It takes weeks or months for most antidepressants to kick in, time that can feel like an eternity to those who need the drugs. But new research suggests that a protein called p11, previously shown to play a role in susceptibility to depression, activates a serotonin receptor in the brain known for producing a rapid antidepressant response. If scientists could develop drugs to target this receptor, then patients might feel the effects of their treatments in as little as two days.
In addition, the findings, reported by Rockefeller University’s Paul Greengard, Jennifer L
Mouse model suggests serotonin might play a role in crib death. This research team created mice with unusually high levels of seratonin receptor 1a (Htr1a), a receptor that binds to seratonin, decreasing the free levels of the neurotransmitter. (In other words, a mouse with high levels of receptor 1a will seem like a mouse with low levels of seratonin, even though its ability to produce seratonin is unimpaired.) They found that the mice periodically went into "crisis" states during which their heart rates and body temperatures plummeted
Dysregulation of brain serotonin (5-HT) neurotransmission is thought to underlie mental conditions as diverse as depression, anxiety disorders, bipolar disorder, autism, and schizophrenia. Despite treatment of these conditions with serotonergic drugs, the molecular mechanisms by which 5-HT is involved in the regulation of aberrant emotional behaviors are poorly understood.
Beside the well-known deficiency in serotonergic neurotransmission as pathophysiological correlate of major depression (MD), recent evidence points to a pivotal role of increased glutamate receptor activation as well. However, cause and interaction of these neurotransmitter alterations are not understood. In this review, we present a hypothesis integrating current concepts of neurotransmission and hypothalamus–pituitary–adrenal (HPA) axis dysregulation with findings on immunological alterations and alterations in brain morphology in MD
Serotonin is a major signaling chemical in the brain, and it has long been thought to be involved in aggressive behavior in a wide variety of animals as well as in humans. Another brain chemical signal, neuropeptide Y (known as neuropeptide F in invertebrates), is also known to affect an array of behaviors in many species, including territoriality in mice.
"In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system."
"The amygdala is a critical site for the acquisition of learned fear memory in mammals, and the formation and long-term maintenance of fear memories are thought to be associated with changes of synaptic strength in the amygdala."