Background Pharmacological and postmortem investigations suggest that patients with major depressive disorder have alterations in function or density of brain serotonin1A(5-HT1A) receptors. The aim of the present study was to use positron emission tomography with the selective 5-HT1Areceptor antagonist [11C]WAY-100635 to measure 5-HT1Areceptor binding in depressed patients before and during treatment with selective serotonin reuptake inhibitors. Methods Positron emission tomographic scans with [11C]WAY-100635 were performed on 25 patients with major depressive disorder. These included 15 unmedicated depressed patients. Ten of these unmedicated patients were scanned again during selective serotonin reuptake inhibitor treatment. A further 10 patients with major depressive disorder were scanned on one occasion only while taking selective serotonin reuptake inhibitors. Comparisons were made with [11C]WAY-100635 positron emission tomographic scans in 18 healthy volunteer subjects. Region of interest analysis and statistical parametric mapping were performed on binding potential images generated using a reference tissue model. Results Binding potential values were reduced across many of the regions examined, including frontal, temporal, and limbic cortex in both unmedicated and medicated depressed patients compared with healthy volunteers. Binding potential values in medicated patients were similar to those in unmedicated patients. Conclusions Major depressive disorder is associated with a widespread reduction in 5-HT1Areceptor binding. This reduced 5-HT1Areceptor binding was not changed by selective serotonin reuptake inhibitor treatment.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/481569/yoa9153.pdf

Brain serotonin1A receptor binding measured by positron emission tomography with [11C]WAY-100635: effects of depression and antidepressant treatment

Forebrain Pathways Mediating Stress-Induced Hormone Secretion ☆ ☆☆

Electrophysiological and autoradiographic approaches were used to assess possible changes in 5-hydroxytryptamine (serotonin) 5-HT1A receptors in the rat dorsal raphe nucleus after a subchronic treatment with fluoxetine or paroxetine, two specific serotonin reuptake inhibitors with antidepressant properties. Fluoxetine or paroxetine were injected daily (5 mg/kg, i.p.) for various time periods up to 21 days. Electrophysiological recordings performed 24 h after the last injection showed that the potency of the 5HT1A receptor agonist, 8-OH-DPAT, to depress the firing of serotoninergic neurons in the dorsal raphe nucleus within brain stem slices was significantly reduced as early as after a 3-day treatment with either drug. The proportion of recorded neurons showing desensitization of somatodendritic 5-HT1A autoreceptors increased along the treatment from ∼40% on the 3rd day to 60–80% on the 21st day. At no time during the treatment, was the specific binding of [3H]8-OHDPAT (agonist radioligand) or [3H] WAY-100 635 (antagonist radioligand) to 5-HT1A receptors modified in the dorsal raphe nucleus or in other brain areas, suggesting that neither the density nor the coupling of these receptors to G-proteins were probably altered in rats injected with fluoxetine or paroxetine for up to 21 days.

Early desensitization of somato-dendritic 5-HT1A autoreceptors in rats treated with fluoxetine or paroxetine

Noradrenergic and Serotonergic Mechanisms in the Neurobiology of Posttraumatic Stress Disorder and Resilience

The aim of the present study was to determine whether alterations in 5-hydroxytryptamine (5-HT)1A receptors would be found in knockout mice lacking the serotonin transporter (5HTT). Hypothermic and neuroendocrine responses to the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetraline (8-OHDPAT) were used to examine the function of 5-HT1A receptors. Initial studies evaluated the dose-response and time course of 8-OH-DPAT-induced hypothermia and hormone secretion in normal CD-1 mice (the background strain of the 5-HTT knockout mice). 8-OH-DPAT dose-dependently produced hypothermic responses that peaked at 20 min postinjection. 8-OHDPAT-induced hypothermia was blocked by the 5-HT1A antagonist WAY-100635. 8-OH-DPAT dose-dependently increased the concentrations of plasma oxytocin, corticotropin, and corticosterone. In the 5-HTT knockout (2/2) mice, the hypothermic response to 8-OH-DPAT (0.1 mg/kg s.c.) was completely abolished. Furthermore, 5-HTT2/2 mice had significantly attenuated plasma oxytocin and corticosterone responses to 8-OH-DPAT. No significant changes in the hypothermic or hormonal responses to 8-OH-DPAT were observed in heterozygous (5-HTT1/2) mice. [ 3 H]8-OH-DPAT- and [ 125 I]MPPI [4-(29-methoxyphenyl)-1-[29-[N-(20-pyridinyl)-iodobenzamido]ethyl]piperazine]-binding sites in the hypothalamus and [ 125 I]MPPI-binding sites in the dorsal raphe were significantly decreased in 5-HTT2/2 mice. The results indicate that lack of the 5-HTT is associated with a functional desensitization of 5-HT1A receptor responses to 8-OH-DPAT, which may be a consequence, at least in part, of the decrease in density of 5-HT1A receptors in the hypothalamus and dorsal raphe of 5-HTT2/2 mice. The 5-hydroxytryptamine (5-HT; serotonin) transporter (5HTT) is an essential component in serotonergic neurotransmission. The 5-HTT regulates 5-HT concentrations in the synaptic cleft and adjacent brain extracellular fluid locations via recycling released serotonin, thus terminating the action of 5-HT. The 5-HTT is the target of serotonin reuptake inhibitors (SRIs), a group of widely used antidepressant and antianxiety agents. The exact mechanism of therapeutic action of the SRIs remains unknown because the onset of clinical improvement usually takes 2 to 4 weeks or longer after the initiation of SRI administration. Adaptive changes in the serotonergic system that are initiated by blockade of 5-HT reuptake have been implicated in these delayed therapeutic effects (Briley and Moret, 1993; Blier and De Montigny, 1998). A number of studies have demonstrated that chronic

Reduction of 5-hydroxytryptamine (5-HT)(1A)-mediated temperature and neuroendocrine responses and 5-HT(1A) binding sites in 5-HT transporter knockout mice.

Attenuation of hormone responses to the 5-HT1A agonist ipsapirone by long-term treatment with fluoxetine, but not desipramine, in male rats

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Attenuation of hormone responses to the 5-HT1A agonist ipsapirone by long-term treatment with fluoxetine, but not desipramine, in male rats