Publications by authors named "Christine Luckhart"
Article Synopsis
- Selective serotonin reuptake inhibitors (SSRIs) are common antidepressants that take weeks to become effective, but chronic use can cause changes in serotonin neurotransmission due to 5-HT1A autoreceptor desensitization.
- Research on mice lacking 5-HT1A autoreceptors showed that while SSRIs like fluoxetine can enhance serotonin levels, they also led to increased anxiety responses, especially in certain behavioral tests.
- The findings suggest that a lack of 5-HT1A autoreceptors may cause an unusual increase in anxiety when using SSRIs, indicating that monitoring these receptors could help predict adverse reactions to SSRI treatment.
Article Synopsis
- The C (-1019) G rs6295 polymorphism in the serotonin-1A receptor gene has mixed associations with major depression, indicating potential compensatory mechanisms that foster resilience.
- The study examined Deaf1-/- mice, which lack the Deaf1 repressor, revealing increased 5-HT1A autoreceptor expression but unchanged receptor function, suggesting adaptations occur over generations.
- Male Deaf1-/- mice showed anxiety-like behavior in certain tests, while females only exhibited increased anxiety in specific situations, highlighting the sex-dependent effects of Deaf1 on anxiety and its possible implications for depression sensitivity.
Recent data has indicated that Zn can modulate serotonergic function through the 5-HT receptor (5-HTR); however, the exact mechanisms are unknown. In the present studies, radioligand binding assays and behavioural approaches were used to characterize the pharmacological profile of Zn at 5-HTRs in more detail. The influence of Zn on agonist binding to 5-HTRs stably expressed in HEK293 cells was investigated by in vitro radioligand binding methods using the agonist [H]-8-OH-DPAT.
View Article and Find Full Text PDFDecreased serotonergic activity has been implicated in anxiety and major depression, and antidepressants directly or indirectly increase the long-term activity of the serotonin system. A key component of serotonin circuitry is the 5-HT1A autoreceptor, which functions as the major somatodendritic autoreceptor to negatively regulate the "gain" of the serotonin system. In addition, 5-HT1A heteroreceptors are abundantly expressed post-synaptically in the prefrontal cortex (PFC), amygdala, and hippocampus to mediate serotonin actions on fear, anxiety, stress, and cognition.
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