Many antidepressant drugs acutely increase synaptic levels of the monoamine neurotransmitter, serotonin, but they may also enhance the levels of two other neurotransmitters, norepinephrine and dopamine. Blue genes and the monoamine hypothesis of depression. A modulatory role for monoamines, based on new findings from monoamine depletion experiments in humans g. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central. Effects of past history of major depression on smoking. A brief history of the development of antidepressant drugs. In this paper, we firstly summarized the evidence challenging the monoamine hypothesis and proposed that the antidepressant efficacy of ssris is not. Looking beyond the monoamine hypothesis touchneurology. Enrol and complete the course for a free statement of participation or digital badge if available. For five decades it has been generally accepted that reserpine, an antihypertensive and antipsychotic drug, causes depression. History and evolution of the monoamine hypothesis of depression by hirschfeld rm department of psychiatry and behavioral sciences, university of texas medical branch, galveston 775550188, usa. The symptoms of depression can be improved by agents that act by various mechanisms to increase synaptic concentrations of monoamines.
The major monoamine hypothesis about depression is that absolute concentrations of norepinephrine, 5ht, or both are deficient. For many years, the prevailing hypothesis of depression has been that a deficit in monoamine neurotransmitters, notably norepinephrine and serotonin. Evidence suggests there is a reduction in activity or transmission of noradrenalin na and or serotonin 5ht in the forebrain areas of depressed patients. The monoamine hypothesis is a theory that suggest that clinical are due to a particular chemical imbalances in neurochemistry in the brain of monoamines, such as dopamine, serotonin, and norepinephrine this hypothesis has been a major focus of research in the fields pathophysiology and pharmacotherapy for over 25 years and led to the development of new classes of drugs. The evidence of this hypothesis has primarily emerged from the apparent success of drugs that increase the. The gabaergic deficit hypothesis of major depressive. The monoamine hypothesis of depression 5 does not only propose the crucial involvement of monoamines in the therapeutic effects of antidepressant drugs but also suggests that depression is directly related to decreased monoaminergic transmission. Jul 21, 2016 the finding that depression is often associated with the short allele of the 5httlpr polymorphism has, sometimes, been touted as evidence against the monoamine hypothesis. Evolutionary approaches to depression are attempts by evolutionary psychologists to use the theory of evolution to shed light on the problem of mood disorders. Home depression psych central professional serotonins. A biological explanation for depression is the monoamine hypothesis. They bind themselves to receptors on the next neuron and pass in their message in the form of a small electric charge. The origins of the monoamine hypothesis of depression.
Sep 28, 2017 the serotonin 5ht hypothesis of depression has played an important role in the history of psychiatry, yet it has also been criticized for the delayed onset and inadequate efficacy of selective serotonin reuptake inhibitors ssris. However, individuals without a personal or family history of major depressive disorder tend to not show any mood changes following tryptophan depletion,8 despite the fact that. Actually, most currently used antidepressants have been considered to act based on the monoamine hypothesis. Neurobiological mechanisms in major depressive disorder. Description unipolar depression has a biological explanation because it runs in families. Monoamines are a group of neurotransmitters that regulate mood. Nov 16, 2010 increasing evidence points to an association between major depressive disorders mdds and diverse types of gabaergic deficits. Current treatment strategies for depression are effective in onethird to half of those seeking treatment, leaving a large unmet need for new therapeutic options.
The main limitation for the monoamine hypothesis of depression is the therapeutic lag between initiation of antidepressant treatment and perceived improvement of symptoms. A brief history of antidepressant drug development. Neuronal plasticity or remodeling is a fundamental concept that underlies central nervous system function as it relates to many types. One explanation for this therapeutic lag is that the initial increase in synaptic serotonin is only temporary, as firing of serotonergic neurons in the dorsal raphe adapt via. Monoamine hypothesis of major depression was formulated almost half a century ago, 21 which stated that deficiency of monoamine neurotransmitters, namely, norepinephrine and or serotonin, underlies clinical depression. In the mid1990s, the life time risk for depression was estimated as 3% to 4% worldwide. The emergence of molecular neurobiology with its powerful analytical techniques is rapidly changing the traditional focus of neuropharmacological research. This hypothesis was first started when doctors noticed that reserpine, a monoamine antagonist, was causing depression as a common side effect. In view of recent developments in molecular biology, it is relevant to consider what the actual. Evolution of the monoamine hypothesis of depression 2019. These theories achieved broad popularity in the mid1960s. Monoamine theories associate depression with reduced brain monoamine levels. Increasing evidence points to an association between major depressive disorders mdds and diverse types of gabaergic deficits.
Blue genes and the monoamine hypothesis of depression stephen m. Neuroendocrine markers of monoamine function in depressed patients. Neurobiology of major depressive disorder and bipolar disorder duration. Keywords history, biological psychiatry, depression, monoamine hypothesis, monoamine theory, psychobiology of depression program, nimh, bibliometrics introduction monoamine theories, perhaps more than any other pathophysiological theories, are said to have inaugurated the modern psychopharmacological era in psychiatry healy, 1997. Neurotransmitters are fast chemical messengers that travel between neurons brain cells by crossing the synapse. The monoamine hypothesis posits that depression is caused by decreased monoamine function in the brain. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central noradrenergic and or serotonergic. The use of ketamine in the acute management of depression. With evolvement of neuroscience, the neuroplasticity hypothesis of major depressive disorder mdd has been proposed and may.
Monoamine hypothesis of depression psychology wiki fandom. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central noradrenergic andor serotonergic. The history of depression and treatment verywell mind. Monoamine neurotransmitter systems occur in virtually all vertebrates, where the evolvability of these systems has served to promote the adaptability of vertebrate species to different environments. History and evolution of the monoamine hypothesis of. Tthe monoamine hypothesis of depression predicts that the underlying pathophysiologic basis of depression is a depletion in the levels of serotonin, norepinephrine, andor dopamine in the central nervous system. Besides the fact that antidepression drugs are all monoamine agonists, there is other evidence that supports the theory. Experimental studies involving patients whose depression is currently in remission may help clarify the role of serotonin in major depressive disorder. Argues that the monoamine hypothesis of depression does not address key issues such as why antidepressants are also effective in other disorders such as panic disorder, obsessivecompulsive disorder, and bulimia, and why all drugs that enhance serotonergic or noradrenergic transmission are not necessarily effective in depression. With evolvement of neuroscience, the neuroplasticity hypothesis of major depressive disorder mdd has been proposed and may provide a better framework for. The monoamine hypothesis of depression is that depression is a result of under activity of monoamines especially serotonin.
Several monoamine based pharmacological drug classes have been. N2 the symptoms of depression can be improved by agents that act by various mechanisms to increase synaptic concentrations of monoamines. Depression biological factors psychology wiki fandom. Manipulation of monoamines by administration of precursors or by depletion strategies. Monoamine hypothesis of unipolar depression youtube. It has been almost 50 years since the monoamine hypothesis of depression was articulated, and just over 50 years since the first pharmacological treatment for mdd was discovered. Hypothesis ofthepathophysiology depression an evolving hypothesis of the pathophysiology and treatment of depression involves adaptation or plasticity of neural systems. This hypothesized pathophysiology appears to be supported by the mechanism of action of antidepressants.
History and evolution of the monoamine theory of depression. Effects of monoamines and antidepressants on astrocyte. The hypothesis originated from early empirical clinical observations and has been generally recognized to mean that low concentrations of synaptic monoamines are a primary factor in the etiology of depression, other monoaminerelated. A 8mark evaluate question awards 4 marks for describing biological explanations of unipolar depression ao1 and 4 marks for evaluating them with reference to treatment ao2. The idea of depression being caused by demons and evil spirits has existed in many cultures, including those of the ancient greeks, romans, babylonians, chinese, and egyptians. Pollard perspectives in medicinal chemistry 2014 10. Neuronal plasticity or remodeling is a fundamental concept that underlies central nervous system function as it. Feb 14, 2012 the monoamine hypothesis posits that depression is caused by decreased monoamine function in the brain. Role in the historical development of the monoamine hypothesis 2003 journal of the history of the neurosciences the monoamine hypothesis has been retained for nearly fifty years, despite a steady accumulation of contradictory evidence, because it remains useful.
The discovery that reserpine depletes brain monoamines was an important factor in the development of the monoamine hypothesis of depression, and it continues to be widely cited in support of this hypothesis. Jan 26, 2005 attempts to validate the monoamine hypothesis by direct measurements of monoamine function in human subjects. The monoamine hypothesis has been accepted as the most common hypothesis of major depressive disorder mdd for a long period because of its simplicity and understandability. Therefore, they knew that monoamine agonist decrease depression, but they can also induce depression. Depression is generally thought of as dysfunction, but it is much more common than schizophrenia, and its prevalence does not increase with age the way dementia and other organic dysfunction commonly does. The functional deficiency of noradrenergic transmission in depression was, then, inferred from the effects of imipraminelike drugs and monoamine oxidase inhibitors on catecholamine. Depression results from a deficiency in the concentrations or in metabolic dysregulation of the monoamines. Evolution a phylogenetic tree showing how a number of monoamine receptors are related to each other. History and evolution of the monoamine hypothesis of depression. Monoamine hypothesis is a biological theory stating that depression is caused by the underactivity in the brain of monoamines, such as dopamaine, serotonin, and norepinephrine in the 1950s the monoamine oxidase inhibitors maois and and tricyclic antidepressants were accidentally discovered to be effective in the treatment of depression.
Ne regulation of 5ht release monoamine interactions. Monoamine hypothesis definition of monoamine hypothesis by. Sep 19, 2017 the monoamine hypothesis has been accepted as the most common hypothesis of major depressive disorder mdd for a long period because of its simplicity and understandability. Attempts to validate the monoamine hypothesis by direct measurements of monoamine function in human subjects. Tthe monoamine hypothesis of depression predicts that the underlying pathophysiologic basis of depression is a depletion in the levels of serotonin, norepinephrine, and or dopamine in the central nervous system. The evolution of the monoamine hypotheses of affective disorders reflects, by and large, the evolution of our understanding of the mode of action of antidepressant drugs. Depression may be caused by a stressinduced deficiency in monoaminergic activation of genes that code for neurotrophic factors. In the 1950s, the amine hypothesis of depression was proposed after it was observed that patients treated for hypertension with reserpine developed depression. According to the monoamine hypothesis, depression can be ascribed to deficits in the monoamine neurotransmitters. Depression monoamine hypothesis psychology wiki fandom. The hypothesis originated from early empirical clinical observations and has been generally recognized to mean that low concentrations of synaptic monoamines are a primary factor in the etiology of depression, other monoamine related disease.
The gabaergic deficit hypothesis of major depressive disorder. Major depressive disorder mdd is a chronic, recurring, and debilitating mental illness that is the most common mood disorder in the united states. You need a conclusion to get a mark in the top band 78 marks. In order to test this hypothesis and more fully characterize the role of serotonin and catecholamines in the pathophysiology of depression and the mechanism of action of antidepressant. T1 history and evolution of the monoamine hypothesis of depression. From the establishment of this hypothesis in the early 1960s through the 1990s, researchers discovered a direct relationship between diminished serotonin pathways and. Is this evidence for or against the monoamine hypothesis of depression reserpine induces depression by inhibiting noradrenaline and 5ht storage.
Monoamine hypothesis depression and neurotransmitters. The original hypothesis that brain monoamine systems have a primary direct role in depression has been through several modifications during the past 30 years. The serotonin 5ht hypothesis of depression has played an important role in the history of psychiatry, yet it has also been criticized for the delayed onset and inadequate efficacy of selective serotonin reuptake inhibitors ssris. Brain and cognition discovery foundation 3,491 views. Because of this belief, it was often treated with methods such as beatings, physical restraint, and starvation in an attempt to drive the demons out.
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