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PubMed1985

Effect of methylphenidate pretreatment on the behavioral and biochemical responses to amphetamine.

After rats were chronically pretreated with methylphenidate (MP), the stereotyped behavioral response to amphetamine (AMPH) was significantly enhanced. In addition, after this pretreatment, the AMPH-induced release of endogenous dopamine from slices of striatum and nucleus accumbens was also enhanced. These effects of MP pretreatment are similar to those reported for AMPH pretreatment and suggest that the sensitization to AMPH that develops after pretreatment with either drug is due to a common mechanism.

Amphetamine↗
PubMed1984

Possible change in noradrenergic receptor sensitivity following methylphenidate treatment: growth hormone and MHPG response to clonidine challenge in children with attention deficit disorder and hyperactivity.

Growth hormone (GH) and 3-methoxy-4-hydroxyphenelethylene glycol (MHPG) response was measured hourly for 4 hours in 8 children with Attention Deficit Disorder with Hyperactivity (ADD+H) following an acute single-dose of clonidine. The clonidine challenge was repeated before, during, and one day after 12 weeks of treatment with methylphenidate (MPH). Before MPH treatment, the plasma growth hormone (GH) rose to 31.3 +/- 4.6 (Mean +/- SE) ng/ml; during MPH treatment, the GH peak was only 14.8 +/- 3.2 ng/ml; one day after discontinuation of MPH, GH rose to only 20.8 +/- 3.9 ng/ml. MHPG release was inhibited by clonidine in all treatment conditions but tended to be more decreased during MPH treatment. Some children with ADD+H may have hypersensitivity of the post-synaptic alpha-1 noradrenergic receptor which is diminished by MPH treatment. The extent to which these effects are pharmacological or represent a change in receptor sensitivity requires further study.

Adolescent↗
PubMed1986

Effects of methylphenidate and pentobarbital on the spontaneous activity levels of rats with selective hippocampal system damage.

The effects of various types of experimentally-induced neural damage involving selective areas of the hippocampal system on spontaneous non-operant activity were studied in adult male rats using stabilimeter apparatus. A hierarchy of lesion-induced activity increases relative to sham-lesioned controls was revealed in which colchicine-induced dentate granule cell lesions produced the greatest increase in activity and kainic acid-induced pyramidal cell lesions produced the least. Methylphenidate (0.2, 0.4, 2.0, 4.0, 8.0 mg/kg) tended to increase this activity in a dose-dependent manner while pentobarbital (0.5, 1.0, 5.0, 10.0 mg/kg) tended to decrease it. These results indicate that such neural damage does not sufficiently alter the responsivity of rats to these drugs to produce a "paradoxical" effect although some lesion group differences in drug responsivity were seen. All this is discussed in light of the neuro-architecture of this system.

Animals↗
PubMed1987

Effects of acute and chronic methylphenidate administration on beta-endorphin, growth hormone, prolactin and cortisol in children with attention deficit disorder and hyperactivity.

The effect of 5 mg/p.o. methylphenidate (MPH) challenge on beta-endorphin (beta-EP), growth hormone (GH), prolactin (Prl) and cortisol was investigated in 16 children suffering from attention deficit disorder with hyperactivity (ADDH) before and after 4 weeks MPH treatment. The study population consisted of 13 males and 3 females aged 6-11 years. All patients were drug free for at least 3 months prior to investigation. The severity of ADDH symptomatology and response to MPH chronic treatment was assessed using parent/teacher abbreviated Conners rating scale. Blood samples for beta-EP, cortisol, Prl and GH were drawn before initiation of treatment (basal pre-treatment level), 2 hours after MPH challenge, 4 weeks after MPH treatment (basal post-treatment level) and 2 hours after re-challenge with MPH. Chronic MPH treatment resulted in a decrease in basal Prl levels (5.5 +/- 2.8 vs 3.7 +/- 1.9 ng/ml; p less than 0.05). Pre-treatment challenge stimulates significantly both beta-EP (15.0 +/- 7.5 vs 12.5 +/- 5.3 pmol/l; p less than 0.05) and cortisol secretion (20.6 +/- 6.6 vs 12.6 +/- 5.8 micrograms/dl; p less than 0.05), and suppressed Prl secretion (4.0 +/- 1.5 vs 5.5 +/- 2.8 ng/ml; p less than 0.05). Re-challenge with MPH enhanced beta-EP levels (14.9 +/- 8.6 vs 10.6 +/- 5.0 pmol/l; p less than 0.05) but failed to affect cortisol, Prl and GH secretion. The acute and chronic neuroendocrine effects of MPH administration might be related to its dopaminergic and adrenergic agonistic activity. It might be that the stimulatory effect of single and repeated acute MPH administration on beta-EP release contributes to the beneficial effect of MPH treatment in ADDH children.

Attention Deficit Disorder with Hyperactivity↗
PubMed1990

Growth hormone and prolactin response to methylphenidate in children with attention deficit disorder.

Utilizing a double-blind, drug-placebo design, we examined growth hormone (GH) and prolactin (Pro) response to oral administration of methylphenidate (MPH) in 14 boys (ages 7.0-12.4 years) with Attention Deficit Disorder (ADD). Four conditions representing three different MPH doses (0.3 mg/kg O.D., 0.3 mg/kg B.I.D., 0.6 mg/kg O.D.) and Placebo were compared in each subject, each condition lasting for a period of 3 weeks. GH and Pro response were measured both as maximum peak GH (DGH) or nadir of Pro (DPro) as well as area under the curve for the first four hours after MPH administration (AUCGH, AUCPro). Behavioral measures included parent ratings on the Yale Children's Inventory and teacher ratings on the Yale and Conners Behavior Rating Scales and Kagan's Matching Familiar Figures Test (MFFT). Prolactin response as measured by AUCPro was significantly increased after MPH compared to placebo (t = 2.04, p less than 0.05, placebo vs all doses MPH). This difference observed for AUCPro between placebo and MPH was evident as well when we considered the number of times AUCPro declined after MPH as compared to placebo (p = .018, Fisher's exact test). Within-subjects analysis of covariance demonstrated significant correlations between the improvement in reaction time on the MFFT and 1) GH response (AUCGH, r = .58, p less than .001) and 2) prolactin response (AUCPro, r = .40, p less than .05) and between improvement in attention as measured on the Yale BRS and GH response (AUCGH, r = .57, p less than .05). Our findings suggest that measures other than GH and prolactin may be more desirable measures of brain catecholaminergic functioning.

Attention Deficit Disorder with Hyperactivity↗
PubMed1994

Methylphenidate decreases regional cerebral blood flow in normal human subjects.

To assess the effects of methylphenidate (MP) on cerebral blood flow (CBF), 5 healthy males were studied using 15O-water and positron emission tomography before and after MP (0.5 mg/kg iv). MP significantly decreased whole brain CBF at 5-10 minutes (25 +/- 11%) and at 30 minutes (20 +/- 10%) after its administration. Decrements in CBF were homogeneous throughout the brain (regional decrements 23-30%) and probably reflect the vasoactive properties of MP. The vasoactive properties of MP should be considered when prescribing this drug chronically and/or when giving it to subjects with cerebrovascular compromise.

Adult↗
PubMed1985

Methylphenidate, but not other CNS stimulants, inhibits red blood cell calcium-activated potassium efflux.

The first-order rate constant of net potassium efflux, measured in human red blood cell (RBC) suspensions by means of a K+-sensitive electrode, was increased 26 fold (from 0.0025 min-1 to 0.0656 min-1) by 0.5 microM of the calcium ionophore A 23187. Both the basal or the calcium-stimulated potassium efflux remained unchanged following the addition of different CNS stimulants (nikethamide (1 mM), pentylenetetrazol (1mM), doxapram (1 mM), strychnine (0.1 mM), picrotoxin (0.1 mM), or nomifensine (0.1 mM). Methylphenidate (10-100 microM), however, inhibited in a concentration-dependent manner the calcium-stimulated, but not the basal potassium efflux. An IC50 of 190 microM was estimated for this effect.

Calcium↗
PubMed1979

A comparison of methylphenidate induced active avoidance and water maze performance facilitation.

Methylphenidate was shown to facilitate both active avoidance and water performance compared to controls. Repetitive errors on both tasks were greater in the drug than the nondrug group and were positively correlated to water maze performance. These results fail to support the view that water maze acquisition is less influenced by performance variables than active avoidance. An unanticipated enhancement of water maze performance was also noted in the control group which had been previously tested on active avoidance compared with naive controls. Moreover, this group made fewer repetitive errors than naive controls, suggesting that previous shock exposure reduced inappropriate responses.

Animals↗
PubMed1980

Differential effects of methylphenidate on signalled and non-signalled reinforcement.

Rats were trained to press a bar with water reinforcement under a variable interval 15-sec (VI 15), variable interval 15-sec signalled-reinforcement (VI SD), or a differential-reinforcement-of-low-rate 10-sec (DRL 10) schedule. Methylphenidate (MP) had little effect on response rates or reinforcements-earned in the VI 15 group. However, MP increased response rates in a dose-related manner in the VI SD and the DRL 10 groups. These findings and additional results reported in the literature suggest that signalled reinforcement does not necessarily antagonize the rate-increasing effects of the amphetamine-type drugs.

Animals↗
PubMed1983

Play soliciting in juvenile male rats: effects of caffeine, amphetamine and methylphenidate.

Three standard CNS stimulants were tested for effect on juvenile play soliciting in prepubertal male rats (n = 120). Three dosages of each stimulant were compared with a saline control. Soliciting behavior was isolated and magnified by a novel method incorporating pretest social deprivation and social response to a standard nonplayful social stimulus pretreated with scopolamine HBr. Caffeine significantly decreased frequency of play soliciting only at the high dose of 40 mg/kg. Methylphenidate and d-amphetamine significantly decreased play soliciting at all dosages tested. The method is proposed as a generally useful experimental paradigm in analyses of drug effects on play soliciting. Advantages include individual measures of soliciting behavior that correlate reliably with measures of rough-and-tumble play fighting.

Amphetamine↗
PubMed1985

Rate-dependency and hyperactivity: methylphenidate effects on operant responding.

The two most common treatment for hyperactivity are psychopharmacological regimens and behavior therapy. Although the concurrent use of stimulant medication has been purported to enhance a child's rate of responding under a behavior management program, studies examining the interaction of the two treatments have been unable to confirm this hypothesis. The present investigation sought to examine the effects of differing levels of methylphenidate hydrochloride (Ritalin) upon operant responding with hyperactive children. After an initial drug-free training period, 10 first through fourth grade hyperactive males performed an operant key-pressing task under a mult VR 5 FI 30 sec reinforcement schedule across four randomly determined, double-blind drug conditions (placebo, 5, 10, 15 mg). Only VR responding changed significantly during medication conditions; however, rate-dependent psychostimulant effects were found within both reinforcement schedules. Discrepancies with animal rate-dependency and implications for treatment and future research are discussed. Medication effects on operant responding appear to depend upon the reinforcement schedule and dose employed.

Attention Deficit Disorder with Hyperactivity↗
PubMed1987

Methylphenidate affects strategic choice behavior in normal adult humans.

The time course of serum concentration and performance on a concurrent probability matching task were evaluated in normal adults receiving 0.15 or 0.3 mg/kg of methylphenidate. The behavioral task, an arcade-like problem-solving game, revealed that drug-treated subjects improved their performance upon repeated testings during pharmacokinetic evaluation at a lower rate than did non-treated controls over the same time span. However, drug-treated subjects failed to adopt the adaptive problem-solving strategies selected by controls.

Adolescent↗
PubMed1987

Effects of methylphenidate and d-amphetamine on timing in the rat.

Rats were trained to press a lever for food pellets provided according to a fixed interval 60-sec schedule of reinforcement. Probe trials (peak trials) assessed responding over two-min periods with no pellet delivered. The low rates of responding found early and late in probe trials were increased by methylphenidate and 1.0 mg/kg d-amphetamine (rate-dependent effect). Further, the mean time of responding (peak time) was shortened for both drugs (timing effect).

Animals↗
PubMed1991

Enantioselective behavioral effects of threo-methylphenidate in rats.

The relative potency of d- and l-threo-methylphenidate (d-MPH and l-MPH) was evaluated using three behavioral paradigms for rats: Responding maintained by a fixed-interval schedule of reinforcement (FI), responding maintained by a concurrent variable-interval schedule of reinforcement (Conc VI VI), and consumption of sweetened condensed milk during a 15-min free-access period. In each case the potency of the d-MPH enantiomer greatly exceeded that of the l-MPH enantiomer. Temporal control of responding was reduced (FI) choice responding was equalized for most rats (Conc VI VI), and milk consumption was suppressed by d-MPH and dl-MPH.

Animals↗
PubMed1994

Methylphenidate treatment following ablation-induced hemiplegia in rat: experience during drug action alters effects on recovery of function.

Two experiments examined the effects of single or multiple administrations of methylphenidate (MPH; Ritalin) and differing amounts of beam-walking trials (symptom relevant experience) during the period of drug action on recovery from hemiplegia following unilateral sensorimotor cortex ablation in rat. The first study tested multiple doses of MPH (10 mg/kg) or sterile saline given once daily, followed by four beam-walk (BW) trials at 1, 2, 3, and 6 h on 3 consecutive days. A significant and enduring enhancement of recovery was only observed 24 h after the third administration of MPH, compared to saline controls. In the second study, a single dose of MPH (10 mg/kg) or saline was administered 24 h after ablation, followed by 12 BW trials beginning 1 h and continuing at 15-min intervals until 3 h after MPH or saline administration. A significant and enduring facilitation of BW ability was produced by this single MPH treatment regimen. These data further support the importance of an interaction between symptom-relevant experience and drugs that increase norepinephrine transmission to enhance functional recovery after brain damage.

Animals↗
PubMed1983

Auditory ERP augmentation-reduction and methylphenidate dosage needs in attention and reading disordered children.

From their event related potentials (ERPs) to tones of four intensity levels, a sample of attention disordered and/or reading disabled children, recommended for a trial on methylphenidate, were classified as auditory augmenters or reducers. The augmenters were blindly titrated at significantly lower dosage levels than the reducers. Moreover, the ameliorative effects of the drug, as assessed by teacher ratings, were more evident in hyperactive augmenters. The children diagnosed either as hyperactive or hyperactive and reading disabled had steeper (or more augmenting) gradients than the nonhyperactive reading disabled and attention disordered subjects. The ERP (N1-P2) gradients were not consistently related to reaction time (RT) gradients to the tones or to an RT measure of nervous system sensitivity. It is suggested that ERPs index registration but not response strength, the first being largely automatic and the second purposive.

Attention Deficit Disorder with Hyperactivity↗
PubMed1991

Methylphenidate and dextroamphetamine treatments of hyperactivity: are there true nonresponders?

The response to stimulant drugs of 48 boys with attention deficit/hyperactivity disorder was measured following dextroamphetamine, methylphenidate, and placebo in a double-blind crossover study. To distinguish lack of behavioral improvement from adverse drug effects, a day hospital setting and a wide dose range were used. Both drugs were highly and equally efficacious for the group as a whole, and frequently one drug or the other was superior for an individual child, or adverse effects occurred only on one of the stimulants. Only one of the 48 boys (2%) was discharged without the recommendation for continued stimulant drug treatment. "Nonresponse" appears to be extremely rare when both stimulants and a wide range of doses are given.

Analysis of Variance↗