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Relevant bibliographies by topics / Serotonergic pathways

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Academic literature on the topic 'Serotonergic pathways'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Serotonergic pathways"

1

Burgard, Edward C., Mathew O. Fraser, and Karl B. Thor. "Serotonergic modulation of bladder afferent pathways." Urology 62, no. 4 (October 2003): 10–15. http://dx.doi.org/10.1016/s0090-4295(03)00590-9.

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Lin, Henry C., Corynn Neevel, Peng-Sheng Chen, Gina Suh, and Jin Hai Chen. "Slowing of intestinal transit by fat or peptide YY depends on β-adrenergic pathway." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 6 (December 2003): G1310—G1316. http://dx.doi.org/10.1152/ajpgi.00230.2003.

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Although the enteric reflex pathway triggered by volume distension is known to depend on an adrenergic nerve, it is not known whether the slowing of intestinal transit by fat or peptide YY (PYY) also depends on an adrenergic pathway. The aim of this study was to test the hypotheses that the slowing of transit by fat or PYY may depend on a β-adrenergic pathway, and this adrenergic pathway may act via the serotonergic and opioid pathways previously observed for the slowing of transit by fat. Eighteen dogs were equipped with duodenal and midgut fistulas. The small intestine was compartmentalized into the proximal and distal half of gut. The role of adrenergic, serotonergic, and opioid pathways was then tested in the slowing of intestinal transit by fat, PYY, and norepinephrine. Intestinal transit results were compared as the cumulative percent marker of recovery over 30 min. We found that the slowing of transit by fat, PYY, or norepinephrine was reversed by propranolol. In addition, the slowing effect of fat was reversed by metoprolol (β1-adrenoreceptor antagonist) but not phentolamine (α-adrenoreceptor antagonist). Furthermore, norepinephrine-induced slowing of transit was reversed by ondansetron (5-HT3 receptor antagonist) or naloxone (opioid receptor antagonist). Extending these physiological results, we also found by immunohistochemistry that β1-adrenoreceptors are expressed by neurons of the intrinsic plexuses of the small intestine. We conclude that the slowing of intestinal transit by fat or PYY depends on a β-adrenergic pathway and that this adrenergic pathway acts on serotonergic and opioid pathways.

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Lam, Daniel D., and Lora K. Heisler. "Serotonin and energy balance: molecular mechanisms and implications for type 2 diabetes." Expert Reviews in Molecular Medicine 9, no. 5 (February 2007): 1–24. http://dx.doi.org/10.1017/s1462399407000245.

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The neurotransmitter serotonin is an important regulator of energy balance. In the brain, serotonergic fibres from midbrain raphe nuclei project to key feeding centres, where serotonin acts on specific receptors to modulate the activity of various downstream neuropeptide systems and autonomic pathways and thus affects ingestive behaviour and energy expenditure. Serotonin, released by intestinal enterochromaffin cells, also appears to regulate energy homeostasis through peripheral mechanisms. Serotonergic effects on energy balance lead to secondary effects on glucose homeostasis, based on a well-established link between obesity and insulin resistance. However, serotonergic pathways may also directly affect glucose homeostasis through regulation of autonomic efferents and/or action on peripheral tissues. Several serotonergic compounds have been evaluated for clinical use in the treatment of obesity and type 2 diabetes; results of these trials are discussed here. Finally, future directions in the elucidation of serotonergic metabolic regulation are discussed.

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Torrico, Bàrbara, Judit Cabana-Domínguez, Anu Shivalikanjli, Noèlia Fernàndez-Castillo, and Bru Cormand. "S68EXPLORING DOPAMINERGIC AND SEROTONERGIC PATHWAYS IN PSYCHIATRIC DISORDERS." European Neuropsychopharmacology 29 (October 2019): S148—S149. http://dx.doi.org/10.1016/j.euroneuro.2019.08.069.

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Áfra, J., C. Ertsey, G. Bozsik, and I. Jelencsik. "Cluster Headache Patients Show Marked Intensity Dependence of Cortical Auditory Evoked Potentials during and outside the Bout." Cephalalgia 25, no. 1 (January 2005): 36–40. http://dx.doi.org/10.1111/j.1468-2982.2004.00801.x.

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Central serotonergic neurotransmission was assessed using intensity dependence of cortical auditory evoked potentials (IDAP) in cluster headache (CH) patients during both the active and interictal period. In 15 episodic CH patients and 13 controls previously described methods were used and amplitude-stimulus intensity function (ASF) slopes were computed. In the cluster group mean ASF slope was significantly steeper than in the control group both during the active period (1.53 + 0.90 vs. 0.77 + 0.85, P = 0031) and interictally (1.85 + 1.20 vs. 0.77 + 0.85, P = 0012). In the cluster group IDAPs of active and interictal period did not differ significantly ( P = 0378). Duration of the disease or the present bout, distance from the last attack did not correlate with ASF slopes. In conclusion, our results are compatible with decreased level of serotonergic neurotransmission in raphe-cortical pathways. Diminished serotonergic activity in raphe-hypothalamic serotonergic pathways might be hypothesized influencing the activity of hypothalamic neurons and thus play a role in the genesis of cluster headache.

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Sawynok, Jana. "The 1988 Merck Frosst Award.: The role of ascending and descending noradrenergic and serotonergic pathways in opioid and non-opioid antinociception as revealed by lesion studies." Canadian Journal of Physiology and Pharmacology 67, no. 9 (September 1, 1989): 975–88. http://dx.doi.org/10.1139/y89-154.

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Both ascending and descending noradrenergic and serotonergic pathways have been implicated in mechanisms of antinociception produced by systemic administration of morphine and the non-opioid drugs, baclofen and clonidine. These agents affect the turnover and release of noradrenaline and 5-hydroxytryptamine in various brain regions and the spinal cord, and alter neuronal activity in regions from which ascending and descending aminergic pathways originate. The role of specific pathways in morphine analgesia has been examined by applying electrolytic lesions to discrete brain regions. However, this technique is limited because lesions are nonselective for a particular neuronal population. More recent studies have used microinjection of the neurotoxins 6-hydroxydopamine and 5, 7-dihydroxytryptamine to lesion specific noradrenergic and serotonergic pathways, respectively. Although more selective, this approach may be limited by the development of receptor supersensitivity or other mechanisms of compensation, as certain changes seen soon after microinjection (days) are no longer apparent at later intervals (weeks). Systemic drug administration reveals drug actions at predominant but not clearly identified sites of action. The role of a particular aminergic pathway can be revealed most clearly by combining microinjection of drugs into discrete brain sites with neurotoxin-induced lesions, and examining the effects of such lesions at a range of time intervals. A differential role of a particular pathway may become apparent following systemic or intracerebral administration.Key words: neurotoxin lesions, antinociception, morphine, noradrenaline, baclofen.

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Keesom, Sarah M., and Laura M. Hurley. "Silence, Solitude, and Serotonin: Neural Mechanisms Linking Hearing Loss and Social Isolation." Brain Sciences 10, no. 6 (June 12, 2020): 367. http://dx.doi.org/10.3390/brainsci10060367.

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For social animals that communicate acoustically, hearing loss and social isolation are factors that independently influence social behavior. In human subjects, hearing loss may also contribute to objective and subjective measures of social isolation. Although the behavioral relationship between hearing loss and social isolation is evident, there is little understanding of their interdependence at the level of neural systems. Separate lines of research have shown that social isolation and hearing loss independently target the serotonergic system in the rodent brain. These two factors affect both presynaptic and postsynaptic measures of serotonergic anatomy and function, highlighting the sensitivity of serotonergic pathways to both types of insult. The effects of deficits in both acoustic and social inputs are seen not only within the auditory system, but also in other brain regions, suggesting relatively extensive effects of these deficits on serotonergic regulatory systems. Serotonin plays a much-studied role in depression and anxiety, and may also influence several aspects of auditory cognition, including auditory attention and understanding speech in challenging listening conditions. These commonalities suggest that serotonergic pathways are worthy of further exploration as potential intervening mechanisms between the related conditions of hearing loss and social isolation, and the affective and cognitive dysfunctions that follow.

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Lin, Henry C., Corynn Neevel, and Jin Hai Chen. "Slowing intestinal transit by PYY depends on serotonergic and opioid pathways." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 4 (April 2004): G558—G563. http://dx.doi.org/10.1152/ajpgi.00278.2003.

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Slowing of intestinal transit by fat is abolished by immunoneutralization of peptide YY (PYY), demonstrating a key role for this gut peptide. How PYY slows intestinal transit is not known. We tested the hypothesis that the slowing of intestinal transit by PYY may depend on an ondansetron-sensitive serotonergic pathway and a naloxone-sensitive opioid pathway. In a fistulated dog model, occluding Foley catheters were used to compartmentalize the small intestine into proximal (between fistulas) and distal (beyond midgut fistula) half of gut. Buffer (pH 7.0) was perfused into both proximal and distal gut, and PYY was delivered intravenously. Ondansetron or naloxone was mixed with buffer and delivered into either the proximal or distal half of gut. Intestinal transit was measured across the proximal half of the gut. The slowing of intestinal transit by PYY was abolished when either ondansetron or naloxone was delivered into the proximal, but not the distal gut, to localize the two pathways to the efferent limb of the slowing response. In addition, 5-HT slows intestinal transit with marker recovery decreased from 76.2 ± 3.6% (control) to 33.5 ± 2.4% (5-HT) ( P < 0.0001) but was reversed by naloxone delivered into the proximal gut with marker recovery increased to 79.9 ± 7.2% ( P < 0.0005). We conclude that the slowing of intestinal transit by PYY depends on serotonergic neurotransmission via an opioid pathway.

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Fajemiroye, James Oluwagbamigbe, Pablinny Moreira Galdino, Joelma Abadia Marciano De Paula, Fagundes Fabio Rocha, Moses A. Akanmu, Frederico Argollo Vanderlinde, Jordan K. Zjawiony, and Elson Alves Costa. "Anxiolytic and antidepressant like effects of natural food flavour (E)-methyl isoeugenol." Food Funct. 5, no. 8 (2014): 1819–28. http://dx.doi.org/10.1039/c4fo00109e.

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Stahl, S. "C.06.03 Targeting dopaminergic and serotonergic pathways in schizophrenia." European Neuropsychopharmacology 25 (September 2015): S667. http://dx.doi.org/10.1016/s0924-977x(15)30954-8.

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Dissertations / Theses on the topic "Serotonergic pathways"

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Series, Hugh George. "The characterisation of two distinct ascending serotonergic projections in rats by anatomical, pharmacological and functional methods." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337566.

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Misra, Bibhu Ranjan. "The role of serotonergic afferents in receptive field organization and response properties of cells in rat trigeminal subnucleus interpolaris." Thesis, This resource online, 1993. http://scholar.lib.vt.edu/theses/available/etd-06302009-040342/.

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Paredes, Zúñiga Susana Carolina. "Behavioral and physiological effects of triadimefon in zebrafish are associated with alterations of the dopaminergic and serotonergic pathways." Tesis, Universidad de Chile, 2018. http://repositorio.uchile.cl/handle/2250/168720.

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Tesis entregada a la Universidad de Chile en cumplimiento parcial de los requisitos para optar al grado de Magíster en Ciencias Biológicas mención Biología Celular, Molecular y Neurociencias
CONICYT beca de maestría (# 333265).

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Lau, D. H. W. "Investigating the role of peripheral serotonergic, purinergic and nitric oxide/cGMP pathways in the normal and pathological erectile process and the effect of Vardenafil on diabetic nephropathy." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1409263/.

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Serotonin (5-HT, 5-hydroxytrptamine), purinergic and nitric oxide (NO)/ cyclic guanosine monophosphate (cGMP) pathways have been implicated in human penile erection and erectile dysfunction (ED) and the later also involved in the pathogenesis of diabetic nephropathy (DN). The role and characterisation of the peripheral serotonergic and purinergic pathway in corpus cavernosal smooth muscle (CCSM) function was investigated. Electrical field stimulation of human and rabbit CCSM strips demonstrated the presence of neuronally-derived 5-HT acting on 5-HT(2A) receptors. Organ bath studies also showed that 5-HT caused CCSM contraction via 5-HT(1A), (1B), (2A) and (4) receptor subtypes, which was inhibited by doxazosin (an α-1 receptor antagonist known to have 5-HT inhibitory action). Immunohistochemistry and Western Blot analysis confirmed the presence of these 5-HT receptor subtypes in human CCSM. The effect of 5-HT and sodium nitroprusside (SNP; NO donor) on CCSM function from normal, diabetic and partial bladder outlet obstructed (PBOO) rabbit models were also assessed as these pathological models are associated with ED. There was no difference in 5-HT-induced CCSM contractions between the control and pathological models. In contrast, SNP-mediated relaxations were impaired in diabetic and PBOO rabbits. Vardenafil (phosphodiesterase type-5 inhibitor) improved the impaired CCSM relaxation in both models. Immunohistochemistry also identified the presence of purinergic P2Y6 receptors in human CCSM, which when activated induced tissue relaxation. Finally, the effect oral vardenafil treatment has on established renal impairment in diabetic rabbits was investigated. Vardenafil increased cGMP accumulation and improved renal function in DN. These findings suggests that targeting the peripheral serotonergic and purinergic pathways may be useful therapeutic options in treating ED. In addition, the use of vardenafil may be beneficial in the management of DN.

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Abushwereb, Hanan. "The median raphe-dorsal hippocampus serotonergic pathway : GABA receptor regulation." Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506562.

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Ismail, Khaled M. K. "Genetics of premenstrual syndrome : investigation of specific polymorphisms in the serotonergic pathway." Thesis, Keele University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.443615.

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Donovan, Lauren Janine. "CONTINUOUSLY ACTIVE TRANSCRIPTIONAL PROGRAMS ARE REQUIREDTO BUILD EXPANSIVE SEROTONERGIC AXON ARCHITECTURES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1567703887338716.

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Silva, Daiany Priscilla Bueno da. "Atividade anti-inflamatória e antinociceptiva de 4-((1-fenil-1h-pirazol-4-il) metil) piperazina-1-carboxilato: um novo derivado piperazínico." Universidade Federal de Goiás, 2015. http://repositorio.bc.ufg.br/tede/handle/tede/5497.

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Submitted by Luciana Ferreira (lucgeral@gmail.com) on 2016-04-20T13:30:13Z No. of bitstreams: 2 Dissertação - Daiany Priscilla Bueno da Silva - 2015.pdf: 1122736 bytes, checksum: fc98524b1ad5d0e3a0cb2e1cc87bc933 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5)
Approved for entry into archive by Luciana Ferreira (lucgeral@gmail.com) on 2016-04-20T13:32:30Z (GMT) No. of bitstreams: 2 Dissertação - Daiany Priscilla Bueno da Silva - 2015.pdf: 1122736 bytes, checksum: fc98524b1ad5d0e3a0cb2e1cc87bc933 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5)
Made available in DSpace on 2016-04-20T13:32:30Z (GMT). No. of bitstreams: 2 Dissertação - Daiany Priscilla Bueno da Silva - 2015.pdf: 1122736 bytes, checksum: fc98524b1ad5d0e3a0cb2e1cc87bc933 (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) Previous issue date: 2015-02-25
Conselho Nacional de Pesquisa e Desenvolvimento Científico e Tecnológico - CNPq
The piperazines derivatives are an important class of chemical compounds with a broad spectrum of biological activities such as anti-infectious activity, anti-carcinogenic, anti-nociceptive, anti-hypertensive, anxiolytic and vasorelaxant and are attractive candidates for development of new analgesics and anti-inflammatories drugs. The aim of this study was evaluate the effects of piperazine compound LQFM-008 (4-[(1-phenyl-1H-pyrazol-4-yl) methyl]1-piperazine carboxylic acid ethyl ester) in acute tests of nociception and inflammation and characterize that the mechanisms are involved in the antinociceptive effect. For this study were used male mice weighing between 25 and 35g. In the formalin test, the treatments with LQFM-008 at doses of 48 and 96 μmol/kg (p.o.) reduced the licking time at both neurogenic and inflammatory phases of this test. The anti-inflammatory activity was confirmed, since LQFM-008 at doses of 48 and 96 μmol/kg (p.o.) reduced the formation of paw edema induced by carrageenan at all hours of the test and LQFM-008 in pleurisy test at dose of 96 μmol/kg (p.o.) also reduced leukocyte migration and protein exudation. In the tail-flick and the hot plate tests, the treatment with LQFM-008 at doses of 48 and 96 μmol/kg (p.o.) increased the latency to thermal stimulus, suggesting the involvement of central mechanisms in the antinociceptive effect LQFM-008. The pre-treatment of animals with naloxone (7.5 μmol/kg s.c.) reversed the antinociceptive effect of LQFM-008 only in the first phase of the formalin test, however, the pre-treatment with NAN-190 (1.3 μmol/kg i.p.) and PCPA (500 μmol/kg i.p.) reversed the antinociceptive effect of LQFM-008 in both phases of the test. Thus, the piperazine derivative LQFM-008 exhibit antinociceptive and anti-inflammatory activities in acute test and the antinociceptive effect is resulting from a central action with involvement of opioid receptors and the serotonin pathway.
Os derivados piperazínicos constituem uma importante classe de compostos químicos com largo espectro de atividades biológicas, tais como atividade anti-infecciosa, anti-cancerígena, antinociceptiva, anti-hipertensiva, vasorrelaxante e ansiolítica, tornando-se candidatos atrativos para desenvolvimento de novos fármacos analgésicos e anti-inflamatórios. O objetivo do presente trabalho foi avaliar os efeitos do composto piperazínico LQFM-008 (4-((1-fenil-1H-pirazol-4-il) metil) piperazina-1-carboxilato) em testes agudos de nocicepção e inflamação, buscando caracterizar quais os mecanismos de ação estariam envolvidos no efeito antinociceptivo. Para este estudo foram utilizados camundongos machos, pesando entre 25 e 35g. No teste da formalina os tratamentos com LQFM-008 nas doses de 48 e 96 μmol/kg (v.o.) reduziram o tempo de reatividade à dor tanto na fase neurogênica quanto na fase inflamatória do teste. A atividade anti-inflamatória foi confirmada, uma vez que LQFM-008 nas doses de 48 e 96 μmol/kg (v.o.) reduziu a formação do edema de pata induzido por carragenina em todas as horas deste teste e no teste de pleurisia LQFM-008 na dose de 96 μmol/kg também reduziu a migração de leucócitos e a exsudação proteica. Nos testes de flexão de cauda e da placa quente, o tratamento com LQFM-008 48 e 96 μmol/kg (v.o.) aumentou a latência ao estímulo térmico, sugerindo o envolvimento de mecanismos centrais no efeito antinociceptivo de LQFM-008. O pré-tratamento dos animais com naloxona (7,5 μmol/kg s.c.) reverteu o efeito antinociceptivo de LQFM-008 apenas na primeira fase do teste da formalina, no entanto, os pré-tratamentos com NAN-190 (1,3 μmol/kg i.p.) e PCPA (500 μmol/kg i.p.) reverteram o efeito antinociceptivo de LQFM-008 em ambas as fases do teste. Assim o derivado piperazínico LQFM-008 apresenta atividade antinoceptiva e anti-inflamatória em testes agudos, sendo efeito antinociceptivo decorrente de uma ação central com envolvimento dos receptores opióides e da via serotoninérgica.

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Books on the topic "Serotonergic pathways"

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van den Boogaard, Mark, and Paul Rood. Delirium in Critically Ill Patients. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199398690.003.0002.

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This chapter addresses delirium in critically ill patients in the intensive care unit (ICU), especially the mixed subtype (alternating hyperactivity and hypoactivity). The Confusion Assessment Method for the ICU and the Intensive Care Delirium Screening Checklist are discussed as useful delirium assessment tools in this setting. Several neurotransmitter pathways have been implicated in delirium, including cholinergic, GABAergic, and serotonergic pathways; cytokines and glucocorticoids also appear relevant. Risk factors for delirium in the ICU include older age, prior cognitive impairment, worse illness severity, recent delirium or coma, mechanical ventilation, admission category (especially trauma or neurological/neurosurgical admission), infection, metabolic acidosis, morphine and sedative administration, urea concentration, respiratory failure, and admission urgency. Prevention and treatment of delirium are discussed, including nonpharmacological interventions (frequent reorientation, providing eyeglasses and hearing aids if needed, promoting nighttime sleep, and early mobilization) and judicious use of opiate, sedative, and antipsychotic medications.

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Graat, Ilse, Martijn Figee, and Damiaan Denys. Neurotransmitter Dysregulation in OCD. Edited by Christopher Pittenger. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228163.003.0025.

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Obsessive-compulsive disorder (OCD) is associated with abnormalities in the cortico-striatal–thalamic–cortical (CSTC) circuitry, and may be associated with dysregulation of neurotransmitters within this network. The major neurotransmitters of the CSTC are serotonin, dopamine, glutamate and γ‎-aminobutyric acid (GABA. This chapter reviews evidence of the involvement of these neurotransmitters in OCD from pharmaocological, genetic, and imaging studies. yielding an integrated neurotransmitter model of OCD. It concludes that the neurotransmitter model of OCD involves dopaminergic and glutamatergic overactivity in frontostriatal pathways, along with diminished serotonergic and GABAergic neurotransmission in frontolimbic systems. These neurotransmitter imbalances may explain frontostriatal hyperactivity and impaired frontolimbic emotion regulation. Advancing our understanding of neurotransmitter abnormalities in OCD, and how abnormalities in different transmitter systems relate to one another, holds promise for the development of new pharmacotherapies.

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Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.

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Book chapters on the topic "Serotonergic pathways"

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Tsao, Tzu-Hsin B., and Robert J. Butera. "Computational Model of TASK Channels and PKC-Pathway Dependent Serotonergic Modulatory Effects in Respiratory-Related Neurons." In Integration in Respiratory Control, 382–86. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-73693-8_67.

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Altieri, Stefanie, Yogesh Singh, and Etienne Sibille. "Serotonergic Pathways in Depression." In Neurobiology of Depression, 143–70. CRC Press, 2011. http://dx.doi.org/10.1201/b11232-8.

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"Noradrenergic and Serotonergic Inhibitory Pathways." In Encyclopedia of Pain, 2304. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_201488.

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Lesch, K. Peter, Jens Benninghoff, and Angelika Schmitt. "The psychopharmacogenetic–neurodevelopmental interface in serotonergic gene pathways." In Pharmacogenetics of Psychotropic Drugs, 95–126. Cambridge University Press, 2002. http://dx.doi.org/10.1017/cbo9780511543944.006.

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Renn, Cynthia L., and Susan G. Dorsey. "Nociceptive Processing." In Pain Care Essentials, edited by Mark Schumacher and Beth B. Hogans, 26–40. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199768912.003.0003.

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Chapter 2 describes the molecular events associated with pain signaling. The mechanisms associated with chemical, thermal, and mechanical pain signaling in the peripheral nerve endings are detailed. Molecular signaling mechanisms occurring in the spinal dorsal horn, including the primary afferent nociceptor, the inhibitory interneurons, and the descending on-cells and off-cells projecting from the nucleus raphe magnocellularis are described. Persistent increases in pain signaling resulting from inflammatory mediators are explained with reference to specific molecules. Signaling events at supraspinal levels, such as the thalamus, cortex, periaqueductal gray, and nucleus raphe magnus, including cannabinoids, opioids, and noradrenergic and serotonergic neurotransmitter events, are described as critical to pain pathways with relevance to potential pain therapies.

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Mann, J. John, and Dianne Currier. "Biological aspects of suicidal behaviour." In New Oxford Textbook of Psychiatry, 963–69. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199696758.003.0123.

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To understand the biological underpinnings of multi-determined behaviours such as suicide and attempted suicide it is necessary to situate them within an explanatory model that can elaborate the causal pathways and interrelations between biological, clinical, genetic, and environmental factors that all play a role in suicidal behaviour. Where possible, such a model should be clinically explanatory, incorporate biological correlates, be testable in both clinical and biological studies, and have some utility in identifying high-risk individuals. We have proposed a stress–diathesis model of suicidal behaviour wherein exposure to a stressor precipitates a suicidal act in those with the diathesis, or propensity, for suicidal behaviour. Stressors are generally state-dependent factors such as an episode of major depression or adverse life event. The diathesis, we have hypothesized, comprises trait characteristics such as impulsive aggression, and pessimism. Uncovering the biological mechanisms relevant to the stress and the diathesis dimensions of suicidal behaviour will facilitate the identification of both enduring and proximal markers of risk, as well as potential targets for treatment. One biological correlate of the diathesis for suicidal behaviour appears to be low serotonergic activity. Abnormal serotonergic function may be the result of numerous factors including genetics, early life experience, chronic medical illness, alcoholism or substance use disorder, many of which have been correlated with increased risk for suicidal behaviour. Moreover, serotonergic dysfunction may underlie recurrent mood disorders or behavioural traits that characterize the diathesis, such as aggression and impulsivity. In terms of stress response, the noradrenergic and HPA axis have been the focus of biological studies in suicidal behaviour. This chapter gives an overview of the major neurobiological findings in suicide and attempted suicide, as well as emerging findings from studies of genes related to those systems.

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Edwards, Sandra, and Anna Valros. "Understanding and preventing tail biting in pigs." In Understanding the behaviour and improving the welfare of pigs, 361–400. Burleigh Dodds Science Publishing, 2021. http://dx.doi.org/10.19103/as.2020.0081.10.

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Tail biting is a behavioural problem of pigs which is associated with welfare detriment for both the perpetrator and victim. It is seen to some extent on most farms worldwide and causes considerable economic loss, leading to widespread adoption of tail docking for risk reduction. Its occurrence is often sporadic and unpredictable, as a result of the many different combinations of chronic and acute risk factors which can be present on individual farms. Understanding of the underlying (neuro)physiological mechanisms which lead an individual pig to initiate tail biting is still incomplete, but stress, pro-inflammatory cytokine production, changes in amino acid metabolism and serotonergic brain pathways have been implicated. Rearing pigs with undocked tails and without tail biting is still challenging in commercial practice and requires a high quality of management and stockmanship to minimise risk, detect early warning signs of biting and intervene appropriately.

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van den Brink, Wim, and Falk Kiefer. "Alcohol use disorder." In New Oxford Textbook of Psychiatry, edited by John R. Geddes, Nancy C. Andreasen, and Guy M. Goodwin, 498–506. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198713005.003.0050.

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Alcohol is one of the most frequently used substances, and alcohol-related disorders are common, especially in western societies. While there is no safe lower drinking level, a clear dose–response relationship has been shown between alcohol intake and organ damage. Conceptualization and diagnostic classification of alcohol use disorders have changed over time, focusing most recently on aspects of craving, loss of control, and continued use despite negative consequences. Alcohol acts via various binding sites in the brain and via downstream effects, including glutamatergic, GABAergic, serotonergic, dopaminergic, opioid, and neuroendocrine pathways. For its long-lasting, habit-forming effects, sensitization within the mesolimbic–mesocortical system is crucial. Psychological treatments traditionally focus on motivational enhancement, cognitive behaviour therapy, and the community reinforcement approach. Pharmacological treatment approaches range from aversive and reward-inhibiting to anti-craving compounds and cognitive enhancers, which target opioid, glutamatergic, and monoamine receptors. Improvement of treatment effects can be achieved by polypharmacy and use of personalized medicine, based on clinical characteristics, biomarkers, and genetic indicators.

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Thomas, Peter, and Izhar A. Khan. "Disruption of Nongenomic Steroid Actions on Gametes and Serotonergic Pathways Controlling Reproductive Neuroendocrine Function by Environmental Chemicals." In Endocrine Disruptors, 3–45. CRC Press, 2004. http://dx.doi.org/10.1201/9781420038866-1.

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Thomas, Peter, and Izhar Khan. "Disruption of Nongenomic Steroid Actions on Gametes and Serotonergic Pathways Controlling Reproductive Neuroendocrine Function by Environmental Chemicals." In Endocrine Disruptors, 3–45. CRC Press, 2004. http://dx.doi.org/10.1201/9781420038866.sec1.

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Conference papers on the topic "Serotonergic pathways"

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Monji, F., PG Adaikan, C. Lau Lang, AM Siddiquee Abrar, B. Said Baharudin, and A. Choolani Mahesh. "Ananas comosus extract mediates uterotonic effect through serotonergic pathway." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608425.

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