A neurotrophic hypothesis of depression: role of synaptogenesis in the
A neurotrophic hypothesis of depression and treatment response. ... Synaptogenesis is a structural change at a subcellular level that takes place in response to synaptic activity, and provides a mechanism for processing and incorporating new information that can be used to make the appropriate, ...
A neurotrophic hypothesis of depression: role of synaptogenesis in the
A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor antagonists ... actions of antidepressant treatment could be mediated in part by blocking or reversing the atrophy caused by stress and depression. Recent studies have identified a novel, rapid-acting antidepressant, ketamine, in treatment-resistant ...
Synaptic Dysfunction in Depression: Potential Therapeutic Targets
Synaptic Dysfunction in Depression: Potential Therapeutic ...
The Neurotrophic Hypothesis of Depression Revisited: New Insights and
Here, we revisit the neurotrophic hypothesis of depression more than 20 years later, restricting our focus to BDNF as the prototypical example best studied in this regard, and discuss evidence in support, as well as challenges to this hypothesis. ... A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor ...
REVIEW Synaptic Dysfunction in Depression: Potential ...
We propose a hypothesis that depression is caused by disruption of homeostatic mechanisms that control synaptic plasticity, resulting in de-stabilization and loss of synaptic connections in mood and emotion circuitry. We compare and contrast the mechanisms underlying typical anti-depressantsandketamine,particularlytheinduction of synaptogenesis.
The evolving neurobiology of depression: from synapses to neurons
Changing paradigms include thinking about the neural circuits involved in depression, the waxing and waning of neurogenesis and synaptogenesis, and realising that there may be important abnormalities of glial cells rather than just abnormalities of neuron to neuron synapses. These shifts in paradigm have occurred within broader developments in ...
A neurotrophic hypothesis of depression: role of synaptogenesis in the
To directly test this hypothesis, the influence of rapamycin, a selective inhibitor of mTOR (figure 3), on synaptogenesis was examined. Rapamycin pretreatment completely blocked ketamine-induction of spine number and function of layer V pyramidal neurons in the PFC [ 42 ].
Dysregulation of adult hippocampal neuroplasticity in major depression
More recently, however, there has been a paradigm shift toward a neuroplasticity hypothesis of depression in which downstream effects of antidepressants, such as increased neurogenesis, contribute ...
(PDF) A neurotrophic hypothesis of depression: Role of synaptogenesis
A neurotrophic hypothesis of depression: Role of synaptogenesis in the actions of NMDA receptor antagonists September 2012 Philosophical Transactions of The Royal Society B Biological Sciences 367 ...
PDF A neurotrophic hypothesis of depression: role of synaptogenesis in the
A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor antagonists ... synapses or synaptogenesis is a key form of neuro-plasticity, and represents a ...
A neurotrophic hypothesis of depression: role of synaptogenesis in the
We have found that ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, causes a rapid induction of synaptogenesis and spine formation in the PFC via stimulation of the mammalian target of the rapamycin signalling pathway and increased synthesis of synaptic proteins. These effects of ketamine rapidly reverse the atrophy of PFC neurons ...
Depression, Antidepressants, and Neurogenesis: A Critical ...
Depression, Antidepressants, and Neurogenesis: A Critical ...
Synaptic Dysfunction in Depression: Potential Therapeutic Targets
Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response.
Synaptic plasticity and depression: New insights from stress and rapid
Abstract. Depression is a common, devastating illness. Current pharmacotherapies help many patients, but there are high rates of partial- or non-response and the delayed onset of the effects of antidepressant leave many patients inadequately treated. However, new insights into the neurobiology of stress and human mood disorders have shed light ...
The neural plasticity theory of depression: assessing the roles of
The neural plasticity theory of depression: assessing the roles of adult neurogenesis and PSA-NCAM within the hippocampus Neural Plast. ... migration, and integration of new neurons to neurite outgrowth, synaptogenesis, and the modulation of mature synapses. This review critically assesses the role of adult hippocampal neurogenesis and the cell ...
[PDF] A neurotrophic hypothesis of depression: role of synaptogenesis
Ketamine causes a rapid induction of synaptogenesis and spine formation in the PFC via stimulation of the mammalian target of the rapamycin signalling pathway and increased synthesis of synaptic proteins, which rapidly reverse the atrophy of PFC neurons caused by chronic stress. Molecular and cellular studies have demonstrated opposing actions of stress and antidepressant treatment on the ...
Leptin in depression: a potential therapeutic target
The classic neurotrophic hypothesis of depression presents that depression risk factors and ... A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor ...
Synaptic Mechanisms Regulating Mood State Transitions in Depression
Depression is an episodic form of mental illness characterized by mood state transitions with poorly understood neurobiological mechanisms. Antidepressants reverse the effects of stress and depression on synapse function, enhancing neurotransmission, increasing plasticity, and generating new synapses in stress-sensitive brain regions. These properties are shared to varying degrees by all known ...
Does neurogenesis relate to depression and do antidepressants ...
Depression is characterized by atrophy in several brain structures, with the hippocampus seemingly particularly affected. A wide variety of cellular mechanisms have been proposed for these structural modifications, including the regression of dendritic branching. While neurogenesis alone appears ina …
The neurobiology of depression—revisiting the serotonin hypothesis. I
The monoamine hypothesis of depression was proposed by Schildkraut , referring essentially to catecholamines. Then, Coppen [ 8 ] emphasized the possible role of 5-HT. In its original formulation, the 5-HT hypothesis postulated a deficit in 5-HT as a primary cause, reversed by antidepressants, which would restore normal function in depressed ...
What Is Depression, Anyway?: The Synapse Hypothesis
According to Duman's Neurobiology of Stress, Depression, and Rapid Acting Antidepressants, it's decreased synaptogenesis, and it's regulated by a protein complex called mTORC1. Neurons communicate with other neurons through branches called dendrites and connections called synapses. Healthy neurons often create new dendrites and synapses ...
Glutamatergic System in Depression and Its Role in Neuromodulatory
Glutamatergic System and Depression. Glutamate is the principal excitatory neurotransmitter in the brain, and glutamatergic mechanisms play significant roles in nearly all key functions affected in depressed states ().Postmortem studies have put forward evidence linking glial cell abnormalities, whose role is synaptic glutamate removal, and the pathophysiology of mood disorders ().
COMMENTS
A neurotrophic hypothesis of depression and treatment response. ... Synaptogenesis is a structural change at a subcellular level that takes place in response to synaptic activity, and provides a mechanism for processing and incorporating new information that can be used to make the appropriate, ...
A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor antagonists ... actions of antidepressant treatment could be mediated in part by blocking or reversing the atrophy caused by stress and depression. Recent studies have identified a novel, rapid-acting antidepressant, ketamine, in treatment-resistant ...
Synaptic Dysfunction in Depression: Potential Therapeutic ...
Here, we revisit the neurotrophic hypothesis of depression more than 20 years later, restricting our focus to BDNF as the prototypical example best studied in this regard, and discuss evidence in support, as well as challenges to this hypothesis. ... A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor ...
We propose a hypothesis that depression is caused by disruption of homeostatic mechanisms that control synaptic plasticity, resulting in de-stabilization and loss of synaptic connections in mood and emotion circuitry. We compare and contrast the mechanisms underlying typical anti-depressantsandketamine,particularlytheinduction of synaptogenesis.
Changing paradigms include thinking about the neural circuits involved in depression, the waxing and waning of neurogenesis and synaptogenesis, and realising that there may be important abnormalities of glial cells rather than just abnormalities of neuron to neuron synapses. These shifts in paradigm have occurred within broader developments in ...
To directly test this hypothesis, the influence of rapamycin, a selective inhibitor of mTOR (figure 3), on synaptogenesis was examined. Rapamycin pretreatment completely blocked ketamine-induction of spine number and function of layer V pyramidal neurons in the PFC [ 42 ].
More recently, however, there has been a paradigm shift toward a neuroplasticity hypothesis of depression in which downstream effects of antidepressants, such as increased neurogenesis, contribute ...
A neurotrophic hypothesis of depression: Role of synaptogenesis in the actions of NMDA receptor antagonists September 2012 Philosophical Transactions of The Royal Society B Biological Sciences 367 ...
A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor antagonists ... synapses or synaptogenesis is a key form of neuro-plasticity, and represents a ...
We have found that ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, causes a rapid induction of synaptogenesis and spine formation in the PFC via stimulation of the mammalian target of the rapamycin signalling pathway and increased synthesis of synaptic proteins. These effects of ketamine rapidly reverse the atrophy of PFC neurons ...
Depression, Antidepressants, and Neurogenesis: A Critical ...
Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response.
Abstract. Depression is a common, devastating illness. Current pharmacotherapies help many patients, but there are high rates of partial- or non-response and the delayed onset of the effects of antidepressant leave many patients inadequately treated. However, new insights into the neurobiology of stress and human mood disorders have shed light ...
The neural plasticity theory of depression: assessing the roles of adult neurogenesis and PSA-NCAM within the hippocampus Neural Plast. ... migration, and integration of new neurons to neurite outgrowth, synaptogenesis, and the modulation of mature synapses. This review critically assesses the role of adult hippocampal neurogenesis and the cell ...
Ketamine causes a rapid induction of synaptogenesis and spine formation in the PFC via stimulation of the mammalian target of the rapamycin signalling pathway and increased synthesis of synaptic proteins, which rapidly reverse the atrophy of PFC neurons caused by chronic stress. Molecular and cellular studies have demonstrated opposing actions of stress and antidepressant treatment on the ...
The classic neurotrophic hypothesis of depression presents that depression risk factors and ... A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor ...
Depression is an episodic form of mental illness characterized by mood state transitions with poorly understood neurobiological mechanisms. Antidepressants reverse the effects of stress and depression on synapse function, enhancing neurotransmission, increasing plasticity, and generating new synapses in stress-sensitive brain regions. These properties are shared to varying degrees by all known ...
Depression is characterized by atrophy in several brain structures, with the hippocampus seemingly particularly affected. A wide variety of cellular mechanisms have been proposed for these structural modifications, including the regression of dendritic branching. While neurogenesis alone appears ina …
The monoamine hypothesis of depression was proposed by Schildkraut , referring essentially to catecholamines. Then, Coppen [ 8 ] emphasized the possible role of 5-HT. In its original formulation, the 5-HT hypothesis postulated a deficit in 5-HT as a primary cause, reversed by antidepressants, which would restore normal function in depressed ...
According to Duman's Neurobiology of Stress, Depression, and Rapid Acting Antidepressants, it's decreased synaptogenesis, and it's regulated by a protein complex called mTORC1. Neurons communicate with other neurons through branches called dendrites and connections called synapses. Healthy neurons often create new dendrites and synapses ...
Glutamatergic System and Depression. Glutamate is the principal excitatory neurotransmitter in the brain, and glutamatergic mechanisms play significant roles in nearly all key functions affected in depressed states ().Postmortem studies have put forward evidence linking glial cell abnormalities, whose role is synaptic glutamate removal, and the pathophysiology of mood disorders ().