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PubMed2006

Juvenile administration of methylphenidate attenuates adult hippocampal neurogenesis.

BACKGROUND: The neural consequences of early-life exposure to methylphenidate (MPH; Ritalin) are of great interest given the widespread, and sometimes inappropriate, use in children. Here we examine the impact of juvenile MPH exposure on adult hippocampal neurogenesis. METHODS: Rats received MPH (2.0 mg/kg, intraperitoneal, twice daily) or saline (SAL) during preadolescence (postnatal days 20-35). Hippocampal cell proliferation (Experiment 1), neurogenesis (Experiment 2), and stress-induced changes in cell proliferation (Experiment 3) were assessed at several developmental stages including adulthood. RESULTS: Juvenile exposure to MPH did not alter proliferation at any developmental time point relative to control rats; however, exposure to MPH significantly decreased the long-term survival of newborn cells in adult rats, particularly in the temporal hippocampus. Although MPH-treated rats had higher levels of corticosterone after restraint stress, they did not show the expected greater decrease in hippocampal cell proliferation relative to control animals. CONCLUSIONS: Early-life exposure to MPH inhibits the survival of adult-generated neurons in the temporal hippocampus and may reduce progenitor sensitivity to corticosterone-induced decreases in proliferation. These findings suggest that decreased adult neurogenesis is an enduring consequence of early-life exposure to MPH and are discussed for their relevance to humans.

Analysis of Variance↗
PubMed2006

Methylphenidate preferentially increases catecholamine neurotransmission within the prefrontal cortex at low doses that enhance cognitive function.

BACKGROUND: Low doses of psychostimulants, such as methylphenidate (MPH), are widely used in the treatment of attention-deficit/hyperactivity disorder (ADHD). Surprisingly little is known about the neural mechanisms that underlie the behavioral/cognitive actions of these drugs. The prefrontal cortex (PFC) is implicated in ADHD. Moreover, dopamine (DA) and norepinephrine (NE) are important modulators of PFC-dependent cognition. To date, the actions of low-dose psychostimulants on PFC DA and NE neurotransmission are unknown. METHODS: In vivo microdialysis was used to compare the effects of low-dose MPH on NE and DA efflux within the PFC and select subcortical fields in male rats. Doses used (oral, 2.0 mg/kg; intraperitoneal, .25-1.0 mg/kg) were first determined to produce clinically relevant plasma concentrations and to facilitate both PFC-dependent attention and working memory. RESULTS: At low doses that improve PFC-dependent cognitive function and that are devoid of locomotor-activating effects, MPH substantially increases NE and DA efflux within the PFC. In contrast, outside the PFC these doses of MPH have minimal impact on NE and DA efflux. CONCLUSIONS: The current observations suggest that the therapeutic actions of low-dose psychostimulants involve the preferential activation of catecholamine neurotransmission within the PFC.

Adrenergic Uptake Inhibitors↗
PubMed2006

Sensory-evoked potentials recordings from the ventral tegmental area, nucleus accumbens, prefrontal cortex, and caudate nucleus and locomotor activity are modulated in dose-response characteristics by methylphenidate.

Most of the studies investigating the effects of methylphenidate (MPD) are using behavioral and biochemical approaches. There are some electrophysiological studies about the effects of MPD on spontaneous electrical activity; however, there is none about the effects of MPD on sensory inputs. The objectives of the present study were to investigate the MPD dose-response characteristics on locomotor activity and sensory inputs using acoustic stimuli. Freely behaving rats previously implanted with semi-microelectrodes were used to record from four brain areas known to be sites of psychostimulant action. For locomotor behavior assessment, rats received saline on experimental day 1 and an acute administration of MPD (0.6, 2.5, or 10.0 mg/kg, i.p.) on experimental day 2. Using an automated, computerized activity-monitoring system, locomotor behavior was recorded for 2-h postinjection on both days. For the electrophysiological experiments, animals were implanted with permanent electrodes in the ventral tegmental area (VTA), nucleus accumbens (NAc), prefrontal cortex (PFC), and caudate nucleus (CN) under general anesthesia. Five to seven days after electrode implantation, they were used to study the effects of three different MPD doses on the response to sensory inputs. The lowest dose of MPD (0.6 mg/kg, i.p.) failed to alter locomotor activity, while the two higher MPD doses (2.5 and 10.0 mg/kg) elicited increase in locomotion, with the 10.0 mg/kg dose increased at least twice as much as the 2.5 mg/kg dose. However, the same three MPD doses elicited significant attenuation of sensory inputs in dose-response characteristics, i.e., as MPD dose increased, evoked sensory inputs decreased. These opposite effects (motor activation and sensory input suppression) were further discussed.

Acoustic Stimulation↗
PubMed2006

Methylphenidate treatment induces oxidative stress in young rat brain.

Methylphenidate (MPH) is frequently prescribed for the treatment of attention deficit/hyperactivity disorder. Psychostimulants can cause long-lasting neurochemical and behavioral adaptations. Here, we evaluated oxidative damage in the rat brain and the differential age-dependent response to MPH after acute and chronic exposure. We investigated the oxidative damage, assessed by the thiobarbituric acid reactive species (TBARS), and the protein carbonyl assays in cerebellum, prefrontal cortex, hippocampus, striatum, and cerebral cortex of young (25 days old) and adult (60 days old) male Wistar rats after acute and chronic exposure to MPH. Chronic MPH-treated young rats presented a dose-dependent increase in TBARS content and protein carbonyls formation in specific rat brain regions. In the acute exposure, only MPH highest dose increased lipid peroxidation in the hippocampus. No difference in protein carbonylation was observed among groups in all structures analyzed. In adult rats, we did not find oxidative damage in both acute and chronic treatment. Chronic exposure to MPH in induces oxidative damage in young rat brain, differentially from chronic exposure during adulthood. These findings highlight the need for further research to improve understanding of MPH effects on developing nervous system and the potential consequences in adulthood resulting from early-life drug exposure.

Age Factors↗
PubMed2005

The role of age, genotype, sex, and route of acute and chronic administration of methylphenidate: a review of its locomotor effects.

Children with attention deficit hyperactivity disorder (ADHD) are treated for extended periods of time with the psychostimulant methylphenidate (MPD). The psychostimulants cocaine, amphetamine, and MPD exhibit similar structural configuration and pharmacological profile. The consequence of the long-term use of psychostimulants such as MPD as treatment for ADHD in the developing brain of children is unknown. Repeated treatment with psychostimulants has been shown to elicit adverse effects in behavior, such as dependence, paranoia, schizophrenia, and behavioral sensitization. Behavioral sensitization and cross-sensitization between two drugs are used as experimental markers to determine the potential of a drug to develop dependence/addiction. Although there are many reviews written about behavioral sensitization involving psychostimulants, scarcely any have focused specifically on MPD-elicited behavioral sensitization and cross-sensitization with other psychostimulants. Moreover, the response to MPD and the expression of ADHD vary among females and males and among different populations due to genetic variability. Since the interpretation and synthesis of the data reported are controversial, this review focuses on the adverse effects of MPD and the role of age, sex, and genetic composition on the acute and chronic effects of MPD, such as MPD-elicited behavioral sensitization and cross-sensitization with amphetamine in animal models. Animal models of drug-induced locomotor stimulation, particularly locomotor sensitization, can be used to understand the mechanisms underlying human drug-induced dependence.

Age Factors↗
PubMed2006

Acute and chronic methylphenidate dose-response assessment on three adolescent male rat strains.

Methylphenidate (MPD), commonly known as Ritalin, is the most frequently prescribed drug to treat children and adults with attention deficit hyperactivity disorder (ADHD). Adolescence is a period of development involving numerous neuroplasticities throughout the central nervous system (CNS). Exposure to a psychostimulant such as MPD during this crucial period of neurodevelopment may cause transient or permanent changes in the CNS. Genetic variability may also influence these differences. Thus, the objective of the present study was to determine whether acute and chronic administration of MPD (0.6, 2.5, or 10.0mg/kg, i.p.) elicit effects among adolescent WKY, SHR, and SD rats and to compare whether there were strain differences. An automated, computerized, open-field activity monitoring system was used to study the dose-response characteristics of acute and repeated MPD administration throughout the 11-day experimental protocol. Results showed that all three adolescent rat groups exhibited dose-response characteristics following acute and chronic MPD administration, as well as strain differences. These strain differences depended on the MPD dose and locomotor index. Chronic treatment of MPD in these animals did not elicit behavioral sensitization, a phenomenon described in adult rats that is characterized by the progressive augmentation of the locomotor response to repeated administration of the drug. These results suggest that the animal's age at time of drug treatment and strain/genetic variability play a crucial role in the acute and chronic effect of MPD and in the development of behavioral sensitization.

Adolescent↗
PubMed2005

Methylphenidate regulates c-fos and fosB expression in multiple regions of the immature rat brain.

Methylphenidate (Ritalin, MPH) is a common psychostimulant used to treat childhood attention-deficit hyperactivity disorder (ADHD). Little is known about the long-term developmental effects on gene expression and behavior, which may occur with extended MPH use. We reported previously that the striatum is a major target of MPH, consistent with human MRI studies. In the present study, we tested the hypothesis that MPH is likely to have widespread effects in extra-striatal regions of the brain. We used the expression of two immediate early genes, c-fos and fosB, as probes to map the response of the immature rat brain to single (1 day) versus repeated (14 days) MPH treatment (2 or 10 mg/kg; s.c.) from postnatal day 25 to 38. Consistent with previous reports, the striatum is a major target of acute MPH action, as indicated by elevated levels of cFOS-immunoreactivity (-ir). Increases in c-fos expression were also seen in the nucleus accumbens, cingulate/frontal cortex and piriform cortex, and Islands of Calleja. FosB expression was elevated only in the striatum following a single stimulation. Chronic MPH treatment (10 mg/kg/day for 14 days) resulted in an attenuation of c-fos expression in the striatum and Islands of Calleja. However, levels of cFOS-ir remained elevated in the nucleus accumbens and frontal cortex. In contrast to the inhibitory effect of repeated MPH exposure on c-fos expression, FOSB-ir was further elevated in the striatum, and an increase was observed in the cingulate/frontal and piriform cortices. Thus, chronic MPH differentially regulated expression of c-fos and fosB in several brain regions. Our data suggest that MPH may exert its stimulant effects at multiple sites in the immature brain, which has implications for long-term treatment in children.

Analysis of Variance↗
PubMed2005

Methylphenidate differentially regulates c-fos and fosB expression in the developing rat striatum.

Methylphenidate (MPH, Ritalin) is a psychostimulant drug used in very young children with attention deficit hyperactivity disorder (ADHD). To explore the central effects of MPH, we compared repeated MPH treatments on c-fos and fosB expression in the striatum of immature and adult rats. Prepubertal (PD25-38) or adult (PD53-66) male rats were treated once daily for: (a) 14 days with either saline or MPH (2 or 10 mg/kg) or (b) 13 days with saline followed by a single dose of MPH (2 or 10 mg/kg) on day 14. To determine long-term effects of MPH, another group of prepubertal rats was allowed a drug-free period of 4 weeks following the initial 14 days of treatment, and received a challenge dose of MPH at adulthood. All rats were sacrificed 2 h post-injection on the final day. Expression of c-fos and fosB was quantified by densitometric analysis of cFOS and FOSB-immunoreactivity (-ir). We demonstrated that FOSB-ir was increased by a single dose of MPH in the prepubertal and adult striatum, and this effect was further elevated by chronic MPH in prepubertal rats, in contrast to the inhibitory effect of MPH (2 and 10 mg/kg) on cFOS-ir. In adult rats, repeated MPH down-regulated cFOS-ir only at the higher dose (10 mg/kg), while fosB expression remained at levels comparable to acute MPH. The reduction in cFOS-ir observed in prepubertal rats given repeated MPH (10 mg/kg) persisted in the adult striatum following MPH challenge at adulthood. Our results suggest that (1) repeated MPH treatment differentially regulates c-fos and fosB expression in the immature and adult brain; (2) MPH-induced changes in gene expression may be enduring, and (3) the immature brain is more sensitive to the stimulant effects of MPH than the adult. Thus, our findings have implications for the long-term use of MPH in ADHD.

Age Factors↗
PubMed2004

Oral methylphenidate challenge selectively decreases putaminal T2 in healthy subjects.

Despite the recent rise in oral methylphenidate (MPH) abuse, few studies have characterized the time course of oral MPH brain effects in human subjects. Accordingly, this study assessed the hemodynamic effects of oral MPH effects in 11 healthy young adults (six women), by measuring brain transverse relaxation times (T2). T2 can be interpreted as a surrogate marker for, and inversely correlated with, steady-state cerebral blood volume (CBV). Data were acquired from the caudate nucleus, putamen, and thalamus, using a 1.5 T MRI scanner at baseline and serially for 2 h following oral MPH administration (0.5 mg/kg). Physiological and subjective measures and plasma MPH levels also were examined. MPH induced a selective T2 decrease (-1.65+/-0.53 ms) in the putamen (F(6,54)=2.68, P<0.03). Heartrate, blood pressure and plasma MPH levels increased significantly after drug administration, as well as subjective ratings of "feeling drug effect". T2 decreases may reflect MPH-induced increases in putaminal blood volume. These data suggest that T2 relaxometry can be used to study the time course of regional cerebral blood volume responses to MPH and perhaps to other stimulant drugs.

Administration, Oral↗
PubMed2006

Treatment of cocaine dependent treatment seekers with adult ADHD: double-blind comparison of methylphenidate and placebo.

The purpose of this double-blind 14-week trial was to compare the efficacy of sustained-release methylphenidate (MPH) to placebo (PBO) in treating adult attention deficit hyperactivity disorder (ADHD) symptoms in current cocaine dependent (CD) treatment seekers. The randomized sample consisted of 106 participants who were predominately male (83%) and 60% Caucasian, 14% Hispanic, 20% African-American and 6% other. All participants met DSM-IV criteria for ADHD and CD. There were no significant demographic differences between the two treatment groups. All participants received weekly individual cognitive behavioral therapy. There was no difference in retention rate based on treatment group (p=.91). The majority of the PBO group and the MPH group reported >30% improvement in their ADHD symptoms (55% versus 47%), with no significant difference between the two groups (p=.44). Using a combined outcome measure (>30% reduction in ADHD symptoms and CGI <3), the response rates were similar for both groups (28% PBO versus 30% MPH; p=.83). Longitudinal analyses of the urine toxicology data using generalized estimating equations, revealed a decrease in the probability of cocaine positive urine samples during the trial for the MPH group compared to the PBO group (p=.001). Further analysis suggested that for the MPH group, ADHD treatment responders, based on a semi structured clinical interview, were more likely to have a reduction in cocaine use compared to the non-ADHD responders. Although sustained-release MPH did not show superiority over PBO in treating ADHD symptoms, this trial provides some evidence that improvement in ADHD symptoms (clinician rated) among those patients receiving MPH, but not placebo, was associated with a reduction in cocaine use.

Adolescent↗
PubMed2006

Methylphenidate and atomoxetine increase histamine release in rat prefrontal cortex.

Using microdialysis in rat prefrontal cortex, we found that 1 mg/kg of the stimulant methylphenidate and the non-stimulant atomoxetine, two widely used treatments for Attention Deficit/Hyperactivity Disorder (ADHD), produce robust increases in the extracellular levels of histamine, which plays a key role in attention, learning and memory. While the clinical response to ADHD drugs is typically attributed to modulation of norepinephrine and dopamine, this finding suggests enhanced histamine release may contribute to their efficacy as ADHD treatments.

Animals↗
PubMed2006

Methylphenidate improves reading performance in children with attention deficit hyperactivity disorder and comorbid dyslexia: an unblinded clinical trial.

Attention Deficit Hyperactivity Disorder (ADHD) and dyslexia are frequently co-occurring disorders. Although methylphenidate (MPH) is the primary treatment for ADHD, the effect on reading in children with these comorbid problems is not yet known. This study was an unblinded clinical trial to evaluate the reading performance before and after treatment with MPH. Reading performance was compared with General Linear Model repeated measures between three groups: (1) an experimental group of children with both ADHD and dyslexia (N = 24), (2) a control group of children with ADHD (N = 9) and (3) a control group of children with dyslexia (N = 10). MPH improved reading performance significantly stronger in the experimental group than in the control groups; the number of correctly read words increased to a larger extent. In conclusion, MPH proved to be an aid in the reading process of children with ADHD and comorbid dyslexia by improving the learning conditions, but MPH cannot cure the reading disorder. Future research should study the effect of MPH on reading in a double-blind clinical trial.

Adolescent↗
PubMed2005

The homozygosity for 10-repeat allele at dopamine transporter gene and dopamine transporter density in Korean children with attention deficit hyperactivity disorder: relating to treatment response to methylphenidate.

The symptoms of attention deficit hyperactivity disorder (ADHD) can be treated with methylphenidate (MPH), a potent blocker of dopamine transporter (DAT). The homozygosity of the 10-repeat allele at the DAT gene (DAT1) seems to be associated with a poor response to MPH in children with ADHD. In the present study, we investigated the association between DAT density using I-123-N-(3-iodopropen-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl)tropane [123I]IPT single photon emission computed tomography (SPECT)] and the homozygosity for 10-repeat allele at DAT1 and response to MPH in Korean children with ADHD. Eleven drug-naive children with ADHD were included in the study and treated with MPH for about 8 weeks. After the genotyping and SPECT were performed, we compared DAT density between ADHD children with and without the homozygosity for 10-repeat allele at DAT1 and investigated the correlation between the homozygosity for 10-repeat allele and response to MPH. ADHD children with 10/10 genotype (n=7) had a significantly greater increase of the DAT density in basal ganglia than the children without 10/10 genotype (n=4). We found that while only 28.6% (2/7) of the subject with 10/10 genotype showed good response to MPH treatment, 100% (4/4) of the subjects without 10/10 genotype showed good response to MPH treatment. Our findings support an association between homozygosity for 10-repeat allele at DAT1 and the DAT density assessed in vivo and correlation between the homozygosity for 10-repeat allele and poor response to MPH.

Alleles↗
PubMed2005

Dose-related effect of methylphenidate on stopping and changing in children with attention-deficit/hyperactivity disorder.

PURPOSE: The effect of methylphenidate (MPH) on inhibitory control as assessed by the stop task in children with attention-deficit/hyperactivity disorder (ADHD) could be influenced by task difficulty and may be mediated by attention. SUBJECTS AND METHODS: Fifteen children with ADHD performed the stop and the change task after placebo, 0.5 and 1.0 mg/kg MPH in a within-subject design. RESULTS: Linear-trend analysis showed a similar effect of MPH in both tasks and a stronger effect for inhibitory control than for attention. Furthermore, a correlation was found between blood serum metabolites of norepinephrine and dopamine for attentional measures and inhibitory control measures, respectively. DISCUSSION AND CONCLUSION: In children with ADHD MPH could act primarily on inhibitory control, and is not influenced by task difficulty. Also, attention and inhibitory control could have differential pharmacological profiles.

Adolescent↗
PubMed2004

Effect of methylphenidate on auditory event related potential in boys with attention deficit hyperactivity disorder.

OBJECTIVE: Event related brain potentials (ERPs) is a non-invasive technique giving knowledge about neural activity associated with sensory and cognitive information processing. The aims of the present study were to investigate amplitude and latency of P100, N200, and P300 in parietal and frontal areas in children with attention deficit hyperactivity disorder (ADHD), and in healthy children, and to determine the effect of methylphenidate (MPH) on these ERPs indices in ADHD group. METHODS: ERP indices, latencies of parietal P3 (PP3L), P1 (PP1L), N2 (PN2L), and frontal P1 (FP1L), N2 (FN2L), P3 (FP3L), and amplitudes of parietal P3 (PP3A), P1 (PP1A), N2 (PN2A), and frontal P1 (FP1A), N2 (FN2A), and P3 (FP3A), using an auditory oddball paradigm were recorded before and under MPH treatment in boys with ADHD, and in 23 healthy children. RESULTS: Before MPH treatment, PP3L was significantly longer and PP3A, PN2A, FN2A, and FP3A smaller in children with ADHD compared to healthy children (all P values < .05). No significant difference was found in PP1L, PP1A, PN2L, FP1L, FP1A, FN2L, and FP3L between ADHD and control group (all P values > .05). MPH treatment resulted in a significant decrease in PP3L, PN2L, and FP3L, and increase in PP3A, PP1A, and FP3A (all P values < .05). There was no significant difference in PP1L, PN2A, FP1L, FP1A, FN2L, and FN2A between before MPH and under MPH treatment in ADHD subjects (all P values > .05). Under MPH treatment, PP3L, PP3A, PP1L, PP1A, PN2L, FP1L, FP1A, FN2L, FP3L, and FP3A were not significantly different between children with ADHD and healthy controls (all P values > .05). However, PN2A and FN2A were significantly smaller in ADHD subjects compared to controls (both P values < .05). CONCLUSION: This study provides indirect evidence that ADHD subjects are associated with abnormalities in signal detection (inattention) and discrimination, and information processing. In addition, present study has shown that except FN2A and PN2A, MPH normalizes ERP indices, which suggested that MPH may be effective on impaired information processing in ADHD, but not on the receiving information.

Adolescent↗
PubMed2005

The effect of methylphenidate on response inhibition and the event-related potential of children with attention deficit/hyperactivity disorder.

Children with Attention Deficit/Hyperactivity Disorder (AD/HD) appear to be deficient in inhibitory processes, as reflected in behavioural and electrophysiological measures. This study examined the effect of methylphenidate (MPH) on response inhibition in children with AD/HD. Event-related potentials (ERPs) and skin conductance level (SCL) were recorded from 18 boys with AD/HD and 18 controls while they performed a cued Go/Nogo task with 70% Go probability. All participants performed the task twice, with an hour interval between test sessions. At the beginning of this interval children with AD/HD took their normal morning dose of MPH. The AD/HD group showed lower SCL than controls pre-medication, a difference not found subsequent to the administration of MPH. While the AD/HD group made more overall errors (omission+commission) pre-medication, and continued to make more omission errors than controls post-medication, the groups became comparable on the number of commission errors, suggesting MPH ameliorates deficits in response inhibition. Children with AD/HD displayed enhanced N1 and P2 amplitudes, and reduced N2 amplitudes relative to controls. These differences were not significant post-medication, at least partly attributable to the action of MPH. This study is unusual in the concurrent examination of electrodermal and electrophysiological measures of medication effects in children with AD/HD, with the retesting of both the AD/HD and control groups allowing a more valid estimate of the effects of medication, rather than assuming that retesting does not have a substantial impact.

Adolescent↗
PubMed2006

Emotional task-dependent low-frequency fluctuations and methylphenidate: Wavelet scaling analysis of 1/f-type fluctuations in fMRI of the cerebellar vermis.

UNLABELLED: Ion channel currents, neural firing patterns, and brain BOLD signals display 1/f-type fluctuations or fractal properties in time. By design, fMRI methods attempt to minimize the contribution of variance from low-frequency physiological 1/f-noise. New fMRI methods are described to visualize and measure 1/f-type BOLD fluctuations in volunteers recalling affectively neutral or emotional memories or meditating (i.e., attending to breathing) then retrospectively rating emotional content. A wavelet scaling exponent (alpha) was used to characterize signals from 0.015625 to 0.5Hz in cerebellar lobules VIII to X of the vermis (posterior inferior vermis; PIV), a region coordinating balance, eye tracking, locomotion, and vascular tone, and a possible site of pathology in attention deficit hyperactivity disorder (ADHD). RESULTS: Changes in alpha and emotional measures were correlated in PIV voxels (r = 0.622, d.f .= 14, P < 0.0005), but not other regions examined. In contrast, conventional means and standard deviations of PIV voxels were unchanged. Methylphenidate, shown to decrease slow oscillations in rodent basal ganglia [Ruskin DN, Bergstrom DA, Shenker A, Freeman LE, Baek D, Walters JR. Drugs used in the treatment of attention-deficit/hyperactivity disorder affect postsynaptic firing rate and oscillation without preferential dopamine autoreceptor action. Biol Psychiatry 2001;49:340-50.], abolished task-dependent alpha changes in the PIV of an adult with ADHD. Wavelet analysis of long BOLD time series appears well suited to fractal physiology and studies of pharmacologically modulated cerebellar-thalamic-cortical function in ADHD or other psychiatric disorders.

Adult↗
PubMed2004

Stuttering priapism associated with withdrawal from sustained-release methylphenidate.

Stuttering priapism is intermittent, prolonged, painful, pathologic erections with intervening periods of detumescence. An adolescent had stuttering priapism associated with withdrawal from sustained-release methylphenidate. To our knowledge, this is the first such report of stuttering priapism associated with stimulant drugs for treatment of attention deficit hyperactivity disorder.

Adolescent↗