Vigabatrin decreases cholecystokinin-tetrapeptide (CCK-4) induced panic in healthy volunteers

P Zwanzger1, T C Baghai, C Schuele

  • 1Department of Psychiatry, University of Munich, Nussbaumstrasse 7, 80336 Munich, Germany. zwanzger@psy.med.uni-muenchen.de

Related Concept Videos

Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias01:25

ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias

Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...
Anxiolytic Drugs: Benzodiazepines and Buspirone01:29

Anxiolytic Drugs: Benzodiazepines and Buspirone

Benzodiazepines are a class of anxiolytic drugs known for their rapid efficacy and high therapeutic-to-lethal dose ratio, but with a potential risk of drug dependence. These drugs are lipophilic, allowing for rapid absorption after oral administration, eventually reaching the central nervous system (CNS). Once in the CNS, benzodiazepines bind to the allosteric site of the GABAA receptor. This binding enhances the inhibitory effects of the neurotransmitter GABA. By doing so, they prevent...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...
Anxiolytic Drugs: Overview01:26

Anxiolytic Drugs: Overview

Anxiolytic drugs are vital in managing anxiety disorders by effectively alleviating symptoms such as excessive fear, tachycardia, and tremors. There are several classes of anxiolytic medications, each with unique mechanisms of action and potential side effects.
Primary Types of Anxiolytic Drugs
1. Benzodiazepines:
Benzodiazepines bind to the GABA-A receptor in the brain, enhancing GABA's interaction. This action reduces neurotransmission, effectively blocking anxiety-associated limbic circuitry.
Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
Two synthetic agonists of THC,...