Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The AP-1 regulatory element has been implicated in the cold-induced expression of tyrosine hydroxylase in the adrenal medulla. Since in this tissue, the cold-induced increase in tyrosine hydroxylase expression is impaired with age and in other tissues, there is some evidence that AP-1 transcription factor binding is diminished with age, we examined the cold-stimulated AP-1 transcription factor binding to an oligonucleotide with the consensus sequence of the AP-1 response element in nuclear extracts from adrenal medulla and hypothalamus of young and senescent rats. AP-1 transcription factor binding activity diminished by 38% with age in unstimulated adrenal medulla. Following cold stimulation, the AP-1 binding activity increased by 21-25% in the adrenal medulla of both young and senescent rats. However, the level of AP-1 binding in cold-stimulated senescent rats was still less than in cold-stimulated younger rats. There were no changes in AP-3 binding activity with either age or cold exposure in the adrenal medulla. Similarly, in the hypothalamus, there was a 25% decrease with age and a 25% increase following cold stimulation in the level of AP-1 binding. There was a 62% age-related increase in AP-3 binding activity but no change with cold exposure. These data indicate that there is reduced AP-1 binding activity in senescent control rats. Moreover, the demonstration that cold stimulus evokes similar increases in AP-1 binding activity in both young and old rats suggests that the stimulation pathway that increases AP-1 transcription factor is maintained in the senescent animal.
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PMID:AP-1 transcription factor binding activity in rat adrenal medulla and hypothalamus with age and cold exposure. 929 71

Adrenal chromaffin cells produce analgesic substances, such as catecholamines and enkephalins, and intrathecal (i.t.) implantation of either allografted adrenal tissue or xenogenic chromaffin cells produce antinociception in animals. We evaluated the analgesic effect of bovine chromaffin cells in a model of central pain in which rats exhibit chronic allodynia-like behavior after photochemically induced ischemic spinal cord injury. Bovine chromaffin cells or endothelial cells were injected i.t. onto the lumbar spinal cord and their effects on mechanical and cold allodynia-like behaviors were studied for up to 8 weeks. The chronic allodynia-like behavior was stable for months without signs of remission and i.t. implantation of human endothelial cells did not alleviate the chronic allodynia-like behavior for the entire observation period. In contrast, 2 weeks after i.t. implantation of bovine chromaffin cells, the mechanical allodynia was abolished in the spinally injured rats, and the enhanced response to cold stimuli was significantly reduced. The overall effects were significant up to 8 weeks after i.t. implantation, although the anti-allodynic effect decreased towards the end of the observation period. No signs of side-effects were noted after i.t. implantation. The allodynia-like state was temporarily restored by naloxone (0.5 mg/kg) or phentolamine (0.3 mg/kg) injected intraperitoneally. Immunohistochemical examination revealed that tyrosine hydroxylase (TH)-positive chromaffin cells could be identified adjacent to the spinal cord up to 4 weeks after i.t. implantation, whereas at 8 weeks the TH-positive cells were sparse. It is concluded that bovine chromaffin cells stay viable in rat spinal cord for a considerable period of time after i.t. administration and alleviate chronic allodynia-like behavior in spinally injured rats, possibly through activation of opioid and alpha-adrenoceptors. The present results further document a new therapeutic approach for the treatment of chronic neuropathic pain.
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PMID:Long-term alleviation of allodynia-like behaviors by intrathecal implantation of bovine chromaffin cells in rats with spinal cord injury. 952 Feb 25

Incomplete peripheral nerve injury often leads to neuropathic pains, some of which are relieved by sympathectomy, and results in sympathetic postganglionic nerve fiber sprouting in the dorsal root ganglion (DRG). This study was performed to see whether the sprouting in the DRG plays a key role in the sympathetic dependence of neuropathic pain. To this aim, we compared two groups of rats, both of which were subjected to unilateral transection of the inferior and superior caudal trunks at the levels between the S1 and S2, S2 and S3, and S3 and S4 spinal nerves, with respect to sympathetic fiber sprouting; one group showed neuropathic pain behaviours (i.e. mechanical and cold allodynia signs) which were very sensitive to phentolamine, alpha adrenergic blocker, and the other group exhibited no sensitivity. Immuno-histochemical staining with tyrosine hydroxylase antibody of the S1-S3 DRGs was not correlated with the sensitivity to phentolamine. These results suggest that the degree of sympathetic dependence of neuropathic pain is not a function of the extent of the sympathetic postganglionic nerve fiber sprouting in the DRG.
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PMID:Amount of sympathetic sprouting in the dorsal root ganglia is not correlated to the level of sympathetic dependence of neuropathic pain in a rat model. 959 46

Stress ulceration of the stomach in mice was investigated from the aspect of the calcium/calmodulin-dependent dopamine synthesizing system in the brain. Cold stress was induced in mice by restraining them at 4 degrees C. Serum and brain calcium levels were increased by cold stress, and an increased brain calcium level was found to enhance dopamine synthesis and a successively increased brain dopamine level induced gastric ulcer formation. Development of gastric ulcers elicited by cold stress was significantly decreased by i.p. pretreatment with EDTA (1 micromol/mouse, 1 h before restraint) or alpha-methyltyrosine (a tyrosine hydroxylase inhibitor, 100 mg/kg, 24 h before restraint), and was further significantly increased by pretreatment with CaCl2 (40 micromol/kg, 1 h before restraint). These findings suggest that the development of gastric ulcers in cold-stressed mice may be linked with the enhancement of calcium/calmodulin-dependent catecholamine synthesis in the brain.
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PMID:Gastric ulcer formation in cold-stressed mice related to a central calcium-dependent-dopamine synthesizing system. 967 76

The success of embryonic neural transplants as a treatment for patients with Parkinson's disease has been limited by poor survival of transplanted dopamine neurons. To see if a new partially intact tissue preparation method improves survival, we have developed a technique for extruding embryonic tissue into strands. We expected this method to reduce cell damage and improve transplant survival as well as provide improved tissue delivery. We have compared transplants of tissue strands with mechanically dispersed suspensions of embryonic day 15 rat ventral mesencephalon. Tissue from ventral mesencephalon was transplanted into a single site in dopamine denervated striatum of unilateral 6-hydroxydopamine (6-OHDA) lesioned rats. To evaluate the effects of striatal cografts and growth factors on dopamine cell survival, dispersed mesencephalic cells were cotransplanted with dispersed striatal cells. Another group had dispersed mesencephalic cells cotransplanted with striatal cells incubated in the cold for 2 h with glial cell line-derived neurotrophic factor (GDNF, 100 ng/ml), insulin-like growth factor-I (IGF-I, 1500 ng/ml), and basic fibroblast growth factor (bFGF, 150 ng/ml). Behavioral improvement was assessed monthly by changes in methamphetamine-induced rotational behavior. Animals were sacrificed after 3 months, and dopamine neurons were identified by tyrosine hydroxylase (TH) immunohistochemistry. Transplants of tissue strands produced better dopamine neuron survival and led to more robust behavioral restoration than did cell suspensions even when suspensions were supported with cografts of striatal cells or pretreatment with growth factors.
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PMID:Strands of embryonic mesencephalic tissue show greater dopamine neuron survival and better behavioral improvement than cell suspensions after transplantation in parkinsonian rats. 973 8

The effects of acute food deprivation and acute cold exposure on 24-hr urinary isatin excretion in rats and a mechanism responsible for changes in urinary isatin excretion during stress were investigated. This is the first study to demonstrate by HPLC that urinary isatin excretion is increased by stress. Both types of stress induced a marked increase in urinary isatin excretion during the 24 hr following the initiation of stress. Dexamethasone administration prevented the increase in urinary isatin excretion induced by both of the different types of stress. Furthermore, administration of either the benzodiazepine receptor agonist diazepam or the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine prevented the increase in urinary isatin excretion induced by acute food deprivation, whereas the dopamine-beta-hydroxylase inhibitor diethyldithiocarbamate proved ineffective. These observations suggest that during stress, activated catecholamine-synthesizing cells and corticotropin-releasing factor cells, both of which play central roles in stress responses, may be involved in total isatin production. Isatin may serve as an endogenously generated marker for some types of stress.
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PMID:Stress-induced increase in urinary isatin excretion in rats: reversal by both dexamethasone and alpha-methyl-P-tyrosine. 977 16

Immunoreactivity of the immediate early gene c-fos was used to investigate changes in the activity of brainstem neurons in response to acute stressors like immobilization, formalin-induced pain, cold exposure, hemorrhage and insulin-induced hypoglycemia. Different stressors induced Fos-like immunoreactivity in different pontine and medullary neurons. A single, 3 hour immobilization was found to be a very strong stimulus that activated brainstem catecholaminergic (tyrosine hydroxylase-immunopositive) neurons and cells in the raphe and certain pontine tegmental nuclei, as well as in the reticular formation. Pain, induced by a subcutaneous injection of formalin was also effective on catecholamine-synthesizing neurons and on others cells in the nucleus of the solitary tract. Cold exposure activated cells mainly in the sensory spinal trigeminal and parabrachial nuclei and in the so-called "pontine thermoregulatory area". Moderate Fos-like immunoreactivity was induced by a hypotonic (25%) hemorrhage in medullary catecholaminergic neurons, the nucleus of the solitary tract and the Barrington nucleus. Among stressful stimuli used, insulin-induced hypoglycemia elicited the smallest Fos activation in the lower brainstem. The present observations indicate that different stressors may use different neuronal pathways in the central organization of the stress response.
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PMID:Stress-induced Fos-like Immunoreactivity in the Pons and the Medulla Oblongata of Rats. 978 41

Partial peripheral nerve injury often results in neuropathic pain that is aggravated by sympathetic excitation and induces sympathetic nerve sprouting in both the injured nerve and corresponding dorsal root ganglia (DRGs). Presently, the functional mechanisms of the interactions between the sprouting and injured somatic afferents remain uncertain. This study was performed to see whether the sprouting in the DRGs plays a key role in the development of neuropathic pain. To this aim, we compared two groups of rats, both of which were subjected to unilateral transection of the superior and inferior caudal trunks at the level between the S1 and S2 spinal nerves, with respect to sympathetic fiber sprouting; one group showed well-developed neuropathic pain behaviors (i.e. mechanical, cold and warm allodynia signs) and the other group showed poorly-developed ones. Immuno-histochemical staining with tyrosine hydroxylase (TH) antibody of the injured S1 DRG taken from both groups of rats after behavioral tests revealed that the magnitude of penetration of TH-positive fibers into the S1 DRG was not significantly different between the two groups. These results suggest that sympathetic nerve sprouting in the injured DRG is not a key factor in the development of neuropathic pain.
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PMID:Is sympathetic sprouting in the dorsal root ganglia responsible for the production of neuropathic pain in a rat model? 1043 May 15

Electron immunocytochemistry was used to examine perivascular nerves of hamster mesenteric and renal arteries during hibernation and 2 h after arousal from hibernation. Vessels from cold-exposed but nonhibernating, and normothermic control hamsters were also examined. During hibernation the percentage of axon profiles in mesenteric and renal arteries that were immunopositive for markers of sympathetic nerves, tyrosine hydroxylase (TH) and neuropeptide Y (NPY), were increased 2-3 fold compared with normothermic and cold control animals. This increase was reduced markedly only 2 h after arousal from hibernation. The small percentage of nitric oxide synthase-1-positive axon profiles found in mesenteric (but not renal) arteries was also increased during hibernation and returned towards control values after arousal. In contrast, the percentage of perivascular axons immunostaining for vasoactive intestinal polypeptide (VIP), a marker for parasympathetic nerves, was reduced in mesenteric arteries during hibernation. There was no labelling of perivascular nerves for substance P in either mesenteric or renal arteries. It is suggested that the increase in percentage of TH- and NPY-immunostained perivascular nerves may account for the increased vasoconstriction associated with high vascular resistance that is known to occur during hibernation. The reduction in the percentage of axons positive for VIP in hibernating animals would contribute to this mechanism since this neuropeptide is a vasodilator.
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PMID:Electron-immunocytochemical studies of perivascular nerves of mesenteric and renal arteries of golden hamsters during and after arousal from hibernation. 1047 99

With aging, circulating catecholamines are elevated in both humans and animals. This may be related to the increased basal levels of dopamine beta-hydroxylase (DbetaH) and tyrosine hydroxylase (TH) mRNA levels and TH enzyme activity in the adrenal medulla of senescent compared with younger animals. Cold exposure induces TH and DbetaH mRNA, and the cholinergic pathway is believed to be involved in the cold-stimulated increase in TH expression in the adrenal medulla. However, TH gene expression in the senescent rat is resistant to stimulation by cold exposure, suggesting that the cholinergic pathway may be impaired with age in the adrenal medulla. To investigate this possibility, we administered carbachol (0.5 mg/kg i.p., every 12 hours for 3 consecutive days), a mixed nicotinic-muscarinic agonist, to young (4-month-old) and senescent (24-month-old) male F-344 rats. We examined the induction of TH mRNA, TH immunoreactivity, and TH enzyme activity in the adrenal medulla in young and old rats. In addition DbetaH and NPY mRNA levels were determined in the adrenal medulla with or without carbachol administration. Basal levels of TH mRNA, TH immunoreactivity, and TH activity as well as DbetaH and neuropeptide Y (NPY) mRNA were 1.5- to 4-fold greater in the adrenal medullae of old rats compared with young rats. Carbachol administration increased TH mRNA, TH immunoreactivity, and TH activity as well as DbetaH and NPY mRNA to the same or a greater extent in the senescent compared with the young rats. The present study indicates that the cholinergic induction of TH or DbetaH are not impaired with age, and that senescent rats retain the capacity to respond to carbachol stimulation. The present findings cannot explain why the adrenal medullae from senescent rats are resistant to the cold-induced elevation of TH mRNA and TH activity observed in young rats.
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PMID:Induction of tyrosine hydroxylase and neuropeptide Y by carbachol: modulation with age. 1056 24


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