Amti psychotic and anti depressants
antipsychotic drug classification dopamine receptor mechanism

A comparison panel of axial diagnostic neuroimaging scans illustrating striatal dopamine D2 receptor occupancy during antipsychotic treatment. Panel A presents structural T1-weighted MRI slices with anatomical segmentations of the basal ganglia from the Harvard-Oxford atlas, highlighting the caudate nucleus (light blue), putamen (red), and nucleus accumbens (dark blue). Panels B and C display co-registered Single-Photon Emission Computed Tomography (SPECT) and MRI fusion images. The color heat map (scale 0–3) represents the specific binding potential of a radioactive tracer to dopamine D2 receptors. Row B shows baseline binding potential (pre-treatment) with high intensity (red/yellow) in the striatum. Row C depicts the same patient after six weeks of treatment with 300 mg of the antipsychotic amisulpride, demonstrating a visible reduction in tracer binding (blue/green shift), corresponding to a mean receptor occupancy of 56%. This visual illustrates the pharmacological mechanism of competitive receptor blockade in psychiatric neuroimaging.
![This diagnostic image displays two side-by-side transaxial Positron Emission Tomography (PET) brain scans using the radiotracer [11C]raclopride, which targets dopamine D2 receptors. The left image represents the 'Baseline' state, showing high radiotracer binding in the striatum (specifically the putamen and caudate nucleus), indicated by warm yellow and orange hues. The right image depicts the 'Drug challenge' state after the administration of 6 mg of aripiprazole. In this scan, there is a visible reduction in radiotracer uptake within the striatal regions, characterized by a shift toward cooler blue and green colors. This visual decrease represents competitive displacement of the radiotracer by aripiprazole, effectively illustrating dopamine D2 receptor occupancy by the antipsychotic medication. The comparison serves as a clinical demonstration of neuropharmacological activity and receptor binding dynamics in the human brain.](/_next/image?url=https%3A%2F%2Fcdn.orris.care%2Fcdss_images%2Fpmc_clinical_VQA_9eb61996d0f81bca0843d76edca579a9b49b2d22a82de92e76818db7572aa7f8.jpg&w=3840&q=75)
This diagnostic image displays two side-by-side transaxial Positron Emission Tomography (PET) brain scans using the radiotracer [11C]raclopride, which targets dopamine D2 receptors. The left image represents the 'Baseline' state, showing high radiotracer binding in the striatum (specifically the putamen and caudate nucleus), indicated by warm yellow and orange hues. The right image depicts the 'Drug challenge' state after the administration of 6 mg of aripiprazole. In this scan, there is a visible reduction in radiotracer uptake within the striatal regions, characterized by a shift toward cooler blue and green colors. This visual decrease represents competitive displacement of the radiotracer by aripiprazole, effectively illustrating dopamine D2 receptor occupancy by the antipsychotic medication. The comparison serves as a clinical demonstration of neuropharmacological activity and receptor binding dynamics in the human brain.
![This diagnostic comparison image features three transversal [123I]IBZM SPECT slices at the level of the striatum, illustrating dopamine D2/3 receptor (D2/3R) availability across different clinical states. The panels represent a patient with treatment-resistant depression (TRD), a TRD patient receiving antipsychotic medication (TRD AP), and a healthy control (HC) subject. In the TRD and HC images, there is a prominent, bilateral, and symmetric high-intensity signal within the striatal regions (caudate and putamen), appearing as well-defined, bright orange-yellow structures against a darker background. In contrast, the TRD AP image demonstrates a marked reduction in signal intensity and distinctness in the striatum. This visual difference indicates high occupancy of D2/3 receptors by antipsychotic dopamine antagonists, which reduces the binding availability for the radiotracer. The comparison serves to illustrate that while TRD alone does not significantly alter striatal D2/3R availability compared to healthy controls, pharmacological intervention with antipsychotics causes a visible and quantifiable decrease in receptor availability.](/_next/image?url=https%3A%2F%2Fcdn.orris.care%2Fcdss_images%2Fpmc_clinical_VQA_340836387dce764e67c5251a1d168b40843d648e503bc7baf69e146346e891f8.jpg&w=3840&q=75)
This diagnostic comparison image features three transversal [123I]IBZM SPECT slices at the level of the striatum, illustrating dopamine D2/3 receptor (D2/3R) availability across different clinical states. The panels represent a patient with treatment-resistant depression (TRD), a TRD patient receiving antipsychotic medication (TRD AP), and a healthy control (HC) subject. In the TRD and HC images, there is a prominent, bilateral, and symmetric high-intensity signal within the striatal regions (caudate and putamen), appearing as well-defined, bright orange-yellow structures against a darker background. In contrast, the TRD AP image demonstrates a marked reduction in signal intensity and distinctness in the striatum. This visual difference indicates high occupancy of D2/3 receptors by antipsychotic dopamine antagonists, which reduces the binding availability for the radiotracer. The comparison serves to illustrate that while TRD alone does not significantly alter striatal D2/3R availability compared to healthy controls, pharmacological intervention with antipsychotics causes a visible and quantifiable decrease in receptor availability.
antidepressant SSRI serotonin reuptake inhibitor mechanism classification

This diagnostic image composite features Positron Emission Tomography (PET) scans illustrating Serotonin Transporter (SERT) availability in the human brain across sagittal, coronal, and axial views. The panels compare a Healthy Control (HC) group with patients with Major Depressive Disorder (MDD) at three intervals: baseline (PET 1), 6 hours post-single dose of a Selective Serotonin Reuptake Inhibitor (SSRI) (PET 2), and after 3 weeks of daily SSRI treatment (PET 3). A colorimetric scale at the bottom indicates SERT binding potential (BPND), ranging from blue (low) to red (high). At baseline (HC and PET 1), high SERT availability is visible in red and yellow within the brainstem (midbrain), thalamus, and subcortical regions, with moderate levels in the cingulate cortex. PET 2 shows a significant reduction in binding potential, represented by a shift toward green and blue, indicating acute SERT occupancy by the SSRI. PET 3 demonstrates sustained and further reduced SERT availability, reflecting long-term therapeutic occupancy. This visual serves as a pharmacological demonstration of antidepressant mechanism of action and brain-wide distribution of serotonin transporters.
![This educational graphic illustrates the effects of a selective serotonin reuptake inhibitor (SSRI) challenge on functional brain responses within the anterior cingulate cortex (ACC). Part (A) features diagnostic neuroimaging (fMRI) consisting of a mid-sagittal and three axial brain slices (Z coordinates 0, 15, 30). Three anatomical regions of interest are highlighted: pregenual area 32 (p32, purple), pregenual area 24 (p24, pink), and subgenual area 25 (s25, green). Part (B) presents three comparison bar charts showing functional activation in arbitrary units [a.u.] across four behavioral event types: violent, attempted, non-violent, and non-intended actions. The charts compare Placebo (PLAC, blue) versus SSRI (yellow) conditions. In pregenual regions p32 and p24, the SSRI significantly enhances deactivation (negative BOLD response) specifically during violent and attempted violent events, indicated by asterisk markers (p < 0.05 and p < 0.01). In contrast, subgenual area 25 (rightmost chart, hatched bars) shows no significant differences between drug conditions. This visual demonstrates the regional specificity of serotonergic modulation on social-emotional processing in the prefrontal cortex.](/_next/image?url=https%3A%2F%2Fcdn.orris.care%2Fcdss_images%2Fpmc_clinical_VQA_c129a0e89e17834eb78d53c1305fe4a8dd2da02864a11ade35493a5b4660f437.jpg&w=3840&q=75)
This educational graphic illustrates the effects of a selective serotonin reuptake inhibitor (SSRI) challenge on functional brain responses within the anterior cingulate cortex (ACC). Part (A) features diagnostic neuroimaging (fMRI) consisting of a mid-sagittal and three axial brain slices (Z coordinates 0, 15, 30). Three anatomical regions of interest are highlighted: pregenual area 32 (p32, purple), pregenual area 24 (p24, pink), and subgenual area 25 (s25, green). Part (B) presents three comparison bar charts showing functional activation in arbitrary units [a.u.] across four behavioral event types: violent, attempted, non-violent, and non-intended actions. The charts compare Placebo (PLAC, blue) versus SSRI (yellow) conditions. In pregenual regions p32 and p24, the SSRI significantly enhances deactivation (negative BOLD response) specifically during violent and attempted violent events, indicated by asterisk markers (p < 0.05 and p < 0.01). In contrast, subgenual area 25 (rightmost chart, hatched bars) shows no significant differences between drug conditions. This visual demonstrates the regional specificity of serotonergic modulation on social-emotional processing in the prefrontal cortex.
![This diagnostic image displays parametric positron emission tomography (PET) scans in a sagittal view, comparing [11C]AZ10419369 radioligand binding before (PET 1) and after (PET 2) treatment with escitalopram, a selective serotonin reuptake inhibitor (SSRI). The radioligand targets 5-HT1B receptors. The images are normalized to Montreal Neurological Institute (MNI) space. A color scale indicates the Non-Displaceable Binding Potential (BPND), ranging from 0.0 (dark purple/blue) to over 2.0 (white/pink). High binding is initially observed in cortical regions and the brainstem. Insets provide a zoomed-in view of the brainstem, specifically highlighting the dorsal brainstem (DBS) region of interest (ROI) outlined in white. Comparison between PET 1 and PET 2 reveals a visible reduction in radioligand binding within the DBS ROI following treatment, characterized by a shift from yellow/green hues (BPND ~1.0-1.5) to cooler blue/purple tones (BPND ~0.5). This visualization demonstrates the pharmacological effect of SSRI treatment on 5-HT1B receptor availability in the human brainstem, relevant for neuroscientific research into Major Depressive Disorder (MDD).](/_next/image?url=https%3A%2F%2Fcdn.orris.care%2Fcdss_images%2Fpmc_clinical_VQA_4520ff6b9e93a0661e35fd89fdd3b4dc406b15cda69343d655b9e210420ee0f6.jpg&w=3840&q=75)
This diagnostic image displays parametric positron emission tomography (PET) scans in a sagittal view, comparing [11C]AZ10419369 radioligand binding before (PET 1) and after (PET 2) treatment with escitalopram, a selective serotonin reuptake inhibitor (SSRI). The radioligand targets 5-HT1B receptors. The images are normalized to Montreal Neurological Institute (MNI) space. A color scale indicates the Non-Displaceable Binding Potential (BPND), ranging from 0.0 (dark purple/blue) to over 2.0 (white/pink). High binding is initially observed in cortical regions and the brainstem. Insets provide a zoomed-in view of the brainstem, specifically highlighting the dorsal brainstem (DBS) region of interest (ROI) outlined in white. Comparison between PET 1 and PET 2 reveals a visible reduction in radioligand binding within the DBS ROI following treatment, characterized by a shift from yellow/green hues (BPND ~1.0-1.5) to cooler blue/purple tones (BPND ~0.5). This visualization demonstrates the pharmacological effect of SSRI treatment on 5-HT1B receptor availability in the human brainstem, relevant for neuroscientific research into Major Depressive Disorder (MDD).
| Chemical Class | Prototype Drug | Potency | EPS Risk | Sedation | Hypotension |
|---|---|---|---|---|---|
| Phenothiazine - Aliphatic | Chlorpromazine | Low | Medium | High | High |
| Phenothiazine - Piperazine | Fluphenazine | High | High | Low | Very Low |
| Phenothiazine - Piperidine | Thioridazine | Low | Low | High | High |
| Thioxanthene | Thiothixene | High | Medium | Medium | Medium |
| Butyrophenone | Haloperidol | High | Very High | Low | Very Low |
| Dibenzoxazepine | Loxapine | Medium | Medium | Medium | Low |
| Drug | Notable Features |
|---|---|
| Clozapine | Most effective for treatment-resistant schizophrenia; risk of agranulocytosis (up to 2%), requires WBC monitoring; very low EPS |
| Risperidone | Broad efficacy; EPS at higher doses; hyperprolactinemia |
| Olanzapine | Effective vs. positive AND negative symptoms; significant weight gain, dyslipidemia, T2DM risk |
| Quetiapine | Low EPS; short t1/2 (twice-daily dosing); metabolic effects intermediate |
| Ziprasidone | Least weight gain among SGAs; QTc prolongation - caution in cardiac disease |
| Aripiprazole | Partial D2 agonist + 5-HT2A antagonist; low weight gain; novel mechanism |
| Paliperidone | Active metabolite of risperidone |
| Lurasidone | Good metabolic profile; indicated for bipolar depression |
| Cariprazine | D2/D3 partial agonist + 5-HT2A antagonist; effective for negative symptoms |
| Brexpiprazole | Similar to aripiprazole; used as MDD adjunct |
| Asenapine | Sublingual formulation; intermediate metabolic effects |
| Pathway | Effect of Blockade |
|---|---|
| Mesolimbic | Reduces positive symptoms (therapeutic) |
| Mesocortical | May worsen negative/cognitive symptoms |
| Nigrostriatal | EPS (akathisia, dystonia, Parkinsonism, tardive dyskinesia) |
| Tuberoinfundibular | Hyperprolactinemia (galactorrhea, amenorrhea, sexual dysfunction) |

| Drug | Half-life | Active Metabolite t1/2 | Notes |
|---|---|---|---|
| Fluoxetine | 48-72 h | 180 h (norfluoxetine) | Longest t1/2; safest in pregnancy context; inhibits CYP2D6/3A4 |
| Sertraline | 22-27 h | 62-104 h | Minimal drug interactions; preferred in cardiac patients |
| Escitalopram | 27-32 h | None | Cleanest receptor profile; good tolerability |
| Citalopram | 33-38 h | None | Dose-limited by QTc (max 40 mg/day) |
| Paroxetine | 20-23 h | None | Most anticholinergic SSRI; teratogenic risk; worst discontinuation syndrome |
| Fluvoxamine | 14-18 h | 14-16 h | Mainly used for OCD |
| Drug | Preferred Indication(s) |
|---|---|
| Venlafaxine | MDD, GAD, panic, social anxiety; at low doses acts like SSRI; NE effect kicks in at higher doses |
| Desvenlafaxine | Active metabolite of venlafaxine; similar profile |
| Duloxetine | MDD, GAD, diabetic neuropathy, fibromyalgia, stress urinary incontinence |
| Levomilnacipran | MDD; more NE-selective than other SNRIs |
| Drug | Selectivity |
|---|---|
| Phenelzine | Irreversible MAO-A + B |
| Tranylcypromine | Irreversible MAO-A + B |
| Moclobemide | Reversible MAO-A (RIMA) |
| Selegiline (transdermal) | Selective MAO-B at low dose; used in Parkinson's |
| Drug | Mechanism | Key Features |
|---|---|---|
| Bupropion | NE + dopamine reuptake inhibitor (NDRI); no serotonergic activity | No sexual dysfunction; used for smoking cessation; lowers seizure threshold; no weight gain; preferred in bipolar depression as less likely to induce mania |
| Mirtazapine | NaSSA (alpha-2 antagonist + 5-HT2/5-HT3 blocker) | Increases NE + 5-HT release; strong sedation (H1); significant weight gain; useful for depression with insomnia/anorexia; no sexual dysfunction |
| Trazodone | 5-HT2A antagonist + weak SERT inhibitor | Mainly used as hypnotic adjunct (at low doses); rare but serious: priapism |
| Nefazodone | 5-HT2A antagonist + SERT inhibitor | Hepatotoxicity risk - rarely used now |
| Vortioxetine | SERT inhibitor + 5-HT1A agonist + 5-HT3/7 antagonist | Multimodal; may improve cognitive symptoms of depression |
| Class/Drug | Bioavailability | t1/2 (h) | Protein Binding (%) |
|---|---|---|---|
| Fluoxetine | 70% | 48-72 | 95 |
| Sertraline | 45% | 22-27 | 98 |
| Venlafaxine | 45% | 8-11 | 27 |
| Duloxetine | 50% | 12-15 | 97 |
| Amitriptyline | 45% | 31-46 | 90 |
| Imipramine | 40% | 9-24 | 84 |
| Condition | Preferred Agent(s) |
|---|---|
| GAD | SSRIs, SNRIs (especially duloxetine, venlafaxine) |
| Panic disorder | SSRIs, TCAs (imipramine) |
| OCD | SSRIs (high dose), clomipramine (most potent for OCD) |
| PTSD | Sertraline, paroxetine (FDA-approved) |
| Neuropathic pain | Duloxetine, TCAs (amitriptyline), SNRIs |
| Fibromyalgia | Duloxetine, milnacipran |
| Smoking cessation | Bupropion |
| Enuresis (childhood) | Imipramine |
| Migraine prophylaxis | Amitriptyline |
