Dextroamphetamine
Pemoline
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Effects of promazine, chlorpromazine, d-amphetamine, and pentobarbital on treadle pressing by pigeons under a signalled shock-postponement schedule. (1/482)
The effects of promazine on treadle pressing to postpone the presentation of electric shock were studied in three pigeons. The effects of chlorpromazine, d-amphetamine, and pentobarbital were studied in two of these pigeons. Each treadle press postponed electric shock for 20 sec and presentation of a preshock stimulus for 14 sec. Selected doses of both promazine and chlorpromazine increased the rates of treadle pressing in all birds. The response-rate increases produced by promazine and chlorpromazine were due to increased conditional probabilities of treadle pressing both before and during the preshock stimulus. d-Amphetamine (1 and 3 mg/kg) slightly increased responding in one of the birds, but not to the extent that promazine or chlorpromazine did. In the other bird, the 10 mg/kg dose of d-amphetamine increased shock rate but did not change response rate. Some doses of d-amphetamine increased the conditional probabilities of responding both in the absence of the preshock signal and during the preshock signal in both birds. Pentobarbital only decreased response rates and increased shock rates. (+info)The effects of d-amphetamine on the temporal control of operant responding in rats during a preshock stimulus. (2/482)
The operant behavior of six rats was maintained by a random-interval schedule of reinforcement. Three-minute periods of noise were superimposed on this behavior, each period ending with the delivery of an unavoidable shock. Overall rates of responding were generally lower during the periods of noise than in its absence (conditioned suppression). These suppressed response rates also exhibited temporal patterning, with responding becoming less frequent as each noise period progressed. The effects of d-amphetamine on this behavioral baseline were then assessed. In four animals the relative response rates during the noise and in its absence suggested that the drug produced a dose-related decrease in the amount of conditioned suppression. However, this effect was often due to a decrease in the rates of responding in the absence of the preshock stimulus, rather than to an increase in response rates during the stimulus. Temporal patterning in response rates during the preshock stimulus was abolished, an effect that was interpreted in terms of rate-dependent effect of d-amphetamine. This study thus extends rate-dependent analyses of the effects of amphetamines to the patterns of operant behavior that occur during a preshock stimulus, and which have been discussed in terms of the disrupting effects of anxiety on operant behavior. (+info)Specification of distinct dopaminergic neural pathways: roles of the Eph family receptor EphB1 and ligand ephrin-B2. (3/482)
Dopaminergic neurons in the substantia nigra and ventral tegmental area project to the caudate putamen and nucleus accumbens/olfactory tubercle, respectively, constituting mesostriatal and mesolimbic pathways. The molecular signals that confer target specificity of different dopaminergic neurons are not known. We now report that EphB1 and ephrin-B2, a receptor and ligand of the Eph family, are candidate guidance molecules for the development of these distinct pathways. EphB1 and ephrin-B2 are expressed in complementary patterns in the midbrain dopaminergic neurons and their targets, and the ligand specifically inhibits the growth of neurites and induces the cell loss of substantia nigra, but not ventral tegmental, dopaminergic neurons. These studies suggest that the ligand-receptor pair may contribute to the establishment of distinct neural pathways by selectively inhibiting the neurite outgrowth and cell survival of mistargeted neurons. In addition, we show that ephrin-B2 expression is upregulated by cocaine and amphetamine in adult mice, suggesting that ephrin-B2/EphB1 interaction may play a role in drug-induced plasticity in adults as well. (+info)Dissociation in effects of lesions of the nucleus accumbens core and shell on appetitive pavlovian approach behavior and the potentiation of conditioned reinforcement and locomotor activity by D-amphetamine. (4/482)
Dopamine release within the nucleus accumbens (NAcc) has been associated with both the rewarding and locomotor-stimulant effects of abused drugs. The functions of the NAcc core and shell were investigated in mediating amphetamine-potentiated conditioned reinforcement and locomotion. Rats were initially trained to associate a neutral stimulus (Pavlovian CS) with food reinforcement (US). After excitotoxic lesions that selectively destroyed either the NAcc core or shell, animals underwent additional CS-US training sessions and then were tested for the acquisition of a new instrumental response that produced the CS acting as a conditioned reinforcer (CR). Animals were infused intra-NAcc with D-amphetamine (0, 1, 3, 10, or 20 microg) before each session. Shell lesions affected neither Pavlovian nor instrumental conditioning but completely abolished the potentiative effect of intra-NAcc amphetamine on responding with CR. Core-lesioned animals were impaired during the Pavlovian retraining sessions but showed no deficit in the acquisition of responding with CR. However, the selectivity in stimulant-induced potentiation of the CR lever was reduced, as intra-NAcc amphetamine infusions dose-dependently increased responding on both the CR lever and a nonreinforced (control) lever. Shell lesions produced hypoactivity and attenuated amphetamine-induced activity. In contrast, core lesions resulted in hyperactivity and enhanced the locomotor-stimulating effect of amphetamine. These results indicate a functional dissociation of subregions of the NAcc; the shell is a critical site for stimulant effects underlying the enhancement of responding with CR and locomotion after intra-NAcc injections of amphetamine, whereas the core is implicated in mechanisms underlying the expression of CS-US associations. (+info)ATP-sensitive potassium channels regulate in vivo dopamine release in rat striatum. (5/482)
ATP-sensitive K+ channels (K(ATP)) are distributed in a variety of tissues including smooth muscle, cardiac and skeletal muscle, pancreatic beta-cells and neurons. Since K(ATP) channels are present in the nigrostriatal dopamine (DA) pathway, the effect of potassium-channel modulators on the release of DA in the striatum of conscious, freely-moving rats was investigated. The extracellular concentration of DA was significantly decreased by the K(ATP)-channel opener (-)-cromakalim but not by diazoxide. (-)-Cromakalim was effective at 100 and 1000 microM concentrations, and the maximum decrease was 54% below baseline. d-Amphetamine significantly increased extracellular DA levels at the doses of 0.75 and 1.5 mg/kg, s.c. with a 770% maximum increase. (-)-Cromakalim had no effect on d-amphetamine-induced DA release, while glyburide, a K(ATP) blocker, significantly potentiated the effects of a low dose of d-amphetamine. These data indicate that K+ channels present in the nigrostriatal dopaminergic terminals modulate basal release as well as evoked release of DA. (+info)Comparison of effects of haloperidol administration on amphetamine-stimulated dopamine release in the rat medial prefrontal cortex and dorsal striatum. (6/482)
Research has shown that there are important neurochemical differences between the mesocortical and mesostriatal dopamine systems. The work reported in this paper has sought to compare the regulation of dopamine release in the medial prefrontal cortex and the anterior caudate-putamen. In vivo microdialysis was used to recover dialysate fluid for subsequent assay for dopamine concentrations. The responses to D2 antagonist (haloperidol) administration, which has been shown to increase impulse-dependent dopamine release, were compared. Results demonstrated a diminished effect of systemic haloperidol administration on dopamine efflux in the prefrontal cortex. The responses to systemic administration of a nonimpulse-dependent, transporter-mediated, dopamine releaser (d-amphetamine) were also contrasted. Results again demonstrated a diminished pharmacological effect in the cortex. The potential interaction of stimulation of these two types of dopamine release was examined by coadministration of these compounds. Haloperidol pretreatment dramatically potentiated the dopamine-releasing effect of amphetamine administration. This effect was observed in both the cortex and the striatum. Subsequent work demonstrated that this effect of haloperidol was mediated by D2-like receptors in the prefrontal cortex. These results are discussed in relation to other neurochemical and neuroanatomical studies demonstrating sparse densities of dopamine transporter sites and dopamine D2 receptors in the cortex compared with the striatum. They demonstrate a functional correlate to the recently reported, largely extrasynaptic localization of dopamine transporter sites in the prefrontal cortex. Furthermore, they demonstrate the existence of cortical D2-like autoreceptors that may normally be "silent" under basal conditions. (+info)Dopamine fluctuations in the nucleus accumbens during maintenance, extinction, and reinstatement of intravenous D-amphetamine self-administration. (7/482)
Moment-to-moment fluctuations of nucleus accumbens dopamine (DA) were determined in rats self-administering or passively receiving "yoked" intravenous infusions of D-amphetamine. The initial lever presses of each session caused elevations in DA concentration, usually to an initial peak that was not maintained throughout the rest of the session. As the initial ("loading") injections were metabolized, DA levels dropped toward baseline but were sustained at elevated plateaus by subsequent lever pressing that was spaced throughout the remainder of the 3 hr sessions. During this period, DA levels fluctuated phasically, time-locked to the cycle of periodic lever pressing. Consistent with the known pharmacological actions and dynamics of amphetamine, peak DA elevations were seen approximately 10-15 min after each injection, and the mean DA level was at a low point in the phasic cycle at the time of each new lever press. During extinction periods when saline was substituted for amphetamine, DA levels dropped steadily toward baseline levels despite a dramatic increase in (now-unrewarded) lever pressing. Noncontingent injections during extinction reinstated lever-pressing behavior and increased nucleus accumbens DA concentrations. These data are consistent with the hypothesis that under the conditions of this experiment-during periods of amphetamine intoxication in well-trained animals-the timing of amphetamine self-administration comes primarily under the control of extracellular DA concentrations. The probability of lever pressing during the maintenance phase is highest when DA concentrations fall near a characteristic trigger point, a trigger point that is significantly elevated above baseline, and falls as DA concentrations fall below or increase above that trigger point. (+info)Operant methodology in the study of learning. (8/482)
A series of experiments is described in which operant methodology is used to study the effects of drugs on "learning." Emphasis is placed on the technique of repeated acquisition as a behavioral baseline for studying this type of transition state. In this technique, each subject is required to learn a new discrimination each session. Multiple-schedule procedures are also described in which acquisition is compared to a "performance" task, where the discrimination is the same each session. The learning baseline is more sensitive to the disruptive effects of a variety of drugs (e.g., cocaine, d-amphetamine, haloperidol) than is the performance baseline. This general finding obtains across procedural variations and species (pigeons and monkeys). The potential usefulness of these procedures for studying both acute and chronic behavioral toxicity is discussed. (+info)Dextroamphetamine is a central nervous system stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. It works by increasing the levels of certain neurotransmitters, such as dopamine and norepinephrine, in the brain. Dextroamphetamine is available as a prescription medication and is sold under various brand names, including Adderall and Dexedrine. It is important to use this medication only as directed by a healthcare professional, as it can have potentially serious side effects if used improperly.
Pemoline is a central nervous system stimulant that was used in the treatment of attention deficit hyperactivity disorder (ADHD). It is a carbamate derivative and its mechanism of action is thought to be related to its ability to increase the levels of dopamine, a neurotransmitter, in the brain. However, due to concerns about liver toxicity, pemoline was withdrawn from the market in many countries including the United States. It's important to note that Pemoline should only be used under the supervision of a physician and it's not commonly used or recommended anymore.
Central nervous system (CNS) stimulants are a class of drugs that increase alertness, attention, energy, and/or mood by directly acting on the brain. They can be prescribed to treat medical conditions such as narcolepsy, attention deficit hyperactivity disorder (ADHD), and depression that has not responded to other treatments.
Examples of CNS stimulants include amphetamine (Adderall), methylphenidate (Ritalin, Concerta), and modafinil (Provigil). These medications work by increasing the levels of certain neurotransmitters, such as dopamine and norepinephrine, in the brain.
In addition to their therapeutic uses, CNS stimulants are also sometimes misused for non-medical reasons, such as to enhance cognitive performance or to get high. However, it's important to note that misusing these drugs can lead to serious health consequences, including addiction, cardiovascular problems, and mental health issues.
Benzhydryl compounds are organic chemical compounds that contain the benzhydryl group, which is a functional group consisting of a diphenylmethane moiety. The benzhydryl group can be represented by the formula Ph2CH, where Ph represents the phenyl group (C6H5).
Benzhydryl compounds are characterized by their unique structure, which consists of two aromatic rings attached to a central carbon atom. This structure gives benzhydryl compounds unique chemical and physical properties, such as stability, rigidity, and high lipophilicity.
Benzhydryl compounds have various applications in organic synthesis, pharmaceuticals, and materials science. For example, they are used as building blocks in the synthesis of complex natural products, drugs, and functional materials. They also serve as useful intermediates in the preparation of other chemical compounds.
Some examples of benzhydryl compounds include diphenylmethane, benzphetamine, and diphenhydramine. These compounds have been widely used in medicine as stimulants, appetite suppressants, and antihistamines. However, some benzhydryl compounds have also been associated with potential health risks, such as liver toxicity and carcinogenicity, and their use should be carefully monitored and regulated.
Sleep deprivation is a condition that occurs when an individual fails to get sufficient quality sleep or the recommended amount of sleep, typically 7-9 hours for adults. This can lead to various physical and mental health issues. It can be acute, lasting for one night or a few days, or chronic, persisting over a longer period.
The consequences of sleep deprivation include:
1. Fatigue and lack of energy
2. Difficulty concentrating or remembering things
3. Mood changes, such as irritability or depression
4. Weakened immune system
5. Increased appetite and potential weight gain
6. Higher risk of accidents due to decreased reaction time
7. Health problems like high blood pressure, diabetes, and heart disease over time
Sleep deprivation can be caused by various factors, including stress, shift work, sleep disorders like insomnia or sleep apnea, poor sleep hygiene, and certain medications. It's essential to address the underlying causes of sleep deprivation to ensure proper rest and overall well-being.
In a medical or physiological context, "arousal" refers to the state of being awake and responsive to stimuli. It involves the activation of the nervous system, particularly the autonomic nervous system, which prepares the body for action. Arousal levels can vary from low (such as during sleep) to high (such as during states of excitement or stress). In clinical settings, changes in arousal may be assessed to help diagnose conditions such as coma, brain injury, or sleep disorders. It is also used in the context of sexual response, where it refers to the level of physical and mental awareness and readiness for sexual activity.
In medical and psychological terms, "affect" refers to a person's emotional or expressive state, mood, or dispositions that are outwardly manifested in their behavior, facial expressions, demeanor, or speech. Affect can be described as being congruent or incongruent with an individual's thoughts and experiences.
There are different types of affect, including:
1. Neutral affect: When a person shows no apparent emotion or displays minimal emotional expressiveness.
2. Positive affect: When a person exhibits positive emotions such as happiness, excitement, or enthusiasm.
3. Negative affect: When a person experiences and displays negative emotions like sadness, anger, or fear.
4. Blunted affect: When a person's emotional response is noticeably reduced or diminished, often observed in individuals with certain mental health conditions, such as schizophrenia.
5. Flat affect: When a person has an almost complete absence of emotional expressiveness, which can be indicative of severe depression or other mental health disorders.
6. Labile affect: When a person's emotional state fluctuates rapidly and frequently between positive and negative emotions, often observed in individuals with certain neurological conditions or mood disorders.
Clinicians may assess a patient's affect during an interview or examination to help diagnose mental health conditions, evaluate treatment progress, or monitor overall well-being.
Psychomotor performance refers to the integration and coordination of mental processes (cognitive functions) with physical movements. It involves the ability to perform complex tasks that require both cognitive skills, such as thinking, remembering, and perceiving, and motor skills, such as gross and fine motor movements. Examples of psychomotor performances include driving a car, playing a musical instrument, or performing surgical procedures.
In a medical context, psychomotor performance is often used to assess an individual's ability to perform activities of daily living (ADLs) and instrumental activities of daily living (IADLs), such as bathing, dressing, cooking, cleaning, and managing medications. Deficits in psychomotor performance can be a sign of neurological or psychiatric disorders, such as dementia, Parkinson's disease, or depression.
Assessment of psychomotor performance may involve tests that measure reaction time, coordination, speed, precision, and accuracy of movements, as well as cognitive functions such as attention, memory, and problem-solving skills. These assessments can help healthcare professionals develop appropriate treatment plans and monitor the progression of diseases or the effectiveness of interventions.
The double-blind method is a study design commonly used in research, including clinical trials, to minimize bias and ensure the objectivity of results. In this approach, both the participants and the researchers are unaware of which group the participants are assigned to, whether it be the experimental group or the control group. This means that neither the participants nor the researchers know who is receiving a particular treatment or placebo, thus reducing the potential for bias in the evaluation of outcomes. The assignment of participants to groups is typically done by a third party not involved in the study, and the codes are only revealed after all data have been collected and analyzed.
Cognition refers to the mental processes involved in acquiring, processing, and utilizing information. These processes include perception, attention, memory, language, problem-solving, and decision-making. Cognitive functions allow us to interact with our environment, understand and respond to stimuli, learn new skills, and remember experiences.
In a medical context, cognitive function is often assessed as part of a neurological or psychiatric evaluation. Impairments in cognition can be caused by various factors, such as brain injury, neurodegenerative diseases (e.g., Alzheimer's disease), infections, toxins, and mental health conditions. Assessing cognitive function helps healthcare professionals diagnose conditions, monitor disease progression, and develop treatment plans.
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Benzphetamine
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Cause of obsessive-compulsive disorder
Controlled Drug in the United Kingdom
Motion sickness
Dopamine hypothesis of schizophrenia
Attention deficit hyperactivity disorder
Phenylisobutylamine
Locomotion in space
Stimulant
Amphetamine type stimulant
List of psychotropic medications
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Sulfate21
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- Ethex Corporation announced yesterday a Dextroamphetamine Sulfate recall for three lots of their generic psychostimulant drug after it was discovered that some tablets could be oversized. (aboutlawsuits.com)
- In a press release issued on October 15, 2008, Ethex Corporation indicated that they recently discovered that some tablets from three different lots of Dextroamphetamine Sulfate 5 mg tablets could be oversized, containing up to twice the labeled amount of active ingredient. (aboutlawsuits.com)
- The FDA and Ethex have requested that any consumers who experienced an adverse reaction or received oversized Dextroamphetamine Sulfate 5mg tablets, should file a report with the FDA's MedWatch Program. (aboutlawsuits.com)
- What is the most important information I should know about Dextroamphetamine Saccharate, Amphetamine Aspartate Monohydrate, Dextroamphetamine Sulfate, and Amphetamine Sulfate Extended-Release Capsules? (nih.gov)
- Dextroamphetamine Saccharate, Amphetamine Aspartate Monohydrate, Dextroamphetamine Sulfate, and Amphetamine Sulfate Extended-Release Capsules have a high chance for abuse and misuse and may lead to substance use problems, including addiction. (nih.gov)
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ADHD12
- Dextroamphetamine is a potent central nervous system (CNS) stimulant and enantiomer of amphetamine that is prescribed for the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. (wikipedia.org)
- Dextroamphetamine is used to treat attention deficit hyperactivity disorder (ADHD) and narcolepsy (a sleep disorder), and is sometimes prescribed off-label for depression and obesity. (wikipedia.org)
- A Cochrane review on the treatment of ADHD in children with tic disorders such as Tourette syndrome indicated that stimulants in general do not make tics worse, but high doses of dextroamphetamine could exacerbate tics in some individuals. (wikipedia.org)
- Our objective was to compare the efficacy of the new wake-promoting drug modafinil to that of dextroamphetamine for the treatment of attention deficit hyperactivity disorder (ADHD) in adults. (nih.gov)
- Twenty-two adults who met DSM-IV criteria for ADHD participated in a randomized, double-blind, placebo-controlled, three-phase crossover study comparing placebo, modafinil, and dextroamphetamine for the treatment of ADHD. (nih.gov)
- Dextroamphetamine is a stimulant drug widely prescribed for treating attention-deficit hyperactivity disorder (ADHD) and narcolepsy. (detox.net)
- Dextroamphetamine is used to treat attention deficit hyperactivity disorder or ADHD and helps an individual to control behavior disorders, stay focused and pay attention on an activity. (savingsonmeds.com)
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- Personally, it ended up not being for me, so I no longer take dextroamphetamine for my ADHD. (medlineplus.gov)
Stimulants5
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Lisdexamfetamine2
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