Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Self-aggression is a behavioural disorder in which an individual damages its own body parts by intense biting or scratching. Self aggression has been reported in human patients in Lesch-Nyhan syndrome and in cases of schizophrenia, depression, and congenital analgesia. In human patients as well as in experimental animals some kind of dysesthesia of the part of the body that is mutilated has been suggested. This study was conducted to find out the underlying pain mechanisms in self-aggressive behaviour arising out of stereotypy. The study was performed in 40 adult male rats. In all these animals, self-aggression was produced as part of amphetamine induced stereotyped behaviour. A predetermined scale was used for quantifying this behaviour. Reserpine and phenoxybenzamine pretreatment led to an increase in the incidence of self-aggression. Naloxone administration in reserpine pretreated animals led to a further significant increase in the incidence of self biting as compared to controls. From these studies it appears that self-aggressive behaviour may be associated with increased pain sensation.
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PMID:Role of opioid receptors in self-aggression in rats. 166 47

Starting from a case of marked pain insensitivity in a patient suffering from catatonic schizophrenia we state in this paper that analgesia seems to be an ubiquitous phenomenon which is not only caused by physical disorders of the central nervous system. Different models of interpretation as to be found in scientific literature are reviewed. On the basis of today's physiological knowledge, five hypotheses on causal explanation of pain insensitivity in schizophrenics are discussed: Hypalgesia and analgesia are an expression of motorial inability to react; a consequence of a disorder of consciousness; an analgetic effect of neuroleptic drugs; a basic deficit in schizophrenia and; a result of a disturbed psycho-physiological development.
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PMID:[Disorders of pain perception in schizophrenia]. 170 99

Vast amounts of research have been done that have attempted to delineate the pharmacological and physiological effects of the endogenous opiate peptides. A great deal of knowledge has also been accumulated in a limited time span concerning the types and locations of the opiate receptors and peptides, as well as their functions. In 1980, reports were made concerning the effects of these peptides on analgesia, on tolerance and dependence, on activity, on learning and memory, on schizophrenia and other types of emotional disturbances, and on physiological responses such as eating and drinking, cardiovascular responses, and sexual function. Additional understanding was also gained concerning their interactions with neurotransmitters, other neuropeptides, and hormones. These and other studies published only in 1980 are reviewed in this paper, which is the third of an annual series.
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PMID:Endogenous opiates: 1980. 611 43

1. In the last ten years basic research on the mechanism of action of opiates has led to the clearcut demonstration of the existence of opiate receptors--possibly several slightly different kinds--in the nervous system. 2. A number of endogenous ligands also called endorphins or enkephalins for these receptors have been discovered that proved to be peptides with opiate-like pharmacological activity and were shown to be localized in strategic neuronal pathways in the brain, spinal cord and pituitary gland. 3. Clinical researchers are beginning to explore the possible role of these opiate-like peptides in a variety of clinical situations such as: pain and analgesia, tolerance and dependence, reinforcement mechanisms, memory processes and learning, and mental illness such as schizophrenia. 4. The discovery of biologically active opioid and other peptides coexisting with more traditional neurotransmitters in the same neurons may lead to a reevaluation of our fundamental notions of how the brain operates. This is viewed as a major advancement not only to our understanding of the theoretical basis of drug actions but also as a first step towards the development of new, practically useful methods for treating the clinical problems associated with drug abuse.
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PMID:Opiate receptors and endogenous opiates: panorama of opiate research. 612 96

A number of compounds have been shown to inhibit the degradation of enkephalins. As expected, these compounds produce naloxone reversible analgesia and potentiate the analgesia produced by enkephalins and by acupuncture. One of these, D-phenylalanine, is also anti-inflammatory. D-phenylalanine has proven to be beneficial in many human patients with chronic, intractable pain. It is proposed the enkephalinase inhibitors may be effective in a number of human "endorphin deficiency diseases" such as depression, schizophrenia, convulsive disorders and arthritis. Such compounds may alleviate other conditions associated with decreased endorphin levels such as opiate withdrawal symptoms.
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PMID:D-phenylalanine and other enkephalinase inhibitors as pharmacological agents: implications for some important therapeutic application. 612 72

Endorphinergic neurons certainly play a role in the brain's processing of painful stimuli. Endorphins act to alter pain appreciation at many levels within the central nervous system including spinal cord, midbrain, thalamus, and cortex. The activity of this pain-suppressing system may play a role in individual differences in the experience of pain. Endorphinergic mechanisms play a major role in analgesia associated with stress and acupuncture, and perhaps mediate placebo-induced analgesia. Chronic pain influences endorphinergic function perhaps depleting endorphinergic neurons of their neurotransmitters. Endorphin function and pain sensibility are prominently affected in affective illness and schizophrenia. It may be that endorphinergic neurons play a fundamental role in selective attention--a kind of sensory filtering of information flow--in somatosensory and other sensory modalities.
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PMID:Endorphins and pain. 631 2

The first indication that histamine might be important in the functioning of the brain was the finding that the centrally penetrating histamine H1 antagonists had marked sedative properties. Subsequently with the development of more specific compounds and drugs for the H1, H2 and H3 receptors a greater understanding of the neurotransmitter/modulator role of histamine in the CNS has been possible. Histamine is now associated with wakefulness, suppression of seizures, hypothermia and emesis. The histamine H1 antagonists have been shown to potentiate opioid-induced analgesia, and modify eating and drinking patterns as well as endocrine secretions from the pituitary gland. Additionally, clinically useful antidepressants have been shown to inhibit histamine-sensitive adenylate cyclase from the mammalian brain. Recently, a possible role for both histamine H1 and H2 receptors in schizophrenia has been reported. As more specific and centrally-penetrating histaminergic compounds are developed, so the roles of histamine as a neurotransmitter/modulator in the brain will be better understood.
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PMID:Histaminergic drugs as modulators of CNS function. 873 45

Behavioral phenotyping of transgenic and knockout mice requires rigorous, formal analyses. Well-characterized paradigms can be chosen from the established behavioral neuroscience literature. This review describes (1) a series of neurological and neuropsychological tests which are effectively used as a first screen for behavioral abnormalities in mutant mice, and (2) a series of specific behavioral paradigms, clustered by category. Included are multiple paradigms for each category, including learning and memory, feeding, analgesia, aggression, anxiety, depression, schizophrenia, and drug abuse models. Examples are given from the experiences of the authors, in applying these experimental designs to transgenic and knockout mice. Extensive references for each behavioral paradigm are provided, to allow new investigators to access the relevant literature on behavioral methodology.
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PMID:A proposed test battery and constellations of specific behavioral paradigms to investigate the behavioral phenotypes of transgenic and knockout mice. 921 34

Recently, much interest has been given to the role of glutamatergic N-methyl-D-aspartate receptors (NMDA) in sensory gating, such as prepulse inhibition (PPI) and reduction of the P50 evoked response potential (ERP). Currently, mainly animal data are available describing the role of NMDA receptors in these stimulus evaluation processes. Human data are virtually lacking and are potentially important, for instance for the understanding of sensory gating deficits observed in schizophrenia. Therefore, the effects of the NMDA antagonist ketamine, in a dose of 0.3 mg/kg i.v., on concurrent assessment of PPI and P50 reduction was studied in 18 healthy male volunteers. Ketamine was administered in a pseudo-steady state model with a subacute loading dose. In addition, the effects of ketamine on behavior, vital signs, homovanillic acid (HVA) plasma levels and secretion of cortisol and luteinizing hormone (LH) were also determined. Ketamine did not significantly alter PPI or the reduction of the P50 ERP. A small but significant increase in Brief Psychiatric Rating Scale (BPRS) total scores and BPRS composite scores "thinking disorder" and "withdrawal/retardation" was observed. Several subjects experienced visual perceptional alterations, but complex hallucinations did not occur. Ketamine induced mild analgesia and coordination problems. In addition, ketamine induced a marked rise in cortisol secretion, while LH secretion was not affected. Finally, systolic and diastolic, blood pressure and heart rate increased during ketamine infusion. Although in humans NMDA receptors may not be involved in the regulation of PPI and P50 reduction, the most likely explanation for the lack of effect of ketamine on these sensory gating paradigms is the dose used in this experiment. However, using a higher dose is hampered by the aspecificity of racemic ketamine. Future studies should use the enantiomer S-ketamine, which is more specific to NMDA receptors, to evaluate the involvement of NMDA receptors in these neurophysiological processes further.
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PMID:The effects of low dose ketamine on sensory gating, neuroendocrine secretion and behavior in healthy human subjects. 968 5

Cholecystokinin (CCK) is the most abundant neuropeptide in the mammalian brain, and in man significant quantities are expressed in all regions of the brain.1,2 Therefore, CCK has been implicated in a variety of CNS functions-such as feeding behavior, anxiety, analgesia and memory functions as well as psychiatric disease like panic disorder and schizophrenia (for review, see2,3). Recently, a number of studies have indicated that a C-36 to T transition in the CCK gene promoter Sp1 element4 (Figure 1) is associated with alcoholism and withdrawal symptoms as well as panic disorder.5-7 Moreover, it has been proposed that the polymorphism plays a direct role in the pathogenesis of the disorders by decreasing the expression and synthesis of CCK peptides. The significance of these findings is still unclear and other studies have failed to demonstrate linkage between the polymorphism and alcoholism.8 In this study we examined the function of the C-36 to T transition in transcription of the human CCK gene. We demonstrate that substitution of the C-36 residue causes a slight reduction of Sp1 and Sp3 binding, but this has no effect on transcription in vivo. Moreover, no difference in the response to physiological stimuli was observed. Taken together the results show that the C to T polymorphism does not play a direct role in the pathogenesis of either alcoholism or panic disorder and that a putative association to these disorders is likely to be the result of co-segregation with a linked mutation.
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PMID:Function of the C-36 to T polymorphism in the human cholecystokinin gene promoter. 1088 57


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