troughs corresponding to the main phases of the movement. Perireach distributions of excitatory and inhibitory unit reactions were similar in the contralateral motor cortex and caudate nucleus of trained rats, but the inhibitory responses started later and were shorter lasting than during standard reaching in naive animals. It is suggested that the task requires tight cortical control of the postural and local movement components manifested by synchronous activation of caudatal and cortical neuronal populations.

Animals↗
PubMed1988

Functional recovery after olfactory bulbectomy in rats: effect of embryonal brain grafts.

Regeneration of olfactory receptor neurones after bulbectomy can lead to formation of extrabulbar synapses, the functional significance of which remains controversial. Adult hooded rats (n = 27) were bilaterally bulbectomized under pentobarbital anaesthesia. Small pieces of brain tissues (1-2 mm3; OB: olfactory bulb; St: corpus striatum) were obtained from embryos of the same strain and placed into the bulbectomy-produced cavity in contact with the exposed brain surface. Smell was tested at 2- to 3-week intervals from 7 weeks to 7 months after the operation. The latency to find hidden food gradually improved and attained the intact control level in bulbectomized rats without grafts, but remained poor in the OB and St transplanted groups. Seven to ten months after transplantation, spontaneous unit activity and unit reactions to amyl acetate vapours were examined with a carbon fibre microelectrode. Unit responses in the transplants resembled those in the normal OB, but were less pronounced. Morphological examination of the transplant and of its connections with the olfactory receptor neurones and with the host brain suggested that functional recovery was mediated by the connections of the olfactory axons with the remnants of the OB, with the anterior olfactory nucleus and/or with the frontal cortex. The adverse effect of OB and St transplants was probably due to their poor connectivity with the host brain which prevented the regenerating olfactory axons from reaching higher olfactory centres.

Analysis of Variance↗
PubMed1987

Systemic ketamine blocks cortical spreading depression but does not delay the onset of terminal anoxic depolarization in rats.

Ketamine (KET)-induced blockade of cortical spreading depression (CSD) was examined in rats (n = 51) anesthetized with pentobarbital (50 mg/kg). CSD was elicited by intracortical injection of 1 microliter of 0.15 mol/l potassium acetate 10-40 min after i.p. injection of 6-50 mg/kg KET. KET was almost ineffective at 6 mg/kg but prevented CSD propagation at 12 mg/kg and at higher dosages. The blockade was maximal 20 min after injection. Terminal anoxic depolarization elicited by N2 breathing developed in control rats after a latency which was not significantly different from that in rats pretreated with 50 and 100 mg/kg KET. The failure of CSD blocking dosages of KET to delay the onset of terminal anoxic depolarization indicates that excitotoxic amino acids play different roles in the mechanism of the anoxia-elicited and CSD-related autoregenerative ionic shifts.

Animals↗
PubMed1987

Functional and metabolic correlates of long series of cortical spreading depression waves in rats.

Repetitive generation of spreading depression (SD) waves may induce metabolic and functional disturbances in the invaded brain regions. In order to better characterize this state, up to 60 SD waves were elicited in the cerebral cortex of anesthetized rats by intracortical injections of 2 microliters of isotonic K-acetate repeated at regular 5-min intervals. Propagation rate of SD between capillary electrodes located 1 mm and 7 mm from the injection site gradually decreased and after 35-45 waves became irregular. In another series of experiments SD-induced changes of cyclic adenosine monophosphate (cAMP) level were examined after 24 SD waves. Although no irregularities of SD propagation were observed, maximum level of cAMP in the SD-invaded cortex decreased from 270% in controls to 170% after 24 waves. Also, the recovery of the nucleotide was slowed down. Metabolic alterations thus preceded irregularities in SD propagation.

Acetates↗
PubMed1987

Conditioned taste aversion induced in rats by intracerebral or systemic administration of monoamine oxidase inhibitors.

Conditioned taste aversion (CTA) elicited by systemic or intracerebral application of the monoamine oxidase inhibitors clorgyline (C), pargyline (P) or deprenyl (D) was studied in 402 rats. Water-deprived animals were allowed 15 min access to 0.1% sodium saccharin (CS) followed 10 min later by IP or by intracerebral injection of the drug. In the latter case, the animals were anesthetized 5 min after saccharin drinking with pentobarbital and the drug was stereotaxically injected (1 microliter/min, 1-2 microliters) into the target structure. CTA was assessed in a two-choice retention test performed 2 days later. A geometric progression of three to six dosages applied to groups of rats (n = 10) was employed to establish the effective doses of the drugs which were 4, 20 and 32 mg/kg with IP and 2.5, 10 and 80 micrograms per rat with intracerebral (n. raphé magnus) injections of C, P, and D, respectively. The ratios of intracerebral to systemic dosages eliciting comparable CTA were 1:300 for C, 1:800 for P and 1:100 for D. Injections of 2.5 micrograms C and 10 micrograms P into the mesencephalic reticular formation, medial hypothalamus and cerebral cortex were ineffective, as were injections of 10 micrograms P into the nucleus of the solitary tract and cerebellum. The results indicate that CTA is elicited more efficiently by inhibition of monoamine oxidase A (selectively inhibited by C) than of monoamine oxidase B (selectively inhibited by D).

Animals↗
PubMed1987

Inefficient licking during forced spout alternation in rats: violation of the law of effect?

The efficiency of the neural control of licking was assessed in rats (n = 6) allowed 30-min daily access to water in a box equipped with two retractable drinking spouts. After completion of a photoelectrically monitored lick, the contacted spout was withdrawn by an electromechanical device which simultaneously made the other spout available at an adjacent wall opening. Although economy of behavior required the animals to lick at each spout only once, computer monitored licking showed that the rats emitted 2.9 +/- 0.2 and 2.5 +/- 0.1 licks per spout presentation (LPSP) on the first and fifth days of training, respectively. The transition time between spouts and the interlick interval were not significantly changed. Separation of the spouts by a vertical partition extending 24 mm into the box prolonged the transition time and increased LPSP to 3.9 and 3.3 on Days 1 and 4 of training, respectively. These values were not changed when the length of the partition was increased to 40 mm. The failure of rats to maximize reward by emitting single licks probably reflects limited control of the generator of licking and/or the tendency to avoid its frequent switching on and off.

Adaptation, Psychological↗
PubMed1987

Spreading depression in the olfactory bulb of rats: reliable initiation and boundaries of propagation.

Spreading depression in the olfactory bulb of rats is an elusive phenomenon, the demonstration of which requires specific conditioning procedures. The present paper describes a simple technique for reliable initiation of bulbar spreading depression with microinjections of potassium acetate. Adult hooded rats were anesthetized with pentobarbital (50 mg/kg) and slow potential changes accompanying spreading depression were recorded with capillary microelectrodes stereotaxically inserted into the olfactory bulb and adjacent forebrain structures. KCl microinjection (0.5-1.0 microliter, 0.134-0.670 mol/l) into the olfactory bulb elicited local depolarization which only exceptionally developed into a propagating spreading depression. Potassium acetate (0.5-1.0 microliter, 0.15 mol/l) injected into the rostral olfactory bulb evoked a negative slow potential wave (amplitude of around 25 mV and duration 30-50 s) propagating at a rate of 3-4 mm/min through all the olfactory bulb layers. Low positive (5 mV) instead of negative waves were recorded in the superficial olfactory nerve layer with reversal in the glomerular layer (200-300 micron). The slow potential decreased in the rostrocaudal direction and expired at the caudal boundary of the olfactory bulb. Bulbar spreading depression never spread to neocortex, and cortical spreading depression never entered into the olfactory bulb but stopped in the anterior olfactory nucleus 7 mm rostral to bregma. Repeated potassium acetate injections into the olfactory bulb occasionally elicited a series of spreading depression waves recurring at regular intervals, probably reflecting reverberation of scroll-shaped waves around the rostrocaudal axis of the olfactory bulb.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Terminal anoxic depolarization proceeds more slowly in the olfactory bulb than in the cerebral cortex of rats.

The time course of terminal anoxic depolarization and of the concomitant [K+]e increase was compared in the cerebral cortex and olfactory bulb of rats anesthetized with pentobarbital. Respiration arrest elicited by (+)-tubocurarine induced a negative slow potential shift which reached 50% of maximum after 90 s in the cortex and after 180 s in the olfactory bulb (n = 10). Bulbar [K+]e increased slowly to 16 mmol/l, then more rapidly to 40 60 mmol/l and reached 90 mmol/l after 10 min asphyxia (n = 10). While the resting and maximal [K+]e levels were the same in the cortex and olfactory bulb, the fast [K+]e rise started in the olfactory bulb at a higher level (16 mmol/l) and proceeded at a slower rate (doubling time 14 s) than in the cortex, where the same values were 11 mmol/l and 5 s, respectively. It is argued that the olfactory bulb resistance to asphyxia is due to a powerful GABAergic inhibition which counteracts the autoregenerative ionic shift and accounts for the absence of spreading depression in this structure.

Animals↗