Cerebral Cortex Of Dogs Research Articles

Galvanometric determination of cerebral cortex currents in the area of tone centers in case of irritation of peripheral auditory organs

At the suggestion of the highly respected prof. VM Bekhterev, I began studying the currents in the cerebral cortex in dogs under the influence of peripheral irritations of the auditory organs with tuning fork currents. Even last year, I performed several experiments in this direction with a Wiedemann-d'Arsonval galvanometer in the physical office of the Military Medical Academy of the much-respected prof. N. G. Egorov with the kind assistance of his assistant N. N. Georgievsky, as well as in the physiological office of prof. Pavlova under the leadership of V.I. Vartanov.

Capillary Lesions Develop in Retina Rather Than Cerebral Cortex in Diabetes and Experimental Galactosemia

To isolate microvessels from cerebral cortex of dogs with alloxan-induced diabetes and dogs with experimental galactosemia to compare the prevalence of microvascular lesions in cerebral cortex with that in retina. Microvessels were isolated from cerebral cortex of experimental animals using a sieving method, and compared with the retinal vasculature isolated from the same animals using the trypsin digestion method. Dogs with diabetes or experimental galactosemia of 5 years' duration had retinopathy that was morphologically indistinguishable from that of humans with diabetes, including microaneurysms, acellular capillaries, and pericyte ghosts. These lesions never were seen in cerebral cortical vessels of the same animals. The only morphologic abnormality observed in cerebral capillaries of dogs with diabetes and dogs fed galactose was thickening of basement membrane. Local influences in the eye apparently play an important role in the development of diabetic retinopathy. Current hypotheses about the pathogenesis of the retinopathy do not account adequately for such differences in the tissue distribution of vascular lesions.

L-glutamate and gamma-aminobutyric acid uptake in synaptosomes from the cerebral cortex of dogs with congenital chronic hepatic encephalopathy.

High affinity [3H]gamma-aminobutyric acid (GABA) and [3H]L-glutamate uptake were determined in synaptosomes prepared from the cerebral cortex of dogs with congenital hepatic encephalopathy and control dogs. The Km value for GABA uptake was increased by 35% but there was a concomitant 34% increase in Vmax suggesting that GABA uptake capacity was not changed in HE dogs. In contrast, mean Vmax for glutamate uptake in HE dogs was 85% greater than mean Vmax in control dogs; mean Km was increased by 25% in HE dogs. Therefore, overall synaptosomal high affinity glutamate uptake capacity was increased in HE dogs compared to controls.

An experimental study on spinal cord ischemia during cross-clamping of the thoracic aorta: the monitoring of spinal cord ischemia with motor evoked potential by transcranial stimulation of the cerebral cortex in dogs.

The usefulness of spinal motor evoked potential by transcranial stimulation of the motor cortex (MEPT) in detecting spinal ischemia and predicting postoperative neurological dysfunction was evaluated using a model of spinal ischemia. Group 1 was comprised of 11 dogs used for measuring the basic wave form of spinal MEPT. The normal spinal MEPT response curve consists of two major peaks: peak I and peak II. The latency of peak I and peak II at T13-L1 was 6.0 +/- 0.6 and 7.1 +/- 0.6 msec, and the amplitude, 3.3 +/- 1.6 and 6.1 +/- 2.6 microV, respectively. Group 2 was comprised of six animals subjected to spinal ischemia, in which a time-related deterioration of the MEPT as well as evoked spinal cord potential (ESP) was demonstrated. The time taken until the loss of peak I and peak II was 19.2 +/- 5.3 and 21.7 +/- 6.2 min, respectively, while the time taken until the loss of ESP was 36.7 +/- 14.0 min. In group 3, comprised of seven animals, the aorta was unclamped and the animals were allowed to recover when the spinal MEPT had disappeared. Four had paraparesis immediately after the operation, two had a normal gait, one died, and one developed spastic paraplegia after 24 h. We concluded that the change in spinal MEPT during spinal ischemia occurred earlier than the change in ESP, and that the loss of MEPT suggested irreversible spinal cord damage.

Cerebellar [3H]kainate and [3H]ampa binding in dogs with congenital portosystemic encephalopathy

Abstract Previous studies have indicated that kainate and AMPA receptors are altered in cerebral cortex of dogs with chronic hepatic encephalopathy (HE). To ascertain whether receptors in dog cerebellum are similarly altered in HE [3H]kainate and [3H]α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) binding assays were performed on crude synaptosomal membranes prepared from cerebellar tissue from dogs with congenital portosystemic encephalopathy (PSE) and control dogs. There was no pathophysiologically relevant difference in the affinity or density of kainate or AMPA binding sites in PSE cerebellar tissue compared with control dogs. The failure to demonstrate alterations in these binding parameters in cerebellar tissue was expected as clinical signs of HE reflect cortical rather than cerebellar dysfunction.

Reduced somatostatin-28-(1–12)-like immunoreactivity in cerebral cortex of dogs with an Eck fistula and somatostatin molecular forms in brain

Somatostatin-28-(1–12)-like immunoreactivity (S28(1–12)LI) in brains of Eck fistula dogs, prepared as an experimental model of hepatic encephalopathy, was measured. Significant reductions of S28(1–12)LI were observed in all cortical regions of Eck fistula dogs. The reductions of S28(1–12)LI were significantly correlated with decreases in somatostatin-14-like immunoreactivity (S14LI) in the cortical region. The ratios of S28(1–12)LI to S14LI in all cortical regions were not different between Eck fistula and normal dogs. Additionally, no difference in gel chromatographic profiles of S28(1–12)LI and S14LI was observed between Eck fistula and normal dogs. These results imply that reduced somatostatin immunoreactivity in hepatic encephalopathy may be caused not by altered degradation but by reduced production of prosomatostatin. Our S28(1–12)LI assay system could detect prosomatostatin(1–76) and S28(1–12) and the S14LI system prosomatostatin, S28 and S14. S28(1–12)LI/S14LI ratios in cortex were 0.64–0.83 and these were significantly different from those (1.02–1.36) in thalamus, midbrain and medulla. Relative proportions of prosomatostatin (20%) and S28 (23–24%) in cortex were larger than those (6–7% and 5–7%, respectively) in thalamus, midbrain and medulla. The differential distribution of these molecular forms suggests that processing of prosomatostatin in cortex may be different from that in thalamus, midbrain and medulla.

Changes of synaptosomal energy metabolism induced by hypoxia during aging.

Synaptosomes were isolated from the motor area of the cerebral cortex of normoxic or hypoxic (PaO2 = 17-19 mmHg, for 15 min) beagle dogs of different ages. Synaptosomes were incubated in Krebs-Henseleit-Hepes buffer (for 10 min at 24 degrees C) and the energetic state was defined by: the balance of the labile phosphates (ATP, ADP, AMP, and creatine phosphate); the respiratory rate; the redox state of the intramitochondrial NAD-couple. By the present experimental model, it is possible to evaluate the potential damage (induced by the "in vivo" hypoxic insult) that synaptosomes cannot reverse under optimal incubation. Aging affected the phosphorylation state of the post-hypoxic incubated synaptosomes. The oxygen consumption rate was quite similar in the synaptosomal fractions from the motor area of hypoxic beagle dogs of different ages, but the cytochrome c and a contents were lower in the preparations from hypoxic older brains. In dogs of different ages, hypoxia always lowered the respiration of the synaptosomes, but aging affected the oxygen consumption rates only in post-hypoxic synaptosomes incubated with succinate. The synaptosomal energetic state was defined also by the redox state of the intramitochondrial NAD-couple (delta Gox-red) and the phosphorylation state of adenine nucleotide system (delta GATP). The free-energy change (delta delta G) for the coupled reactions was calculated, too. In synaptosomes isolated from the cerebral cortex of dogs submitted to hypoxia, the equilibrium (calculated for the mitochondrial electron transfer chain and the phosphorylation of adenine nucleotides) was markedly altered as function of aging.(ABSTRACT TRUNCATED AT 250 WORDS)

Posthypoxic changes in the cerebral cortex of dogs in the late recovery period after hypovolemic hypotension for 4 hours

On the 14th–21st day of the recovery period after hypovolemic hypotension lasting 4 h the total RNA level in the tissue of the gray matter of the brain fell by 20.9% and the DNA level by 13%. In the postmitochondrial supernatant the concentration of prealbumins fell by 26.5%, of α-globulins by 19.2%, and of γ-globulins by 59.8%; the concentration of albumins and β-globulins increased by 12.6 and 50% respectively. Activity of acid cathepsins rose by 50% and of acid phosphatase by 44%. Activity of total lactate dehydrogenase (LD) and glutamate dehydrogenase did not differ significantly from the control values. However, the LD isozyme spectrum showed a decrease in LD3+4+5 from 31.9 to 14.2%. Analysis of densitograms of electrophoresis in polyacrylamide gel showed changes in the physiocochemical properties of the protein molecules similar to denaturation in nature. The number of Purkinje cells in the cerebellar cortex was 41.3% below the control level.

Changes in phosphatase and acid cathepsin activity in the cerebral cortex of dogs in terminal states

The activity of acid and alkaline phosphatases and acid cathepsins in subcellular fractions (especially in the postmitochondrial supernatant) of the gray matter of the dog brain rises proportionally to the duration of compression ischemia. The activity of the last two enzymes also rises during clinical death from blood loss preceded by hypotension of varied duration or with different levels of the arterial pressure. Comparison of the changes observed in the specific activity of these enzymes in subcellular fractions of the gray matter indicates the existence of a general mechanism for the activation of proteolysis in nerve tissue in the terminal states investigated.

Cerebral cortical metabolism after chronic exposure to ozone.

This study represents a biochemical survey of cerebral cortex in dogs, in which an increased latency of evoked electroencephalogram EEG potentials of visual cortex had been observed after prolonged exposure to ozone. Portions of occipital and parietal cortex were analyzed from 44 dogs which had been exposed to 1 to 3 ppm O3 for 18 months. Contents of norepinephrine and epinephrine, lipid hydroperoxides, K+, Na+, and Cl- were measured. In addition, the activity of the following enzymes was determined: monoamine oxidase, catechol-O-methyltransferase, cholinesterase, 5’-nu-cleotidase, and Na+, K+, and Mg++ adenosine triphosphatases (ATP’ases). Catechol-O-methyltransferase activity showed a steady decline as the daily exposure to 1 ppm O3 was increased from 8 to 24 hours. Concurrently, the catecholamine content of the tissues declined.

Effects of local pressure on cortical electrical activity and cortical vessels in the dog.

✓ Suppression of the cortical electrical activity and resistance of cortical vessels to collapse were investigated under various pressures applied locally by an inflatable balloon over the cerebral cortex of dogs. The locally applied pressure and the transmitted general intracranial pressure were measured by a special pressure switch. To produce a 50% suppression of the electrical activity required an average of 45.4 mm Hg local pressure; for 100% suppression, an average of 164 mm Hg. Thus, suppression of the cortical electrical activity is proportional to the pressure applied. In separate experiments with transparent cranial windows, collapse of the cortical veins was produced by an average local pressure of 48.5 mm Hg and collapse of the cortical arteries by an average of 188 mm Hg. It is concluded that the cortical electrical activity is suppressed as a result of changes in local blood flow which are in turn a result of local compression and tissue distortion.

Slow potential changes recorded from cerebral cortex of dogs : A. Kamp, A. J. van Rijn, and J. M. Zwart (Utretch, The Netherlands)

Slow potential changes recorded from cerebral cortex of dogs : A. Kamp, A. J. van Rijn, and J. M. Zwart (Utretch, The Netherlands)

Resting Saliva of Men as a Reflex

This chapter discusses experimental studies focusing on resting saliva of humans as a reflex. Artificial conditioned reflexes, positive, as well as negative, can be established by Pavlov's method in humans in the same way as in dogs, even though humans have resting saliva. The resting saliva must be a reflex saliva, of which the receptor stimulation is a special mechanical stimulus due to the attachment of a suction cup, and of which the reflex center was situated at the gyrus coronarius in the cerebral cortex of dogs. Calculation of the amount of established conditioned saliva can be obtained by subtracting the resting one measured before and after the experiments. The positive, as well as negative, conditioned salivary reflex in humans could be established in the same way as in dogs. Intravenously injected vitamin B 1 augmented the positive conditioned saliva and reduced the negative one; on the contrary, γ-amino-β-hydroxy-butyric acid (GABOB) and vitamin B 6 reduced the positivity and enhanced the negativity in the conditioned salivary reflex. It is concluded that the inhibition in the conditioned reflexes is due to the increasing inhibitory chemical transmitter in the synapse of nerve cells concerned in the formation of the conditioned reflexes. The increase in the chemical transmitters should be due to the enhanced activities of enzyme systems at the site of synapses.

Electromyographic effects of stimulation of the motor points of the cerebral cortex in dogs after hemisection of the spinal cord

Electromyographic effects of stimulation of the motor points of the cerebral cortex in dogs after hemisection of the spinal cord

Measurement of blood flow in the cerebral cortex of dogs, by the clearance of krypton-85.

Measurement of blood flow in the cerebral cortex of dogs, by the clearance of krypton-85.

Changes in the bioelectrical activity in various areas of the cerebral cortex in dogs, during the formation of a temporary connection

Under the combined effect of two stimuli (non-rhythmic light and passive raising of the forelimb), a considerable change occurred in the character of the bioelectric activity in various cortical areas.

Recurrent inhibition in cerebral cortex.

RECURRENT inhibition via interneurones (Renshaw cells) was recently invoked by Brooks and Wilson1 to account for changes in monosynaptic spinal reflexes following antidromic activation. This mechanism, which confines stretch reflexes to their paths of afferent origin, operates through a cholinergic synapse between the motoneurone axon collateral and the Renshaw cell2, which liberates an unknown inhibitory transmitter. Presumably the same mechanism functions with respect to disynaptic pathways through the cord. The purpose of this communication is to describe an analogous system in the cerebral cortex of dogs, operated under ether and immobilized by succinylcholine.

痙攣時における犬大脳皮質の各種電解質の変動に関する実験的研究

痙攣時における犬大脳皮質の各種電解質の変動に関する実験的研究

CORTICAL MASTICATION AND ITS EFFERENT PATHWAY IN DOGS

1. In the cerebral cortex of dog, there was an area which produces mastication through (appropriate) electrical or chemical stimulation. The extension of the area covers gyrus coronarius, ectosylvius anterior, compositus anterior and con-nected through operculum to gyros hippocampi.2. The above area was a part of the area which produces clonic convulsion, so that, there would be located the motor cells of mastication and at the same time the motor cells of clonic convulsion.3. The representation of mastication was physiologically divided into two, the one was the area covered gyrus coronarius, ectosylvius anterior, compositus anterior, which initiated the cortical mastication, and the other was operculum and gyrus hippocampi, which initiated the mastication through the former area. If the former area would be thought to correspond with the motor area for clonic con-vulsion, the latter would correspond to the extramotor area of it.4. The cortical mastication which was initiated from the motor area descends a pathway to homolateral ventral nucleus of thalamus, within which there is first relay cells. From thalamus it passes to the contralateral rostral outer part in the substantia reticularis of midbrain, which is the executing center of mastica-tion connected as a bilateral functional level. From where the third neurone descends to the motor nuclei of the trigeminal and hypoglosal.5. Thus the efferent pathway of the cortical mastication had at least three relay till the cranial motor nuclei, so that, this system must be considered as a system of the extrapyramidal motor systems, with which the relation of voluntary move-ment was discussed in the text.

Blood pressure changes in response to electrical and chemical (acetylbetamethylcholine) stimulation of the cerebral cortex in dogs: Kremer, W. F.: Am. J. Physiol. 152:314 (Feb.), 1948

Blood pressure changes in response to electrical and chemical (acetylbetamethylcholine) stimulation of the cerebral cortex in dogs: Kremer, W. F.: Am. J. Physiol. 152:314 (Feb.), 1948