Psychotropic management of behavioral disorders after head trauma.
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A rational basis for the psychopharmacologic management of behavioral disturbances after head trauma has been presented that is predicated on research in neurotransmitter changes that evolve subsequent to head trauma. The paucity of human studies in this area mandates the use of experimental models and evidence garnered from provocative challenges to suggest the underlying neurotransmitter profile in various behavioral abnormalities. Multiple neurotransmitter circuits exist that provide parallel, duplicate, and redundant systems for these behaviors. Certainly, alternative explanations could be offered for the examples cited above. Furthermore, measurement of neurotransmitter metabolite concentration in cerebrospinal fluid does not allow specific inferences to be made regarding topographic correlation and neurotransmitter function. Nor does it afford assessment of regional differences in psychotropic influence on neurotransmitter receptors. New imaging techniques (eg, positron emission tomography) will certainly aid in this determination. Current investigations, however, support the concept that neurotransmitter changes do occur after head injury, that these alterations exist during the time that "recovery" occurs, and that psychotropic agents influence this recovery process. Further research is needed to clarify neurotransmitter changes after head injury and to identify psychotropic intervention strategies that facilitate the recovery process.Keywords:
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The brain is composed of numerous neurons, and information is chemically transmitted between neurons by neurotransmitters. In other words, the function of the brain is the sum of synaptic transmission phenomena. Therefore, to clarify physiological brain function and pathophysiology of involuntary movements, quantification of both neurotransmitters and receptors are indispensable. In the present paper, changes in neurotransmitters and receptors in the brain of various type of involuntary movements are reviewed. In spite of the fact that changes in neurotransmitter systems are the cardinal pathological lesions in involuntary movements, there is little evidence to support the view that these changes are actually related to the generation of involuntary movements. It is required to summarize all informations from neurotransmitter system analysis, behavioral pharmacology, clinical observations and animal models for clarifying the pathophysiology and developing a better therapeutic strategy against various involuntary movements.
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Mild traumatic brain injury (TBI) often results in pathophysiological damage that can manifest as both acute and chronic neurological deficits. In an attempt to repair and reconnect disrupted circuits to compensate for loss of afferent and efferent connections, maladaptive circuitry is created and contributes to neurological deficits, including post-concussive symptoms. The TBI-induced pathology physically and metabolically changes the structure and function of neurons associated with behaviorally relevant circuit function. Complex neurological processing is governed, in part, by circuitry mediated by primary and modulatory neurotransmitter systems, where signaling is disrupted acutely and chronically after injury, and therefore serves as a primary target for treatment. Monitoring of neurotransmitter signaling in experimental models with technology empowered with improved temporal and spatial resolution is capable of recording in vivo extracellular neurotransmitter signaling in behaviorally relevant circuits. Here, we review preclinical evidence in TBI literature that implicates the role of neurotransmitter changes mediating circuit function that contributes to neurological deficits in the post-acute and chronic phases and methods developed for in vivo neurochemical monitoring. Coupling TBI models demonstrating chronic behavioral deficits with in vivo technologies capable of real-time monitoring of neurotransmitters provides an innovative approach to directly quantify and characterize neurotransmitter signaling as a universal consequence of TBI and the direct influence of pharmacological approaches on both behavior and signaling.
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The study of the ontogenesis of neurotransmitter systems is relevant not only to understand the development of the central nervous system. The new horizons that have appeared in research into the use of stem cells in the repair of damaged neurons are allowing attempts to be made to imitate the differentiation and maintenance of the type of affected neuron. To achieve this, it is necessary to understand which signals direct the differentiation and the molecules that guide their maturation, their survival and the maintenance of their functionality. Furthermore, the early emergence of these systems during ontogenesis has led us to question their participation in the regulation of the development of the central nervous system.To describe the most significant events in the development of the neurotransmitter systems and to discuss some of the processes that take part in the ontogenesis of the nervous system.The study will offer a chronological review of the sequence of molecular events in the main neurotransmitter systems that allow the phenotype to be established and the appearance of receptors and transporters. Likewise, the role they play in events like neurogenesis, proliferation, differentiation and neuronal migration will also be outlined.The neurotransmitter systems regulate events that range from neurogenesis to both radial and tangential cortical migration, as well as intervening in the correct maturation of their own system.
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Is functional neuroimaging a royal way to understand brain function or is it a new phrenology without an exact understanding what we measure? After two decades of imaging revolution, more and more authors ask this question. Brain functions are multidimensional, which can be approached from the point of (1) behavioural measures, (2) brain activation as reflected by blood flow and metabolic changes, (3) electrical activity of cells and cell-populations, and (4) neurotransmitter dynamics (release, receptor binding and reuptake). Using imaging techniques, we must take into consideration that even during the simplest task all of these processes operate in a closely interacting manner. Therefore, before drawing final conclusions about brain functions on the basis of a single aspect of these mechanisms, we must clarify the exact relationship among them. In this paper, we address this issue in order to draw attention to a number of uncertainties and controversies in the relationship of the four facets of brain functions.
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A rational basis for the psychopharmacologic management of behavioral disturbances after head trauma has been presented that is predicated on research in neurotransmitter changes that evolve subsequent to head trauma. The paucity of human studies in this area mandates the use of experimental models and evidence garnered from provocative challenges to suggest the underlying neurotransmitter profile in various behavioral abnormalities. Multiple neurotransmitter circuits exist that provide parallel, duplicate, and redundant systems for these behaviors. Certainly, alternative explanations could be offered for the examples cited above. Furthermore, measurement of neurotransmitter metabolite concentration in cerebrospinal fluid does not allow specific inferences to be made regarding topographic correlation and neurotransmitter function. Nor does it afford assessment of regional differences in psychotropic influence on neurotransmitter receptors. New imaging techniques (eg, positron emission tomography) will certainly aid in this determination. Current investigations, however, support the concept that neurotransmitter changes do occur after head injury, that these alterations exist during the time that "recovery" occurs, and that psychotropic agents influence this recovery process. Further research is needed to clarify neurotransmitter changes after head injury and to identify psychotropic intervention strategies that facilitate the recovery process.
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The transmitter phenotype of a neuron has long been thought to be stable for the lifespan. Much as eyes have one color and do not change it over time, neurons have been thought to have one neurotransmitter and retain it for their lifetime. Both principles, exclusivity and stability, are challenged by recent data. More and more neurons in different regions of the brain appear to coexpress two or more neurotransmitters. Moreover, the profile of neurotransmitter expression of a given neuron has been shown to change over time, both during development and in response to changes in activity. The present review summarizes recent studies of this neurotransmitter phenotype plasticity (NPP). Homeostatic mechanisms of plasticity are aimed at maintaining the system within a functional range. They appear to be critical for optimal network operations and have been thought to operate largely by regulating intrinsic excitability, synapse number and synaptic strength. NPP provides a new and unexpected level of regulation of network homeostasis. We propose that it provides the basis for NT coexpression and discuss emerging issues and new questions for further studies in coming years.
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Neurotransmitters should fulfil the following main three criteria; 1) they should be localized in synaptic terminals, 2) they should have certain actions on neurons, 3) they should be released from the terminals after nerve stimulation. In addition to the above three, recent studies have revealed that neurotransmitters should have their own receptors. Moreover, recent immunohistochemical studies have revealed certain neurons to have two or more neurotransmitter candidates; one classic and the other non-classic neurotransmitter candidate. These progresses in the field of neurotransmitter science were briefly reviewed. As an extension of the basic studies mentioned above, clinical studies of measurements of neurotransmitter markers in brains of neurodegenerative disorders are now actively performed. Based on my own studies in the same line, it is possible to summarize the fundamental patterns of neurotransmitter alterations in neurodegenerative disorders as follows: 1) they decrease as a result of degeneration of neuron groups (the most popular pattern); 2) they decrease in spite of the morphologically normal appearance of neurons ("biochemical non-functioning"); 3) they increase in the projecting regions of certain neurons which escaped degeneration. This may be a result of simple condensation of normal nerve terminals or real increase based on the compensatory mechanisms.
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