Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add filters








Language
Year range
1.
Medical Journal of Cairo University [The]. 2009; 77 (3): 245-250
in English | IMEMR | ID: emr-97588

ABSTRACT

Cyclooxygenase-3 [Cox-3] is a recently identified cyclooxygenase which is inhibited by paracetamol related drugs rather than traditional non-steroidal anti-inflammatory. In this study the distribution of Cox-3 has been studied in the rat nervous system both in the central and peripheral nervous system. Ten adult male Wistar rats weighing 300-400 g were killed by decapitation under brief anesthesia. Nervous system; brains, spinal cords, spinal ganglia and spinal nerves were removed and processed for immunohistochemisty using an antibody raised against Cox-3. Cox-3 was widely distributed in the rat nervous system. The expression appeared mainly neuronal. In the central nervous system, Cox-3 was localized in neurons in the brain and spinal cord. In the brain Cox-3 was highly expressed in cerebral cortex, hippocampus and cerebellum. In the peripheral nervous system Cox-3 was localized in neurons in the spinal ganglia and in the spinal nerves. Cox-3 was widely distributed in the nervous system. Thus, this isoform could be contributing to the generation of the physiological levels of prostaglandins normally for needed for homeostatic regulation in the nervous system. Localisation of Cox-3 in areas associated with nociception and pain such as brain, spinal cord and spinal ganglia support the hypothesis that Cox-3 may be the central target of paracetamol and other related centrally acting analgesics/antipyretics


Subject(s)
Animals, Laboratory , Nervous System , Rats , Anti-Inflammatory Agents, Non-Steroidal
2.
Egyptian Journal of Histology [The]. 2009; 32 (2): 246-252
in English | IMEMR | ID: emr-136351

ABSTRACT

Periodontal disease is a common chronic inflammatory disease in humans, It is believed that neurogenic inflammation plays an important role in pathogenesis of this disorder. Therefore the neuronal expression of the pro-inflammatory mediators are altered. This study was to determine the neuronal profile of neuropeptides mRNA in the trigeminal ganglia in a model of experimental periodontitis in rats, Periodontitis was induced in male rats by intragingival injection of lipopolysaccharide adjacent to the second right mandibular molar, The animals were killed seven days after lipopolysaccharide injection and the right trigeminal ganglia were processed for in situ hybridisation for neuropeptides [beta-preprotachykinin, alpha-calcitonin gene-related peptide mRNAs and somatostatin]. Expression of these neuropeptides' mRNAs was significantly increased only in small neurons in the mandibular division of the trigeminal ganglion from the periodontitis Group. No significant changes in neuropeptide mRNA levels were seen in the maxillary and ophthalmic divisions of the trigeminal ganglia. The upregulation of neuropeptides mRNAs in periodontal disease suggests a role for neurogenic mechanisms in the development of periodontal disease

3.
Egyptian Journal of Histology [The]. 2009; 32 (2): 410-416
in English | IMEMR | ID: emr-136367

ABSTRACT

Nitric oxide [NO] is produced in the nervous system by the activity of the neuronal nitric oxide synthase [nNOS]. Nitric oxide is involved in nociceptive processing and is an important molecule in the regulation of cranial blood flow and arterial diameters. Thus it is a key molecule in the generation of headache. Headaches are hypothesised to be due to neural activation in the trigeminal pathway resulting in vasodilatation of meningeal blood vessels leading to pain. In this study we investigated the cellular source of NO in structures known to be involved in headache by studying the expression of nNOS mRNA and protein along the trigeminal pathway. Fifteen Wistar adult male rats weighing 300-400g were killed by decapitation under brief anesthesia. The dura mater, trigeminal ganglia and trigeminal nerves were removed and processed for in situ hybridization to study nNOS mRNA expression and for immunohistochemistry to study nNOS protein localization. In situ hybridization showed nNOS mRNA expression in all divisions of the trigeminal ganglia, exclusively in neuronal cell bodies. Immunohistochemistry showed nNOS localization in the trigeminal ganglia both in neuronal cell bodies and neuronal process. Neuronal NOS was also localized in trigeminal nerves and in the dura mater. In the dura mater nNOS immunoreactivity was exclusively localized in meningeal nerve fibers but neither in dural vessels nor in dural cells. These data provide evidence that nNOS mRNA and protein are expressed in neuronal but not vascular structures known to be involved in pathogenesis of headache. Therefore, nNOS could be contributing to the production of dural NO which is known to be a key factor in generation of headache

4.
Egyptian Journal of Histology [The]. 2009; 32 (1): 9-16
in English | IMEMR | ID: emr-100858

ABSTRACT

Prostaglandins are synthesized by the activity of cyclooxygenase [Cox] isoforms. The newly discovered isoform [Cox-3] has been shown to be potently inhibited by centrally-acting analgesics, such as acetaminophen [paracetamol] which are widely used in treatment of headache. Vascular headaches such as migraine are hypothesized to be due to neural activation in the trigemino-vascular system. This results in vasodilatation of meningeal blood vessels leading to activation of trigeminal sensory afferents and pain. Headache is thus attributable to a neurovascular interaction. In this study the localisation of Cox-3 has been studied in structures known to be involved in pathogenesis of headache including rat dura mater and trigeminal pathway [trigemino-vascular system]. Fifteen adult male Wistar rats weighing 300-400g were killed by decapitation under brief anaesthesia. The dura mater, the trigeminal ganglia and brain were removed and processed for immunohistochemistry using an antibody raised against Cox-3. Dura mater showed Cox-3 immunoreactivity in meningeal blood vessels, perivascular nerve fibres and mast cells. In the trigeminal ganglia, Cox-3 immunoreactivity was localised in neurons of different sizes and in trigeminal nerve fibres. In the brain stem, Cox-3 was localised in neurons in the trigeminal nuclei. These data provide evidence that Cox-3 is expressed in both neuronal and vascular structures known to be involved in pathogenesis of vascular headache. These data support the hypothesis that Cox-3 may be a central target of paracetamol and related analgesics


Subject(s)
Animals, Laboratory , Meninges/blood supply , Trigeminal Ganglion , Trigeminal Nuclei , Brain Stem , Acetaminophen , Migraine Disorders , Headache , Rats
SELECTION OF CITATIONS
SEARCH DETAIL