Synaptic plasticity is a property of adult as well as developing or young cortex, and reflects how synaptic strength changes with experience. Its relevance to psychiatry is seen in the course of the illnesses psychiatrists treat. Clinical research supports the notion that psychiatric illnesses progress and become more refractory to treatment over time. This has been demonstrated most clearly in bipolar disorders and schizophrenia. The expression or severity of an illness changing over time implies an underlying change in the neurobiology of the illness. Neuroscience studies of learning and memory have helped to illuminate the plasticity of adult cortex, which can be used as a blueprint for brain changes associated with psychiatric illnesses. What evidence is there for structural brain changes with learning?
[...] This suggests that extrapyramidal and antipsychotic effects can be dissociated in terms of their respective molecular neuroanatomies. Antidepressant treatments increase intracellular phosphorylation of cAMP-responsive proteins (e.g., CRE) that lead to transcription of specific genes. One of these genes, brain-derived neurotrophic factor, has also been implicated in neuronal plasticity and may play a role in the potential restitutive effects of treatment with antidepressant medications. These recent observations on the intracellular effects of psychiatric medications have potentially far-reaching implications for the understanding of mental illness and approaches to their treatments. The traditional [...]
[...] Neuronal Plasticity Synaptic plasticity is a property of adult as well as developing or young cortex, and reflects how synaptic strength changes with experience. Its relevance to psychiatry is seen in the course of the illnesses psychiatrists treat. Clinical research supports the notion that psychiatric illnesses progress and become more refractory to treatment over time. This has been demonstrated most clearly in bipolar disorders and schizophrenia. The expression or severity of an illness changing over time implies an underlying change in the neurobiology of the illness. [...]
[...] Protein kinases are enzymes that phosphorylate multiple substrates, altering their functioning, altering neuronal physiology, and increasing synaptic strength. When protein kinases become autonomously activated, they are independent of the second messenger. This explains how a short-lived increase in second messengers results in longer- lasting changes in synaptic strength. Protein kinases involved in LTP include protein kinase C calcium/calmodulin-dependent kinase II (CaMKII), the cyclic adenosine monophosphate (cAMP) dependent protein kinase and protein tyrosine kinase (PTK). Substrates for phosphorylation implicated in long-term potentiation include GAP-43 for PKC, the glutamate receptor by CaMKII, and synaptophysin, the nicotinic acetylcholine receptor, and the glutamate receptor by PTKs. [...]
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