36 results match your criteria: "and the Department of Psychiatry at the University of California San Diego[Affiliation]"

Norepinephrine and dopamine work in a cooperative yet reciprocal manner to regulate information processing at pyramidal neurons in the prefrontal cortex.

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Voltage sensitive calcium channels (VSCCs) have unique structures and functions that distinguish them from other ion channels, especially the voltage sensitive sodium channels (VSSCs). Modulation of VSCCs by certain drugs such as pregabalin and gabapentin via binding to the alpha2delta subunits of VSCCs can lead to anticonvulsant, anxiolytic, and chronic pain-relieving actions.

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Article Synopsis
  • Novel antiemetic drugs target neurokinin-1 or serotonin-3 receptors to prevent vomiting.
  • Studies on how substance P and serotonin work together in the brain are revealing new potential uses for neurokinin-1 antagonists.
  • These insights could lead to additional treatments for conditions like depression and stress beyond just anti-nausea effects.
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The art of psychopharmacology derives from the science of psychopharmacology, but still requires wisdom, judgment, and experience to translate findings from clinical trials of a new drug into clinical practice.

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We have entered an exciting new era in which the nearly completed mapping of the human genome is now leading to the ability to characterize the human proteome, thereby expanding the horizon for new drug development by 3 orders of magnitude. Figuring out which proteins are involved in which disorders and in which individuals with any given disorder holds the promise of highly individualized therapeutics in the not so distant future.

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Three new cholinesterase inhibitors, donepezil, rivastigmine, and galantamine, all inhibit the enzyme AChE. Rivastigmine also inhibits BuChE, which could lead to additional benefits in late-stage Alzheimer's disease, but also cause more GI side effects at initiation of therapy. Galantamine is also an allosteric modulator of nicotinic receptors, which could lead to additional efficacy for attention and for behaviors mediated by neurotransmitters other than ACh.

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Neurotransmitters activate genes in their target neurons by precipitating a molecular cascade, which may be the ultimate consequence of chemical neurotransmission. When this transfer is aberrant, a mental disorder may be manifest. When drugs act upon neurons to change gene expression, this could lead to therapeutic actions, side effects, and the long-term consequences of drug abuse.

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Chemical neurotransmission begins when receptor occupancy by a neurotransmitter is converted into an intracellular second messenger that carries the information from the neurotransmitter deep into the target neuron. For clinicians, it is this transfer of neurotransmitter information all the way to the genome that hypothetically explains the therapeutic actions of many psychotropic drugs. This also accounts for why drugs that modify neurotransmission may take time to fully develop their clinical actions.

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Antipsychotic polypharmacy is a surprisingly frequent occurrence that can be both justified and unjustifed, depending on how it is used. To the extent that this phenomenon has been unrecognized and is not being studied, it is a "dirty little secret." To the extent that careful clinicians have uncovered a useful strategy for boosting the effectiveness of available antipsychotic monotherapies, it represents an opportunity to improve the outcomes of patients with psychotic illnesses.

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