Related Experiment Video
Updated: Aug 7, 2026
09:28
A Method of Nodose Ganglia Injection in Sprague-Dawley Rat
Published on: November 25, 2014
Stimulating effects of H1-antagonists
Eef L Theunissen1, Annemiek Vermeeren, Eric F P M Vuurman
1Experimental Psychopharmacology Unit, Brain and Behavior Institute, Faculty of Psychology, Maastricht University, The Netherlands. e.theunissen@psychology.unimaas.nl
Current Pharmaceutical Design
|July 18, 2006
Summary
Some antihistamines, like terfenadine and fexofenadine, may offer mild performance boosts, particularly in attention-demanding tasks. This contrasts with their typical sedative effects, and the exact mechanism requires further investigation.
Area of Science:
- Pharmacology
- Neuroscience
Background:
- Antihistamines are commonly associated with sedative side effects.
- Histamine plays a complex role in arousal and cognitive functions.
Purpose of the Study:
- To review the performance effects of specific H1-antihistamines.
- To explore potential mechanisms behind observed stimulating effects.
Main Methods:
- Literature review of studies on H1-antihistamines (terfenadine, ebastine, fexofenadine, desloratadine).
- Analysis of performance in attention-based tasks (divided attention, vigilance, driving).
Main Results:
- Mild stimulating effects on performance observed for terfenadine, ebastine, fexofenadine, and desloratadine.
- Stimulating effects were dose-dependent but not always linear.
- Effects were most prominent in high-attention tasks.
Conclusions:
- Certain H1-antihistamines may have paradoxical stimulating effects.
- Mechanisms may involve neurotransmitters (dopamine, GABA) or H3 histamine receptors.
- Further research is needed to clarify histamine's role in arousal and antihistamine effects.
Related Concept Videos
01:30Adrenergic Agonists: Direct-Acting Agents
Drugs that mimic the action of endogenous catecholamines like noradrenaline and adrenaline are called adrenergic agonists or sympathomimetics. Based on their mechanism of action, sympathomimetics can be classified as direct-, indirect-, or mixed-acting sympathomimetics. Direct-acting adrenergic agonists activate adrenoceptors without affecting presynaptic neurons, making them independent of neuronal catecholamine-depleting agents like reserpine and guanethidine.
These agents can be classified...
These agents can be classified...
01:30Adrenergic Agonists: Therapeutic Uses
Adrenergic agonists have diverse therapeutic uses across various medical conditions and emergencies.
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and anaphylaxis:...
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and anaphylaxis:...
01:28Adrenergic Agonists: Mixed-Action Agents
Mixed-action adrenergic agonists, like ephedrine and pseudoephedrine, directly and indirectly affect adrenergic receptors. These agents stimulate adrenoceptors and indirectly release stored neurotransmitters, amplifying the adrenergic response.
Ephedrine and pseudoephedrine lack a catecholamine group, making them less susceptible to degradation by metabolic enzymes. They have increased oral bioavailability and lipophilicity, resulting in a longer duration of action. Their response is reduced by...
Ephedrine and pseudoephedrine lack a catecholamine group, making them less susceptible to degradation by metabolic enzymes. They have increased oral bioavailability and lipophilicity, resulting in a longer duration of action. Their response is reduced by...
01:28Cholinergic Antagonists: Pharmacological Actions
Antimuscarinic drugs block muscarinic receptors in multiple systems, including the gut, eye, smooth muscles, respiratory tract, cardiovascular, and central nervous systems. They produce similar effects with varying selectivity depending on the specific agent and tissue. Here are the key pharmacological actions of antimuscarinics:
Gastrointestinal Effects: Antimuscarinics reduce gut contractions, increase gastric emptying, and slow intestinal transit. They partly inhibit gastric acid secretion...
Gastrointestinal Effects: Antimuscarinics reduce gut contractions, increase gastric emptying, and slow intestinal transit. They partly inhibit gastric acid secretion...
01:23Drugs Acting on Autonomic Ganglia: Stimulants
Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
01:25Adrenergic Agonists: Indirect-Acting Agents
Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...