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Dopaminergic Pathways (dopaminergic + pathway)
Selected AbstractsContribution of perospirone and risperidone to reduce delirium in senile patientsPSYCHOGERIATRICS, Issue 1 2008Michikazu USHIJIMA Abstract Background:, Serotonin,dopamine antagonists (SDAs) inhibit dopaminergic transmission in the mesolimbic system less than in the nigrostriatal dopaminergic pathway, which relates to the extrapyramidal side-effects of these drugs. The SDAs seem to have an adequate receptor binding profile for the management of the behavioral and psychiatric symptoms of dementia. However, clinicians are discouraged from prescribing SDAs for elderly patients because of an advisory statement from the US Food and Drug Administration that warns about an increased mortality rate among elderly patients treated with atypical antipsychotics. Methods:, We conducted a retrospective study involving 16 elderly patients (mean age 84.9 years; range 67,94 years) with delirium who were treated with one of two SDAs, namely perospirone (4,12 mg/day) or risperidone (1,2 mg/day). The time-course of their psychiatric symptoms was assessed using subcategories of the Delirium Rating Scale (DRS) before treatment and on Days 10 and 24 of treatment. Results:, Total DRS scores were significantly decreased from baseline in both treatment groups. Both agents led to significant improvements from baseline in psychomotor behavior and lability of mood. Of interest, perospirone decreased hallucinations and delusions and improved sleep,awake cycle disturbances compared with baseline. No serious side-effects were seen with either drug. Conclusions:, Both perospirone and risperidone are effective in the management of delirium in elderly patients. The improvement in the sleep,awake cycle with perospirone may be derived from its short pharmacological half-life. [source] Ephrin-A5 regulates the formation of the ascending midbrain dopaminergic pathwaysDEVELOPMENTAL NEUROBIOLOGY, Issue 1 2009Margaret A. Cooper Abstract Dopaminergic neurons from the substantia nigra and the ventral tegmental area of the midbrain project to the caudate/putamen and nucleus accumbens, respectively, establishing the mesostriatal and the mesolimbic pathways. However, the mechanisms underlying the development of these pathways are not well understood. In the current study, the EphA5 receptor and its corresponding ligand, ephrin-A5, were shown to regulate dopaminergic axon outgrowth and influence the formation of the midbrain dopaminergic pathways. Using a strain of mutant mice in which the EphA5 cytoplasmic domain was replaced with ,-galactosidase, EphA5 protein expression was detected in both the ventral tegmental area and the substantia nigra of the midbrain. Ephrin-A5 was found in both the dorsolateral and the ventromedial regions of the striatum, suggesting a role in mediating dopaminergic axon-target interactions. In the presence of ephrin-A5, dopaminergic neurons extended longer neurites in in vitro coculture assays. Furthermore, in mice lacking ephrin-A5, retrograde tracing studies revealed that fewer neurons sent axons to the striatum. These observations indicate that the interactions between ephrin-A ligands and EphA receptors promote growth and targeting of the midbrain dopaminergic axons to the striatum. © 2008 Wiley Periodicals, Inc. Develop Neurobiol, 2009 [source] Cytokines and Cognition,The Case for A Head-to-Toe Inflammatory ParadigmJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 12 2002Craig J. Wilson MBBS The brain is not only immunologically active of its own accord, but also has complex peripheral immune interactions. Given the central role of cytokines in neuroimmmunoendocrine processes, it is hypothesized that these molecules influence cognition via diverse mechanisms. Peripheral cytokines penetrate the blood-brain barrier directly via active transport mechanisms or indirectly via vagal nerve stimulation. Peripheral administration of certain cytokines as biological response modifiers produces adverse cognitive effects in animals and humans. There is abundant evidence that inflammatory mechanisms within the central nervous system (CNS) contribute to cognitive impairment via cytokine-mediated interactions between neurons and glial cells. Cytokines mediate cellular mechanisms subserving cognition (e.g., cholinergic and dopaminergic pathways) and can modulate neuronal and glial cell function to facilitate neuronal regeneration or neurodegeneration. As such, there is a growing appreciation of the role of cytokine-mediated inflammatory processes in neurodegenerative diseases such as Alzheimer's disease and vascular dementia. Consistent with their involvement as mediators of bidirectional communication between the CNS and the peripheral immune system, cytokines play a key role in the hypothalamic-pituitary-adrenal axis activation seen in stress and depression. In addition, complex cognitive systems such as those that underlie religious beliefs, can modulate the effects of stress on the immune system. Indirect means by which peripheral or central cytokine dysregulation could affect cognition include impaired sleep regulation, micronutrient deficiency induced by appetite suppression, and an array of endocrine interactions. Given the multiple levels at which cytokines are capable of influencing cognition it is plausible that peripheral cytokine dysregulation with advancing age interacts with cognitive aging. [source] Androgen Decreases Dopamine Neurone Survival in Rat MidbrainJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2010M. L. Johnson Clinical studies show that men are more likely to develop disorders affecting midbrain dopaminergic pathways, such as drug addiction and Parkinson's disease (PD). Although a great deal of focus has been given to the role of oestrogen in the maintenance of midbrain dopaminergic pathways, little is known about how testosterone influences these pathways. In the present study, we used stereological analysis of tyrosine hydroxylase-immunoreactive (TH-IR) cell bodies to determine how testosterone influences the dopaminergic cell bodies of the substantia nigra pars compacta (SNpc) and ventral tegmental area (VTA). Rats and mice were castrated at postnatal day (PN) 60, and these midbrain cell populations were counted on PN 90. One month after castration, TH-IR cell number had increased in the SNpc and VTA of rats and mice. Replacement with testosterone or the non-aromatisable analogue dihydrotestosterone (DHT) in castrated animals reduced TH-IR cell number in the SNpc and VTA in rats. In mice, the decrease of TH-IR cell number with testosterone or DHT replacement was observed only in the SNpc. The apparent increase in TH-IR neurone number after castration is not explained by an increase in TH expression because the number of nondopaminergic cells (TH-immunonegative, TH-IN) did not decrease proportionally after castration. TH-IN cell number did not change after castration or hormone replacement in rat or mouse SNpc or VTA. These findings suggest that testosterone may play a suppressive role in midbrain dopaminergic pathways. [source] Blink rate variability in patients with panic disorder: New trial using audiovisual stimulationPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 5 2002MAKI KOJIMA Abstract Several lines of evidence have implicated central dopaminergic pathways in the modulation of spontaneous blink rate (BR). Furthermore, previous studies have indicated a relationship between spontaneous BR and anxiety and/or depression. However, to our knowledge, there is no report on the examination of BR in a group of patients with panic disorder (PD). During the conditions of rest and with audiovisual stimulation, exposed to a video of imaginary experiences, such as driving a motor vehicle or diving into the sea, BR was examined in 11 male patients with PD and compared with the BR of 16 age-matched normal controls. The BR was significantly higher in PD patients relative to normal controls under both conditions. In particular, the PD group had a higher BR score during the sea scene as relaxation compared with the normal controls. In conclusion, although the sample size was small the present preliminary study, these findings suggest that BR may have potential for application in the assessment of anxiety state, which is consistent with previous studies. [source] Behavioral genetics in antisocial spectrum disorders and psychopathy: A review of the recent literatureBEHAVIORAL SCIENCES & THE LAW, Issue 2 2010Tracy D. Gunter M.D. Behavioral geneticists are increasingly using the tools of molecular genetics to extend upon discoveries from twin, family, and adoption studies concerning the heritability of antisocial spectrum disorders and psychopathy. While there is a substantial body of research concerning antisocial spectrum disorders in the behavioral genetics literature, only a few studies could be located using the phenotype of psychopathy. In this report we summarize some of the recent molecular genetics work concerning antisocial spectrum disorders and psychopathy, with a focus on genes involved in the serotonergic and dopaminergic pathways, while also mentioning some of the novel genetic factors being considered. Monoamine oxidase (MAOA) and the serotonin transporter (5HTT) are reviewed at length, as these genes have received significant scientific attention in recent years and are sites of high biological plausibility in antisocial spectrum disorders and psychopathy. Copyright © 2010 John Wiley & Sons, Ltd. [source] Depression in Parkinson's disease , a reviewACTA NEUROLOGICA SCANDINAVICA, Issue 1 2006A. Lieberman Major depression is present, at any given time, in 20,40% of Parkinson's disease (PD) patients, several times the prevalence in the general population. In addition, depression may precede the diagnosis of PD. These observations and reports of depression during deep brain stimulation of regions contiguous to the substantia nigra, as well as reports of dopamine agonist improving depression, suggest depression, rather than being mainly a psychological reaction to a debilitating disease, is part of PD. It is postulated that mesolimbic and mesocortical dopaminergic pathways that mediate affect, behavior, and cognition, contribute to depression in PD. [source] | ||||||||||