First report of the histopathological effect of electrocautery using on the urethral taste rosea during glans penis injury by incision in rabbits.

Objective: Currently, electrocautery devices have frequently been used in penile surgical procedures. We hypothesized that electrocautery using during penile surgical procedures may harm the taste rosea and the dorsal nerve of the penis or clitoris. Methods: Eighteen young age male New Zealand rabbits were studied: five in the control (Group I, n=5), five in the penile surgery without using electrocautery (sham group, Group II, n=5), eight in the monopolar cautery (study group, Group III, n=8) groups under general anesthesia. The animals were followed for 3 weeks and sacrificed. Penile tissue-pudendal nerve root complexes and dorsal root ganglion of sacral 3 level were examined using stereological methods. The results were compared statistically. Results: The live and degenerated taste bud-like structures and degenerated neuron densities of pudendal ganglia (mean±standard deviation, n/mm3) were estimated as 198±24/mm3, 4±1/mm3, and 5±1/mm3 in Group I; 8±3/mm3, 174±21/mm3, and 24±7/mm3 in Group II; and 21±5/mm3, 137±14/mm3, and 95±12/mm3 in Group III, respectively. Neurodegeneration of taste buds and pudendal ganglia was significantly different between groups. Conclusion: Intact spinal cord and normal parasympathetic and thoracolumbar sympathetic networks are crucial for human sexual function. The present study indicates that the glans penis injury by using electrocautery may lead to pudendal ganglia degeneration. Iatrogenic damage to taste rosea and retrograde degeneration of the pudendal nerve may be the cause of sexual dysfunction responsible mechanism.

New Evidence for Regulatory Role of Trigeminal Ganglion on the Intraocular Pressure Following Subarachnoid Hemorrhage.

BACKGROUND: Increased intraocular pressure (IOP) likely secondary to an activated oculo-trigeminal reflex network is an important issue following subarachnoid hemorrhage (SAH). The relationship between the IOP and trigeminal ganglion (TGG) following experimental SAH was investigated in this study. METHODS: Twenty-three rabbits were used in this study. Five rabbits (n = 5) were used as the control group, another 5 as the sham group (n = 5), and the remaining 13 (n = 13) as the study group. The study group was further divided into two groups of animals with mild (n = 6) and severe (n = 7) TGG degeneration. The IOP values were recorded. After 2 weeks, the animals were decapitated. The mean degenerated neuron density of TGGs was estimated by stereological methods and analyzed statistically. RESULTS: The average IOP values were 11.85, 14.12, and 21.45 mm Hg in the control (n = 5), sham (n = 5), and study (n = 13) groups, respectively. The mean degenerated neuron density was 34, 237, and 3,165 mm3 in the control, sham, and study groups, respectively. CONCLUSION: According to the findings of this study, the experimental SAH leads to changes in IOP by affecting the TGG. By predicting and preventing IOP elevation in the setting of SAH, our findings will shed light on secondary sequelae such as glaucoma and irreversible blindness.

Overlooked evidence for transmission deficit of pupillary light reflex can be secondary to trigeminal nerve ganglion degeneration following subarachnoid hemorrhage; preliminary experimental study.

OBJECTIVE: Although the effect of oculomotor and cervical sympathetic networks on pupil diameter is well known; the effect of the trigeminal nerve on pupil diameter has not been investigated yet. This subject was investigated. MATERIALS AND METHODS: Five of 23 rabbits were used as a control group (GI; n = 5); 0.5 ccs saline solution into cisterna magna injected animals used as SHAM (GII; n = 5); autologous blood injected to produce SAH used as the study group (GIII; n = 13) and followed up three weeks. Light-stimulated pupil diameters were measured with an ocular tomography device before, middle, and at the end of the experiment. Considering the sclera area/pupil area ratio index (PRI) as the pupillary reaction area, we used this equation for the pupil's rush to light. Degenerated neuron densities of trigeminal ganglia and pupil diameters compared with the Mann-Whitney U test. RESULTS: The PRI, degenerated neuron density of trigeminal ganglia (n/mm3) were: (2.034 ± 0.301)/(13 ± 3) in GI; (1.678 ± 0.211)/(46 ± 9) in GII; and (0.941 ± 0.136)/(112 ± 21) in GIII. P-values between groups as: p < 0.005 in GI/GII; p < 0.0001 in GII/GIII and p < 0.00001 in GI/GIII. CONCLUSION: Light stimulates the cornea which is innervated by the trigeminal nerves. This experimental study indicates that the pupil remains mydriatic as the cornea is damaged by trigeminal ischemia following SAH and blocks the light flow.

Interaction between Neurogenic Pulmonary Edema and Thoracic 3 DRG Degeneration Following Spinal Subarachnoid Hemorrhage: First Experimental Study.

BACKGROUND: Neurogenic pulmonary edema (NPE) following subarachnoid hemorrhage (SAH) is still one of the most catastrophic complications with high morbidity and mortality rates. Systemic sympathetic hyperactivity has been considered in the pathogenesis, but it has not been clarified. In this study, we investigate the relationship between the degeneration of the T3 dorsal root ganglion (DRG) and the development of NPE following spinal SAH. METHODS: The study was conducted on 23 rabbits. Five rabbits were used as the control group, 5 as the sham group (n = 5), and 13 as the study group. The correlation between the degenerated neuronal densities of the T3 nerve axons and neurons in the DRG and NPE scores was analyzed statistically. RESULTS: A correlation between the neuronal degeneration of the T3 nerve, its DRG, and high NPE scores was found in the study group and the sham group. Massive NPE was detected in the study group along with neural degeneration of T3 axons and ganglia. CONCLUSION: The present study indicates that NPE and pulmonary artery vasospasm can be prevented by reducing T3 DRG degeneration.

Olfactory bulbectomy leads to prolonged induction phase of sevoflurane anesthesia in rats.

The effect of olfactory bulb lesions on the induction time of sevoflurane has never been studied. We aimed to investigate this issue. In this study, we found that the volume of olfactory bulbs and the pore of the fila olfactoria were significantly lower with the fibrosis of olfactory bulbs in animals subjected to olfactory bulbectomy. Volatile anesthetics induction times were measured in all groups. Prolonged induction was observed in olfactory bulbectomy group. It was concluded that increased induction times of sevoflurane may be due to the olfactory bulb lesion.

New histopathological evidence for the relationship between hydromyelia and hydrocephalus following subarachnoid hemorrhage: An experimental study.

Objectives: Subarachnoid hemorrhage (SAH) is a serious pathology with a high death and morbidity rate. There can be a relationship between hydromyelia and hydrocephalus following SAH; however, this subject has not been well investigated. Materials and Methods: Twenty-four rabbits (3 ± 0.4 years old; 4.4 ± 0.5 kg) were used in this study. Five of them were used as the control, and five of them as the SHAM group. The remaining animals (n = 14) had been used as the study group. The central canal volume values at the C1-C2 levels, ependymal cells, numbers of central canal surfaces, and Evans index values of the lateral ventricles were assessed and compared. Results: Choroid plexus edema and increased water vesicles were observed in animals with central canal dilatation. The Evans index of the brain ventricles was 0.33 ± 0.05, the mean volume of the central canal was 1.431 ± 0.043 mm3, and ependymal cells density was 5.420 ± 879/mm2 in the control group animals (n = 5); 0.35 ± 0.17, 1.190 ± 0.114 mm3, and 4.135 ± 612/mm2 in the SHAM group animals (n = 5); and 0.44 ± 0.68, 1.814 ± 0.139 mm3, and 2.512 ± 11/mm2 in the study group (n = 14). The relationship between the Evans index values, the central canal volumes, and degenerated ependymal cell densities was statistically significant (P < 0.05). Conclusions: This study showed that hydromyelia occurs following SAH-induced experimental hydrocephalus. Desquamation of ependymal cells and increased cerebrospinal fluid secretion may be responsible factors in the development of hydromyelia.

Important Finding for COVID-19 Pandemic: Hydrocephalus-producing effect of Vaporized Alcohol Disinfectant.

BACKGROUND: Alcohol exposure may cause hydrocephalus, but the effect of vaporized nasal alcohol exposure on the choroid plexus, and ependymal cells, and the relationship between alcohol exposure and developing hydrocephalus are not well known. This subject was investigated. METHODS: Twenty-four male (∼380 g) Wistar rats were used in this study. The animals were divided into three groups, as the control, sham and study groups. The study group was further divided into two groups as the group exposed to low or high dose of alcohol. The choroid plexuses and intraventricular ependymal cells and ventricle volumes were assessed and compared statistically. RESULTS: Degenerated epithelial cell density of 22 ± 5, 56 ± 11, 175 ± 37, and 356 ± 85/mm3 was found in the control, sham, low alcohol exposure, and high alcohol exposure groups, respectively. The Evans index was <34% in the control group, >36% in the sham group, >40% in the group exposed to low alcohol dose (low-dose alcohol group), and >50% in the group exposed to high dose of alcohol (high-dose alcohol group). CONCLUSIONS: It was found that alcohol exposure caused choroid plexus and ependymal cell degeneration with ciliopathy and enlarged lateral ventricles or hydrocephalus. In the COVID-19 pandemic era, our findings are functionally important, because alcohol has often been used for hygiene and prevention of transmission of the Sars-Cov-2-virus.

New experimental finding of dangerous autonomic ganglia changes in cardiac injury following subarachnoid hemorrhage; a reciprocal culprit-victim relationship between the brain and heart.

OBJECTIVE: The vagal, stellate, and cardiac ganglia cells changes following subarachnoid hemorrhage (SAH) may occur. This study aimed to investigate if there is any relation between vagal network/stellate ganglion and intrinsic cardiac ganglia insult following SAH. MATERIALS AND METHODS: Twenty-six rabbits were used in this study. Animals were randomly divided as control (GI, n = 5); SHAM 0.75 cc of saline-injected (n = 5) and study with autologous 1.5 cc blood injection into their cisterna magna(GIII, n = 15). All animals were followed for three weeks and then decapitated. Their motor vagal nucleus, nodose, stellate, and intracardiac ganglion cells were estimated by stereological methods and compared statistically. RESULTS: Numerical documents of heart-respiratory rates, vagal nerve- ICG, and stellate neuron densities as follows: 276 ± 32/min-22 ± 3/min-10.643 ± 1.129/mm3-4 ± 1/mm3-12 ± 3/mm3 and 2 ± 1/cm3 in the control group; 221 ± 22/min-16 ± 4/min-8.699 ± 976/mm3-24 ± 9/mm3-103 ± 32/mm3 and 11 ± 3/cm3 in the SHAM group; and 191 ± 23/min-17 ± 4/min-9.719 ± 932/mm3-124 ± 31/mm3-1.542 ± 162/mm3 and 32 ± 9/cm3 in the SAH (study) group. The animals with burned neuro-cardiac web had more neurons of stellate ganglia and a less normal neuron density of nodose ganglia (p < 0.005). CONCLUSION: Sypathico-parasympathetic imbalance induced vagal nerve-ICG disruption following SAH could be named as Burned Neurocardiac Web syndrome in contrast to broken heart because ICG/parasympathetic network degeneration could not be detected in classic broken heart syndrome. It was noted that cardiac ganglion degeneration is more prominent in animals' severe degenerated neuron density of nodose ganglia. We concluded that the cardiac ganglia network knitted with vagal-sympathetic-somatosensitive fibers has an important in heart function following SAH. The neurodegeneration of the cardiac may occur in SAH, and cause sudden death.

Protective Felix Culpa Effect of Superior Sympathetic Cervical Ganglion Degenerations on Prevention of Basilar Artery Spasm After Subarachnoid Hemorrhage: A Preliminary Experimental Study.

BACKGROUND: Posterior cerebral blood flow is regulated by the basilar arteries (BAs). Vasospasm of BAs can occur after subarachnoid hemorrhage (SAH). Superior cervical sympathetic ganglia (SCG) fibers have a vasoconstrictor effect on the BA. We aimed to investigate the relationship between the degenerated neuron density of the SCG and the severity of BA vasospasm after experimental SAH. METHODS: Twenty-four rabbits were used. Five were used as the control group, and 5 were used as the sham group. Experimental SAHs were performed in the remaining 14 animals (study group) by injecting homologous blood into the cisterna magna. After 3 weeks of injection, neuron densities of SCG and the severity of BA vasospasm index values (VSI) were examined histopathologically and compared statistically. RESULTS: The mean VSI was 0.669 ± 0.1129 in the control group, 0.981 ± 0.159 in the sham group, and 1.512 ± 0.298 in the study group. The mean degenerated neuronal density of SCG was 436 ± 79/mm3 in severe vasospasm (n = 3), 841 ± 101/mm3 in moderate vasospasm (n = 4), and 1.921 ± 849/mm3 in the less vasospasm detected animals (n = 6). CONCLUSIONS: This study shows an inverse relationship between the degenerated neuronal density in the SCG and VSI values. This finding indicates a diminished sympathetic input from the SCG, resulting in a beneficial effect (the felix culpa) by dilating the lumen diameter of the BA, so SCG degeneration after SAH protects the BA spasm.

Predictive role of trigeminal ganglion ischemia on scalp survival affected by temporal artery diameters: The first experimental study.

Scalp arteries are mainly innervated by trigeminal, facial, and vagal nerves. The ischemic neurodegeneration of the trigeminal ganglion can impede scalp circulation via vasospasm-creating effects. This study was designed to investigate whether there is any link between the vasospasm index of deep temporal arteries and ischemic neuron densities of the trigeminal ganglion after subarachnoid hemorrhage. The study subjects included five normal control rabbits, six sham rabbits, and nine rabbits chosen from a formerly established experimental subarachnoid hemorrhage group created by cisternal homologous blood injection (0.75 mL). These rabbits, all male, were followed up for 3 weeks. The trigeminal ganglion and deep temporal artery vasospasm indexes were examined by stereological methods. Ischemic neuron densities of the trigeminal ganglion and vasospasm index values of deep temporal arteries were compared statistically. Postmortem examinations showed important vasospasms of deep temporal arteries, foramen magnum herniations, and neurodegeneration of the trigeminal ganglion. The mean vasospasm index values and degenerated neuron densities of the trigeminal ganglion were determined as 1.03 ± 0.13 and 10 ± 3/mm3 (p > 0.5) in the control group, 1.21 ± 0.18 and 35 ± 9/mm3 in the sham group (p < 0.005 for sham vs. control), and 2.54 ± 0.84 and 698 ± 134/mm3 in the experimental group (p < 0.0005 for sham vs. control and p < 0.00001 for study vs. control). There was an inverse relationship between the vasospasm index values and the degenerated neuronal density of the trigeminal ganglion. The high degenerated neuron density in the trigeminal ganglion had a facilitative effect on temporal artery vasospasm. Trigeminal ganglion neurodegeneration may promote temporal artery vasospasms after subarachnoid hemorrhage, which has not been previously mentioned in the literature.

Assessment relationship between the femoral artery vasospasm and dorsal root ganglion cell degeneration in spinal subarachnoid hemorrhage: an experimental study.

STUDY DESIGN: Animal proof of principle study. OBJECTIVES: To investigate neurodegeneration in rabbit L4-dorsal root ganglion (DRG) cells by creating experimental spinal subarachnoid hemorrhage (SAH), we aimed to show the neuronal pathway between L4-DRG and femoral artery. SETTING: Ataturk University, Medical Faculty, Animal Laboratory, Erzurum, Turkey. METHODS: This study was designed on 20 rabbits, which were randomly divided into three groups: Spinal SAH (n = 8), SHAM (n = 6), and control (n = 6) groups. Animals were followed for 20 days and then killed. Vasospasm index values of the femoral artery and neuron density of L4-DRG were analyzed. RESULTS: The number of degenerated neurons in DRG was higher in the spinal SAH than the control and SHAM groups (p < 0.001). But, the difference between the control group and the SHAM group was not significant. Normal neuron densities were significantly lower in the spine SAH group compared to the SHAM and the control groups. There was a statistically significant increase in vasospasm index values of the spinal SAH group compared to the other two groups (p < 0.001). CONCLUSIONS: Decreased volume of the femoral artery lumen was showed in animals with spinal SAH compared with control and SHAM groups. Increased degeneration of the L4 dorsal root ganglion in animals with spinal SAH was also demonstrated. Our findings might shed light on the planning of future experimental studies and evaluating the clinical relevance of such studies.

Estimating basilar artery upper rupture limit by dangerous alarming diameter of arteries (DADA) following bilateral common carotid artery ligation; a new theorem.

BACKGROUND: Although many theories have been established to explain the mechanism of aneurysm development following steno-occlusive or hypertensive disease, the effect of the geometrical shape of the inner elastic membrane on the maximum dilatation capacity of arteries has not been adequately investigated so far. This subject was investigated. METHODS: This study was conducted in 24 rabbits. The rabbits were divided into 3 groups: as the control, (n = 5), the SHAM (n = 5), and the study group (n = 14). In the study group, BCCAL was performed. After decapitation, the basilar artery vasodilatation index (VDI) and the actual length of the inner elastic membrane (IEM) were estimated. The relationship between the true length of IEM and VDI values was compared statistically using the Mann-Witney -U test. RESULTS: Mean blood pressures were 113 ± 7 mmHg in animals at the beginning of the experiment (n = 24), and 119 ± 9 mmHg in GII and 122 ± 11mmHg in GIII after BCCAL (n = 12). Before decapitation, the mean blood pressures were 115 ± 10 mmHg in GI, 116 ± 10 mmHg in GII, and 127 ± 11mmHg GIII. The DADA values of animals were 20 ± 4mm in GI; 28 ± 6mm in GII and 37 ± 9mm in GIII. The VDI value of BA was 1.390 ± 0.220 in GI; 1.013 ± 0.108 in GI; 0.019 ± 0.011in GII group. CONCLUSION: An inverse relationship was discovered between the DADA/VDI values. BCCAL may lead to severe dangerous histopathological changes at the BA. Lower DADA or higher VDI values may lead to severe basilar enlargement, endothelial losing, inner elastic membrane rupture, and aneurysm formation after BCCAL.

Important interaction between urethral taste bud-like structures and Onuf's nucleus following spinal subarachnoid hemorrhage: A hypothesis for the mechanism of dysorgasmia.

BACKGROUND: We previously postulated that orgasmic sensation may occur through recently discovered genital taste bud-like structures. The interaction between the pudendal nerve and Onuf's nucleus may be important for developing orgasmic information. The study aims to investigate whether ischemic damage to Onuf's nucleus-pudendal network following spinal subarachnoid hemorrhage (SAH) causes taste bud degeneration or not. METHODS: The study was conducted on 22 fertile male rabbits who were divided into three groups: control (GI; n=5), SHAM (GII; n=5) and study (GIII; n=12). Isotonic solution, .7cm3, for the SHAM, and .7cm3 homologous blood was injected into spinal subarachnoid spaces at S2 level of the study group. Two weeks later, Onuf's nucleus, pudendal ganglia and the taste bud-like structures of the penile urethra were examined histopathologically. Degenerated neuron densities of Onuf's nucleus, pudendal ganglia and atrophic taste bud-like structures were estimated per mm3 and the results analyzed statistically. RESULTS: The mean degenerated neuron densities of taste bud-like structures, Onuf's nucleus and pudendal ganglia were estimated as 2±1/mm3, 5±1/mm3, 6±2/mm3 in GI; 12±4/mm3, 35±9/mm3, 188±31/mm3, in GII and 41±8/mm3, 215±37/mm3, 1321±78/mm3, in GIII. Spinal SAH induced neurodegeneration in Onuf's nucleus, pudendal ganglia and taste bud atrophy was significantly different between GI/GII (p<.005); GII/GIII (p<.0005) and GI/GIII (p<.0001). CONCLUSION: Ischemic neuronal degenerations of Onuf's nucleus and pudendal ganglia following spinal SAH lead to genital taste bud-like structure atrophy. This mechanism may be responsible for sexual anhedonia and sterility in cases with spinal cord injury, which has not been documented so far. More studies are needed.

New description of vagal nerve commanted intrapancreatic taste buds and blood glucose level: An experimental analysis.

Introduction: There have been thousands of neurochemical mechanism about blood glucose level regulation, but intrapancreatic taste buds and their roles in blood glucose level has not been described. We aimed to investigate if there are taste buds cored neural networks in the pancreas, and there is any relationship between blood glucose levels. Methods: This examination was done on 32 chosen rats with their glucose levels. Animals are divided into owned blood glucose levels. If mean glucose levels were equal to 105 ± 10 mg/dL accepted as euglycemic (G-I; n = 14), 142 ± 18 mg/dL values accepted as hyperglycemic (G-II; n = 9) and 89 ± 9 mg/dL accepted as hypoglycemic (G-III; n = 9). After the experiment, animals were sacrificed under general anesthesia. Their pancreatic tissues were examined histological methods and numbers of newly described taste bud networks analyzed by Stereological methods. Results compared with Mann-Whitney U test P < 0.005 considered as significant. Results: The mean normal blood glucose level (mg/dL) and taste bud network densities of per cm3 were: 105 ± 10 mg/dL; 156±21 in G-I; 142 ± 18 mg/dL and 95 ± 14 in G-II and 89 ± 9 mg/dL and 232 ± 34 in G-III. P values as follows: P < 0.001 of G-II/G-I; P < 0.005 of G-III/G-I and P < 0.0001 of G-III/G-II. We detected periarterial located taste buds like cell clusters and peripherally located ganglia connected with Langerhans cells via thin nerve fibers. There was an inverse relationship between the number of taste buds networks and blood glucose level. Conclusion: Newly described intrapancreatic taste buds may have an important role in the regulation of blood glucose level.

Dry Mouth Caused by Facial Nerve Ischemia due to Subarachnoid Hemorrhage: An Experimental Study.

OBJECTIVE: Parasympathetic network damage results in facial nerve damage, sublingual ganglion degeneration, sublingual gland dysfunction, and dry mouth. In this study, subarachnoid hemorrhage (SAH) was considered to be the cause of dry mouth. METHODS: We assessed 23 hybrid rabbits, including 5 control (group 1, Control). One milliliter of serum saline was injected into the cisterna magna of 5 animals (group 2). SAH was induced by injecting 1 mL of autologous blood into the cisterna magna of 13 animals (group 3). The animals were killed after 3 weeks of induction. The animals' sublingual ganglion and sublingual gland were excised for histopathological examination. The number of degenerated cells in the sublingual ganglion, secretory vesicles, and secretory granules in the sublingual gland that contain salivary components were estimated using Sequential Window Acquisition of All Theoretical Mass Spectra data analysis. The values were compared by the Mann-Whitney U-test. RESULTS: The numbers of secretory vesicles in the sublingual gland were 5.3 ± 1.1 × 103 (group 1), 4.23 ± 0.45 × 103 (group 2), and 1.56 ± 0.22 × 103 (group 3); the numbers of secretory vesicles containing saliva in the sublingual gland were 324 ± 12.18 (group 1), 263 ± 36.23 (group 2), and 114 ± 23.14 (group 3); and the numbers of degenerated cells in the sublingual ganglion were 11 ± 3/mm3 (group 1), 98.43 ± 15.54/mm3 (group 2), and 346 ± 12.28/mm3 (group 3) (P < 0.05). CONCLUSIONS: Clinical findings in infection and diseases such as Sjögren syndrome, aseptic meningitis, and SAH are similar. However, until now, SAH has not been demonstrated experimentally to cause dry mouth. Discovering that SAH might cause dry mouth might prevent unnecessary use of antibiotics and decrease morbidity due to the wrong or late diagnosis.

First emerging evidence of the relationship between Onuf's nucleus degeneration and reduced sperm number following spinal subarachnoid haemorrhage: Experimental study.

Lumbosacral pathologies can lead to infertility. Onuf's nucleus changes in these pathologies may have a role in low sperm number. This study aims to investigate the relationship between Onuf's nucleus degeneration and sperm number following spinal subarachnoid haemorrhage. 22 rabbits were used. They were divided into three groups; five of them were used as the control (GI), five as the SHAM (GII) and twelve as the study groups (GIII). The study group received 0.7 ccs autologous blood into the spinal subarachnoid space at the T12-L1 level. After two weeks, all animals were decapitated, and S1-S3 laminectomy was done. Neurodegenerative changes of Onuf's nucleus, pudendal ganglia (S3) following two weeks after spinal SAH, were examined; sperm numbers were calculated. Degenerated neuron density of the Onuf's nucleus (n/mm3 ), the pudendal ganglia (S3) (n/mm3 ) and mean sperm numbers were calculated as 5 ± 2, 8 ± 3/mm3 and 98.345 ± 12.776/mm3 in the control (GI), 20 ± 5/mm3 , 243 ± 66/mm3 and 91.841 ± 9.654/mm3 in the SHAM (GII), 143 ± 39/mm3 , 2,350 ± 320/mm3 and 68.549 ± 5.540/mm3 in the study group (GIII). In conclusion, there were statistically significant differences between groups. Onuf's nucleus may be responsible for decreased sperm number following spinal SAH.

A new experimental evidence that olfactory bulb lesion may be a causative factor for substantia nigra degeneration; preliminary study.

Background: Anosmia has been considered as the first diagnostic criteria of Parkinson disease (PD), we investigated the effect of the olfactory bulbectomy (OBX) on histopathological features of the substantia nigra in an animal model.Methods: Twenty-seven male rats were used in this study. Animals were divided into three groups as five (control), six SHAM and sixteen study (OBL) groups. Nothing was done in the control group, the only burr hole was done in the SHAM group, OBL was not applied, and bilateral OBL was performed in the study group, and followed ten weeks, then animals were decapitated. Olfactory bulb volumes were measured by macro anatomically. The olfactory bulbs and substantia nigra sections were analyzed by a stereological method to evaluate olfactory glomerulus and neuron density of substantia nigra per cubic centimeter and compared with statistically.Results: The mean olfactory bulb volume, degenerated olfactory glomerulus density and degenerated neuron density of substantia nigra were measured as:(4.14 ± 0.20) mm3, (1 ± 1)/mm3 and (7 ± 2)/mm3 in control (Group I); (3.6 ± 0.16)/mm3, (4 ± 1)/mm3 and(32 ± 7)/mm3 in SHAM (Group II) and (2.2 ± 0.9)/mm3, (112 ± 18)/mm3 and (1543 ± 115)/mm3in study group (Group III). Diminished olfactory bulb volume was observed in Group III animals.Conclusions: We concluded that OBL may lead to the degeneration of substantia nigra.

Relationship between subarachnoid and central canal hemorrhage and spasticity: A first experimental study.

Objective: Spastic disorders are considered as important cerebral complications of subarachnoid hemorrhage (SAH). However, there has been no research concerning the pathophysiological mechanism of its link with the spinal cord. The present study aimed to assess the relationship between the development of spasticity and neuronal degeneration after SAH and increase in spinal cord pressure after central canal hemorrhage (CCH).Participants: Twenty-three rabbits were included.Outcome measures: Of all rabbits, 5, 5, and 13 were allocated in the control, SHAM and study groups, respectively. Moreover, 1 cc of saline and 1 cc of autologous arterial blood were injected into the cisterna magna of the SHAM and study groups, respectively. The Muscle spasticity tension values (MSTVs) were determined according to the modified Ashworth scale. Degenerated neuron densities (DND) in the gray matter (GM) of each animal's spinal cord were stereologically calculated.Results: The average MSTV of each group was as follows: control group (n = 5) 2; SHAM group (n = 5) 3-5; and study group (n = 13) 8-10. The DND values of the spinal cord of each group were as follows: control group, 2 ± 1/mm3; SHAM group, 12 ± 3/mm3; and study group, 34 ± 9/mm3. Results showed an important linear relationship between the MSTVs and the DND of the spinal cord (P < 0.001).Conclusion: Spasticity may be attributed to other causes such as ischemic neurodegenerative process that develops after spinal SAH and the de-synchronization of the flexor-extensor muscles due to the spontaneous discharge of interneuronal structures, which are crossed within the spinal cord owing to the build-up of pressure after CCH.

First histopathological bridging of the distance between Onuf's nucleus and substantia nigra after olfactory bulbectomy-new ideas about the urinary dysfunction in cerebral neurodegenerative disease: an experimental study.

OBJECTIVES: Olfactory bulbectomy (OBX) in experimental studies induces neurochemical, neurodegenerative changes in various parts of the body. But no information is available about how OBX affects the spinal cord in rats. Our study aims to investigate this question. METHODS: Twenty-eight male rats were used. The rats were divided into three groups: six as the control, six as the SHAM, and 16 as the study group in which OBX was performed. The animals were followed for 10 weeks. After decapitation of the animals, olfactory bulb (OB) volumes, the olfactory glomerulus (OG), and the neuron density of the ON (Onuf nucleus) per cubic centimeter at the L4-S4 level were examined histopathologically and analyzed stereologically. RESULTS: The mean OB volume, remaining normal OG density, and degenerated neuron density (DND) of the ON was measured as 4.32 ± 0.21/mm3 , 1842 ± 114/mm3 , and 4 ± 1 /mm3 in the control (group I); 3.3 ± 0.14/mm3 , 1321 ± 114/mm3 , and 43 ± 8/mm3 in the SHAM (group II); and 1.672 ± 0.12/mm3 , 852 ± 93/mm3 , and 154 ± 11/mm3 in the study group (group III). There was a statistically significant difference between the SHAM and the study group (P < .05). CONCLUSIONS: In this study, histopathological bridging between ON-related lower urinary tract symptoms (LUTS) and OBX was shown the first time. According to the findings, LUTS may be reversed by the protection of the affected spinal cord through the correction of olfaction impairment in neurodegenerative disease.

Toward the first definition of taste rosea in female breasts: histological analysis / La primera definición del sabor rosea en mamas femeninas: análisis histológico

Although various neuropsychochemical theories have been established about why breastfeeding mothers feel hedonic sensation, the underlying neural mechanism has not been adequately clarified. We aimed to investigate if there is hedonic sensation-initiated taste-bud like structures stimulated by sugars in the milk-secreting lactiferous ducts of mammary glands of breastfeeding female rats. In this study, twenty-two female rats were chosen which six of the virgin (n=6), six of pregnant (n=6) and ten of breastfeeding (n=10). We examined lactiferous ducts/nipples of mammary glands of all animals. They were sacrificed following intracardiac formalin injection, and their breast tissues were removed with covering tissues and fixed with 10 % of formalin solution. After current histological procedures, the tissues were examined by light microscope to assess taste-bud like structures, and their numerical densities were calculated by using stereological methods. Results were analyzed statistically. Taste-buds like structures with neuron-like appendages at the apical ends were discovered in lactiferous ducts. The taste rosea numbers were estimated as 3±1/mm3 in virgins, 167±27/mm3 in pregnant and 375±63/mm3 in breastfeeding animals. The taste rosea numbers were greater in breastfeeding rats than those of virgins and pregnant rats. They named as taste rosea resembling flower bucket which has not been mentioned in the literature so far.

Existen varias teorías neuropsicoquímicas, referente a la sensación hedónica que sienten las mujeres al amamantar, y el mecanismo neural subyacente. No obstante, estas aún no se aclaran adecuadamente. El objetivo de este estudio, fue investigar si existen estructuras hedónicas iniciadas por la sensación gustativa estimuladas por los azúcares en los conductos mamarios secretores de leche, de las glándulas mamarias de las ratas durante el período de lactancia. En este estudio, se eligieron 22 ratas hembras, seis de estas no preñadas como grupo control, seis preñadas y diez en período de lactancia. Examinamos los conductos lactíferos / pezones de las glándulas mamarias de los tres grupos. Los animales fueron sacrificados por medio de inyección intracardíaca de formalina. El tejido mamario se fijó en solución de formalina al 10 %. La muestras histólogicas fueron examinadas a través microscopía óptica con la finalidad de evaluar estructuras con características morfológicas similares a las papilas gustativas. Su densidad de número se calculó utilizando métodos estereológicos. Los resultados fueron analizados estadísticamente. En los conductos mamarios se observaron dos estructuras con con características morfológicas tipo papilas gustativas con apéndices neuronales en los extremos apicales. Los números se estimaron en 3±1/mm3 en el grupo control, 167±27/mm3 en gestantes y 375±63/mm3 en animales lactantes. El número de estructuras características morfológicas similares a las papilas gustativas fue mayor en las ratas amamantando que en el grupo control y que en las ratas preñadas. Conocido como sabor rosea debido a que se asemeja a un ramo de flores, lo que hasta ahora no se ha mencionado en la literatura.