Number Density Of Neurons Research Articles

Morphofunctional Changes in Neurons, Glial Cells and Synapses in the Sensorimotor Cortex after Severe Traumatic Brain Injury

The aim of the study was to investigate morphofunctional modifications in neurons, glial cells and synaptic terminals in the sensorimotor cortex of the brain in rats after severe traumatic brain injury (STBI).Material and methods. STBI simulation in white rats (main group, n=30) was performed on a device with a special shock mechanism. Intact animals (n=6) were included in the control group. The sensorimotor cortex (SMC) of the brain in rats was studied histomorphologically on sections stained with hematoxylin and eosin and thionin according to Nissl. Synaptophysin and GFAP were detected immunohistochemically, then morphometry was performed. On serial frontal sections of the SMC, neurons, neuroglia, and interneuronal synapses were studied in animals of the control group and in animals exposed to STBI in 1, 3, 7, 14, and 30 days after STBI simulation. The number density of neurons, neuroglia, and synaptic terminals was determined per a unit area of the section of layers I (terminals only), III, and V of the cerebral SMC. Statistical hypotheses were tested using nonparametric methods in the Statistica 10.0 program.Results. In animals of the control group, typical normochromic pyramidal neurons predominated, synaptic terminals were clearly verified; this was combined with unaltered neuropil. In animals exposed to STBI, there were signs of tinctorial, hydropic, dehydration and necrobiotic changes in neurons, reactive astrogliosis, fields of "loss" of neurons appeared; the overall numerical density of neurons and synapses decreased. The maximally increased content of pycnomorphic neurons was detected in 1 day after STBI (in layer III of the SMC, by 11.6%; in layer V of the SMC, by 18.5%). The peak in the number density of shadow cells and hyperchromic non-wrinkled neurons was noted in 3 days. The numerical density of synaptic terminals in different layers of the SMC decreased by 1.5-2 times. The altered balance of the destruction and restoration processes of the synaptic pool after STBI was evidenced by statistically significant data on the decreased and increased numerical density of terminals during 30 days of the study. There was no complete recovery of the studied parameters of neurons and synapses to control values within 30 days.Conclusion. The SMC of the brain in rats remains functioning after STBI; this occurs in the context of long-term preservation of reversibly and irreversibly damaged neurons, reactive neurogliosis, and permanent reorganization of interneuronal relationships due to activated reparative neuro- and synaptic plasticity. The data obtained will specify reorganization of the components of various neuronal complexes of the SMC (layers I, III, and V) after STBI.

Morphofunctional Characteristics of the Hippocampus of White Rats in the Acute Period After Severe Traumatic Brain Injury During the Use of L-lysine Aescinat

Aim of study. The study is devoted to the effect of L-lysine aescinat on the nervous tissue of the CA1 and CA3 fields of the hippocampus of the brain of white rats in the acute period after severe traumatic brain injury (TBI).Material and methods. TBI was simulated by applying a blow to the parieto-occipital region with a freely falling weight weighing 200-250 grams from a height of 50 cm using a special rail rack. The objectives of the study were: 1) comparative morphometric assessment of the degree of hydration, cyto- and glioarchitectonics of different layers of CA1 and CA3 fields after ischemia without treatment; 2) the effect of L-lysine aescinat on these indicators. We used histological (staining of sections with hematoxylin-eosin and Nissl), immunohistochemical (for NSE, MAP-2 and GFAP) and morphometric methods. On thin (4 μm) serial frontal sections of the hippocampus, neurons, astrocytes, microvessels and neuropiles were studied in control (intact animals, n=5) and 1 and 3 days after injury without treatment (n=10, comparison group) and with treatment ( n = 10, main group). The number density of neurons was determined using the Nissl staining of cells and by the reaction to NSE. The cytoskeleton of neurons was studied by detecting MAP-2, and astroglia by GFAP. On color raster images (staining with hematoxylin and eosin, x100) using the Find Maxima plug-in filter, the zones of maximum brightness were determined, which were then analyzed using Analyze Particles from the ImageJ 1.52s program. Zones of maximum brightness corresponded to areas of the hippocampus with a high degree of hydration of the nervous tissue - edema-swelling. The nature of the distribution, statistical hypotheses, and plotting were checked using Statistica 8.0 software and R environment.Results. In control animals, normochromic neurons without signs of changes in the cytoskeleton prevailed in all layers of fields CA1 and CA3, and a low degree of hydration of the nervous tissue was noted (the relative proportion of zones of maximum brightness was 5–8%). One and 3 days after TBI, there was a statistically significant increase in the focal content of dystrophic and necrobiotically altered neurons (95% confidence interval: 52–78%), manifestations of reactive gliosis were noted, and the proportion of zones of maximum brightness increased to 16%. Statistically significant layer-by-layer differences were revealed between the CA1 and CA3 fields of the hippocampus. The use of L-lysine aescinat had a statistically significant effect on the morphometric parameters of the nervous tissue of the hippocampus.Conclusion. In the early post-traumatic period after TBI, the degree of hydration of the nervous tissue of the hippocampus increased. Heteromorphicity of dystrophic and necrobiotic changes in different layers of CA1 and CA3 fields was noted. L-lysine aescinate had a statistically significant positive effect on these changes. To a greater extent, this is typical for the CA3 field. The revealed changes are considered not only as patho-, but also as sanogenetic structural mechanisms of protection and reorganization of the hippocampus in the acute post-traumatic period.1. In the acute period (1−3 days) after severe traumatic brain injury, the degree of hydration of all components of the hippocampal nervous tissue increased. In the group without treatment, 3 days after injury, the relative volume of edema-swelling zones varied from 10 to 13% in CA1 (control 3-7%) and from 8 to 16% in CA3 (control 5–10%).2. The heteromorphism of hydropic changes in the molecular layer, the layer of pyramidal neurons and the polymorphic layer was established. The maximum increase in the volume of free water (more than twofold) was characteristic of the molecular and polymorphic layer CA1, as well as the polymorphic layer CA3.3. The use of L-lysine aescinat in the acute period significantly changed the manifestations of hydropic dystrophy. One day after injury, the volume of free water increased in comparison with animals without treatment, and then, after 3 days, decreased, but remained higher than in the comparison group. The maximum effect of the drug was noted in field CA3.

Comparative Characteristics of Structural and Functional Changes in the Hippocampal CA<sub>3</sub> Region in White Rats After Acute Ischemia and Brain Injury

The aimof the study was to study pyramidal neurons and astrocytes of the hippocampal CA3region in dynamics in white rats after acute ischemia and severe traumatic brain injury.Material and methods.Acute ischemia was simulated by 20-minute occlusion of the common carotid arteries (CCA), and severe traumatic brain injury (TBI) by a free-falling weight impact. The Nissl staining, hematoxylin and eosin staining, immunohistochemical reactions for NSE, MAP-2, p38, GFAP were used in the study. The proliferative activity of the cells was assessed using the Ki-67 response. The study was carried out on thin (4 μm) serial frontal sections in the animals of the control group (animals without pathological factors, n=5) in 1, 3, 7 and 14 days after the experimental modeling of CCA occlusion (n=20) and TBI (n=20). Morphometric analysis was performed using the ImageJ 1.52s software. The relative area of edema-swelling zones in the neuropil, the number density of pyramidal neurons, the content of dystrophic and necrobiotically altered neurons, the content of neurons with one or more nucleoli, proliferating cells, the density of large trunks of pyramidal neurons dendrites, the total number density and the relative area of giant synaptic terminals in stratum lucidum was detected. The distribution of variation series, the verification of statistical hypotheses, and the construction of graphs were assessed using the Statistica 8.0 software and the R.Results.Mortality between groups did not differ and did not exceed 7%. In a day after CCA occlusion and TBI, there was a statistically significant increase in the relative volume of edema-swelling, the content of dystrophic and necrobiotically altered neurons, the total number density and the relative area of the terminals decreased, but the total number density of neurons did not change. In 3, 7 and 14 days, the mechanisms of neuroglio- and synaptic plasticity were activated. The content of neurons with two or more nucleoli increased, the total number and content of hypertrophied astrocytes increased, the cytoskeleton of damaged neurons was restored, and the content of interneuronal synapses increased. During the period from 3 to 14 days, the total number density of neurons in CCA occlusion decreased by 16.3%, and in TBI – by 33.7% (p=0.001). Pathological and compensatory-restorative changes were of a diffuse-focal nature and were more pronounced after TBI.Conclusion.Thus, the same type of focal heterochronous and heteromorphic dystrophic, necrobiotic and compensatory-restorative changes in the nervous tissue were observed after CCA occlusion and TBI in the hippocampal CA3region. Structural and functional recovery occurred together with a decrease in the total numerical density of pyramidal neurons and edema-swelling of the nervous tissue. More pronounced dystrophic and necrobiotic changes in TBI were combined with more pronounced compensatory-restorative changes in astrocytes and giant interneuronal synapses of the hippocampal CA3region. The revealed changes were considered as the basis for the standard permanent compensatory-restorative reorganization of the nervous tissue of the hippocampus in the postischemic and post-traumatic periods.

Number of Brain States in an N-Body Dynamical Scenario According to the Universal Bekenstein Entropy Bound.

There is an intense interest in the modulation of brain neural circuits and its correlations with different behavioral states, memory, learning, as well as neuropsychological disorders. It is believed that brain cells form functional circuits, process information and mediate behavior. Therefore, the brain system may be thought of as a super-computing machine that turns information into thoughts, memories, and cognitions. Moreover, according to the quantum brain dynamics and quantum conscience hypotheses, quantum theory, the most fundamental theory of matter, may help explain the function of the brain. In the intersection of the architecture of the brain's biological substrate, the processing of information and entropy (as a measure of information processing capacity), and the generation of input to this system (either externally or internally), one may expect to find the foundations of cognition and behavior as an emergent phenomenon. In this chapter, we calculate the entropy Bekenstein bound of the brain, and from that the number of information N in bits that is required to describe the brain down to its tiniest detail. Furthermore, we define the quantity cmbRb as brain quantum of action b. Next, we estimate the possible number of states b in the human brain as related to the number of information bits N. Furthermore, we derive an expression for the kinetic energy of a pair of neurons as a function of brain temperature T, the number of information N in bits, and the neuron mass mn as well as the number density of neurons n. We introduce the conjecture that the time rate of r(t) might represent the velocity at which a pair of neurons can approach or recede from each other upon experiencing a transfer of N number of information bits.

The effect of prenatal and postnatal diminishing of litter number on some parameters of rat brain development in milk period of ontogenesis

The authors studied the brain of 14 day old rats born in diminished by number litters (n=7,7±0,7), received from mating females having been exposed to the removal of right uterine horn (1,5 month before mating) and a day after delivery – with litter diminishing up to 5-6. The control group included rats from the litters with an average amount 10,8±1,1, which were off spring from intact males and females. At the age of 14-days experimental animals had a higher body mass, and adrenals mass (P<0,05), and testes (P>0,05) than the control group. Their brain and cerebral hemispheres had increased mass. The thickness of cortex and parietal lobe proper layer I did not show any reliable diff erences between the groups. Number density of neurons in layer II and V in the experimental rats was decreased, the size of cytoplasm of hippo-campus neurons and nucleoli in the neuron layer II PLP were reliably increased compared to the control group. The obtained data confi rm than diminished number of animals in a litter in the prenatal and early postnatal periods odontogenesis is refl ected on the parameters of brain development. At the same time, the diff erences with the control are of the same type and are more pronounced than when the number of animals in a litter is decreased straight after birth.

Neuron density in the hippocampus in rat strains with contrasting nervous system excitability after prolonged emotional-pain stress

A model system consisting of two rat strains bred for nervous system excitability in response to electric shocks was used to study changes in the number density of neurons in hippocampal field CA3 at 24 h, two weeks, and two and six months after prolonged emotional-pain stress (PEPS). Neuron density in hippocampal field CA3 decreased after completion of PEPS. These changes arose at different time points in the different rat strains (one day for low-excitability rats, two months for high-excitability rats) and persisted to six months. Thus, this is the first demonstration that persistent differential effects of stress on the number density of neurons in hippocampal field CA3, which plays an important role in learning and memory processes, depend on genetically determined constitutive characteristics of the nervous system.