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Biomedical subjects

Rodney J Croft

Publications and source records attributed to Rodney J Croft.

At least 19 recordsLinked to original sources
PubMed2006

Acute serotonin and dopamine depletion improves attentional control: findings from the stroop task.

Schizophrenia is associated with impairments of attentional control on classic experimental paradigms such as the Stroop task. However, at a basic level the neurochemical mechanisms that may be responsible for such impairments are poorly understood. In this study, we sought to investigate the influence of brain monoamine function on Stroop task performance in healthy participants using the established methods of acute dietary serotonin, dopamine, and combined monoamine depletion. The study was a double-blind placebo controlled design in which 12 healthy male participants completed the Stroop task under four acute treatment conditions: (a) balanced/placebo control, (b) acute tryptophan depletion, (c) acute tyrosine/phenylalanine depletion, and (d) acute tyrosine/phenylalanine/tryptophan depletion (combined monoamine depletion). Decreased Stroop interference indicating improved attentional control was observed after both tryptophan depletion and tyrosine/phenylalanine depletion, while there was no significant change in interference after combined monoamine depletion. Findings suggest that reduced tonic dopamine or serotonin activity within specific neural circuits (such as the striatum, anterior cingulate, or prefrontal cortex) may play a critical role in attentional control, possibly by improving gating of information via reducing noise in monoaminergic systems. These findings enhance our understanding of the neurochemical basis of attentional control and the possible cause of attentional control deficits in schizophrenia.

Adult↗
PubMed2006

Pindolol does not augment central serotonin function increases to citalopram in humans: an auditory evoked potential investigation.

Animal studies have demonstrated that the co-administration of pindolol and selective serotonin reuptake inhibitors (SSRIs) potentiate serotonergic functioning to a greater degree than SSRIs alone. However, clinical trials of pindolol augmentation in patients with major depressive disorder have reported contradictory findings, and the central effects of this treatment regime on serotonin functioning in humans are unknown. The current double-blind placebo controlled repeated measures investigation used the loudness dependence auditory evoked potential (LDAEP) to assess central serotonin functioning in healthy participants across three acute treatment conditions: placebo, citalopram (20 mg), and pindolol (10 mg)+citalopram (20 mg). The current paper focuses on the effects of pindolol augmentation of citalopram as compared to the administration of citalopram alone. Enhancement of serotonin function with citalopram in comparison to placebo decreased the slope of the LDAEP (i.e. weaker LDAEP). However, there were no significant differences between the changes in the LDAEP induced by co-administration of pindolol and citalopram compared to citalopram. The present results indicate that, in healthy controls, pindolol augmentation of SSRIs does not potentiate central serotonin function to a greater degree than the administration of an SSRI alone. The findings may provide further support for why pindolol may not be an effective therapeutic strategy to augment serotonin function and antidepressant response.

Adult↗
PubMed2006

Dopamine receptor stimulation does not modulate the loudness dependence of the auditory evoked potential in humans.

RATIONALE: The Loudness Dependence of the Auditory Evoked Potential (LDAEP) has been suggested as a reliable measure of central serotonin function in humans; however, its specificity for the serotonin system remains a topic of debate, with possible modulation of this purported serotonin marker by other neurotransmitters, including dopamine. OBJECTIVES: We examined the effect of dopaminergic modulation on the LDAEP using the D1/D2/D3 dopamine receptor agonist pergolide and the D2/D3 agonist bromocriptine. METHODS: The study was a double-blind, placebo-controlled repeated-measures design in which healthy participants were tested under three acute treatment conditions: placebo, bromocriptine (2.5 mg), and pergolide (0.1 mg). Changes in the amplitude of the N1/P2 at intensities (60, 70, 80, 90, and 100 dB) were examined at C Z. RESULTS: Acute stimulation of D1/D2/D3 receptors with pergolide and D2/D3 receptors with bromocriptine in comparison with placebo had no effect on the LDAEP. CONCLUSION: These findings indicate that acute stimulation of dopamine D1, D2, and D3 receptors does not modulate the LDAEP in humans. Although the findings suggest that the LDAEP may not be modulated by acute changes in dopamine neurotransmission, further studies are needed to fully characterize its dopaminergic sensitivity.

Acoustic Stimulation↗
PubMed2006

Quantitative EEG in low-IQ children with attention-deficit/hyperactivity disorder.

OBJECTIVE: This study investigated EEG differences between children with attention-deficit/hyperactivity disorder (AD/HD) and matched control subjects, with either normal or low IQs. METHODS: Twenty normal-IQ and 20 low-IQ children with AD/HD, and 40 age-, IQ- and sex-matched control subjects participated in this study. EEG was recorded from 21 sites during an eyes-closed resting condition and Fourier transformed to provide estimates for total power, and absolute and relative power in the delta, theta, alpha and beta bands. RESULTS: Children with AD/HD had increased theta activity with decreased levels of alpha and beta activity compared to control subjects. IQ was not found to impact on the EEG. No significant differences were found between subjects with normal and low IQs, with the low- and high-IQ AD/HD groups having similar EEG profiles. CONCLUSIONS: Low-IQ children with AD/HD have similar EEG abnormalities to those with normal IQs, and IQ does not appear to impact on EEG power measures. SIGNIFICANCE: This is the first study to investigate EEG differences in low-IQ children with and without AD/HD.

Adolescent↗
PubMed2006

The acute effects of d-amphetamine and methamphetamine on attention and psychomotor performance.

RATIONALE: It is not clear how the deleterious effects of amphetamines on driving performance are mediated in terms of select cognitive processes. OBJECTIVES: The current three separate experiments assessed the acute effects of an oral dose of either 0.42-mg/kg d-amphetamine, d,l-methamphetamine and d-methamphetamine on driving-related cognitive functions in a total of 60 healthy non-fatigued adults. MATERIALS AND METHODS: Three separate repeated measures counterbalanced, double-blind, placebo-controlled designs were employed in which 20 volunteers completed two treatment conditions, either d-amphetamine, d,l-methamphetamine or d-methamphetamine and placebo. Performance was assessed on a range of attentional, psychomotor and perceptual speed tasks. RESULTS: Mean blood concentrations at 120-, 170- and 240-min postdrug administration were 83, 98 and 96 ng/ml, respectively, for d-amphetamine, 90, 95 and 105 ng/ml, respectively, for d,l-methamphetamine and 72, 67 and 59 ng/ml, respectively, for d-methamphetamine. The amphetamines, in general, improved various aspects of attention (Digit Vigilance, Digit Symbol Substitution Test and Movement Estimation Performance) with some evidence to suggest possible enhancement in psychomotor functioning (Tracking ability) and perceptual speed (Inspection Time). CONCLUSIONS: The current series of studies primarily provides evidence of low-level amphetamine-related enhancement of function; however, it also provides evidence of less conservative movement estimation that might contribute to amphetamine-related road fatalities.

Administration, Oral↗
PubMed2006

Investigating evoked and induced electroencephalogram activity in task-related alpha power increases during an internally directed attention task.

This study sought to explore whether the so-called 'paradoxical' task-related increases in the alpha bandwidth of the human electroencephalogram result from increases in evoked (phase locked), as opposed to induced (non-phase locked), activity. The electroencephalograms of 18 participants were recorded while they engaged in both auditory sensory-intake tasks (listening to randomly generated 'tunes') and internally directed attention tasks (imagining the same randomly generated tunes) matched for auditory input. Measures of evoked (phase locked) and induced (non-phase locked) activity were compared between tasks. Increases in induced alpha power were found during internal attention. No experimental effects were observed for evoked activity. These results are not entirely consistent with proposals that 'paradoxical' alpha indexes the evoked inhibition of task irrelevant processing.

Acoustic Stimulation↗
PubMed2006

Direct evidence that acutely enhancing serotonin with the selective serotonin reuptake inhibitor citalopram modulates the loudness dependence of the auditory evoked potential (LDAEP) marker of central serotonin function.

The loudness dependence of the auditory evoked potential (LDAEP) has been suggested as a reliable measure of central serotonin function in humans. The most convincing evidence for a direct relationship between serotonergic function and LDAEP to date has come from animal studies, while evidence in humans has been circumstantial and inconsistent. In the current study, we examine the direct effect of serotonergic modulation with the selective serotonin reuptake inhibitor (SSRI) citalopram on the LDAEP. The study was a double-blind placebo controlled design in which healthy participants were tested under two acute treatment conditions: placebo and citalopram (20 mg). Enhancement of serotonin function with citalopram in comparison to placebo decreased the slope of the LDAEP (i.e. weaker LDAEP). The findings provide direct evidence in humans, of a relationship between central serotonin function and the LDAEP, supporting findings previously observed in animals and clinical populations. Together the results provide further support for the validity of the LDAEP as a non-invasive in vivo measure of central serotonin function in humans.

Acoustic Stimulation↗
PubMed2006

Estrogen prevents 5-HT1A receptor-induced disruptions of prepulse inhibition in healthy women.

The sex steroid hormone, estrogen, has been proposed to be protective against schizophrenia. This study examined the effects of estrogen treatment on modulation of prepulse inhibition (PPI) by the serotonin-1A (5-HT1A) receptor partial agonist, buspirone. PPI is a model of sensorimotor gating, which is deficient in schizophrenia and other mental illnesses. A total of 11 healthy women were tested following four acute treatment conditions: placebo, buspirone (Buspar; 5 mg), estradiol (Estrofem; 2 mg), and combined buspirone and estradiol. Electromyogram activity was measured across three interstimulus intervals (ISI): 30, 60, and 120 ms. There was no significant effect of either drug treatment on startle amplitude or habituation. At 120 ms ISI, buspirone caused a significant disruption of PPI and pretreatment with estrogen prevented this disruption. Estrogen treatment, administered in the appropriate experimental conditions, prevented PPI deficits induced by 5-HT(1A) receptor activation and may therefore also play a protective role in sensorimotor gating deficits in schizophrenia.

Acoustic Stimulation↗
PubMed2006

Dynamics of narrow-band EEG phase effects in the passive auditory oddball task.

Evidence suggests that the component frequencies of the electroencephalogram (EEG) are dynamically adjusted to provide particular brain states at stimulus occurrence, and that these facilitate cortical processing of the stimulus. We examined relationships between stimulus intensity, the phase of narrow-band EEG activity at stimulus onset, and the resultant event-related potentials (ERPs) in a passive auditory oddball task, using a novel conceptualization of orthogonal phase effects (cortical negativity vs. positivity, negative driving vs. positive driving, waxing vs. waning). EEG responses to the standard stimuli (50 vs. 80 dB, varied between subjects) were analysed. Prestimulus narrow-band EEG activity (in 1-Hz bands from 1 to 13 Hz) at Cz was assessed for each trial by digital filtering. For each frequency, the cycle at stimulus onset was used to sort trials into four phases, for which ERPs were derived from both the filtered and unfiltered EEG activity at Fz, Cz and Pz. Preferred brain states at various frequencies were indicated by 16-34% differential occurrence within the orthogonal phase dimensions explored. The preferred states were associated with smaller N1, N2 and N3, larger P2 and P3, shorter N1, P2, N2 and P3 latencies, and some intensity effects. These effects reflected the operation of three separate phase-influenced mechanisms, involving anticipatory potentials and prestimulus/poststimulus amplitudes in various EEG frequencies. Results indicate that, even in paradigms with a slightly varying interstimulus interval, brain dynamics provide preferred brain states at the moment of stimulus presentation, which differentially affect the EEG correlates of stimulus processing.

Acoustic Stimulation↗
PubMed2005

The effect of electromagnetic fields emitted by mobile phones on human sleep.

Previous research has suggested that exposure to radiofrequency electromagnetic fields increases electroencephalogram spectral power in non-rapid eye movement sleep. Other sleep parameters have also been affected following exposure. We examined whether aspects of sleep architecture show sensitivity to electromagnetic fields emitted by digital mobile phone handsets. Fifty participants were exposed to electromagnetic fields for 30 min prior to sleep. Results showed a decrease in rapid eye movement sleep latency and increased electroencephalogram spectral power in the 11.5-12.25 Hz frequency range during the initial part of sleep following exposure. These results are evidence that mobile phone exposure prior to sleep may promote rapid eye movement sleep and modify the sleep electroencephalogram in the first non-rapid eye movement sleep period.

Adolescent↗
PubMed2005

Is the P300 wave an endophenotype for schizophrenia? A meta-analysis and a family study.

INTRODUCTION: We assessed the usefulness of the P300 wave as endophenotype for schizophrenia by means of a meta-analysis of the literature as well as our own family study. METHOD: Meta-analysis: We conducted a systematic search for articles published between 1983 and 2003 that reported P300 measures in non-psychotic relatives of schizophrenic patients and in healthy controls. Meta-regression analyses were performed using a random effects procedure. The pooled standardized effect size (PSES) was calculated as the difference between the means of the two groups divided by the common standard deviation. Local study: We examined the P300 wave with a standard two-tone oddball paradigm in 30 patients with schizophrenia, 40 non-psychotic relatives, and 40 controls using linear mixed models. RESULTS: Meta-analysis: We pooled 472 relatives and 513 controls. The P300 amplitude was significantly reduced in relatives (PSES = 0.61; 95% CI: 0.30 to 0.91; P < 0.001). The P300 latency was significantly delayed in relatives (PSES of -0.50; 95% CI: -0.88 to -0.13; P = 0.009]. Local study: The patients showed a trend for amplitude reductions (P = 0.06) and significant latency delays (P < 0.01). The relatives displayed normal amplitude but had significant latency delays (P = 0.01). The P300 amplitude and especially the P300 latency are promising alternative phenotypes for genetic research into schizophrenia.

Adolescent↗
PubMed2005

An evaluation of the sensitivity of the standardised field sobriety tests to detect the presence of amphetamine.

RATIONALE: The Standardised Field Sobriety Tests (SFSTs), designed and validated to assess impairment associated with alcohol intoxication, are currently being employed by the Victoria Police (Australia) for the identification of driving impairment associated with drugs other than alcohol. OBJECTIVES: The aim of this study was to evaluate whether the SFSTs are a sensitive measure for identifying the presence of dexamphetamine and methamphetamine. METHODS: Three studies each employed a repeated-measures, counterbalanced, double-blind placebo-controlled design. In each study, 20 healthy volunteers completed two treatment conditions: either 0.42 mg/kg d,l-dexamphetamine and placebo, 0.42 mg/kg d,l-methamphetamine and placebo, or 0.42 mg/kg d-methamphetamine and placebo. Performance was assessed using the SFSTs, consisting of the Horizontal Gaze Nystagmus test, the Walk and Turn test, and the One Leg Stand test. Blood and saliva samples were obtained before and immediately after the administration of the SFSTs (120 and 170 min post drug administration). RESULTS: At 120 and 170 min post drug administration, d,l-dexamphetamine blood levels were 83.16 and 98.42 ng/ml, respectively; d,l-methamphetamine levels were 90 and 95 ng/ml, respectively; and d-methamphetamine blood levels were 72 and 67 ng/ml, respectively. None of the three amphetamine doses impaired performance on the SFSTs. Using the SFSTs, the presence of dexamphetamine was identified in 5% of cases, d-methamphetamine in 5%, and d,l-methamphetamine in 0% of cases. CONCLUSIONS: Under these conditions, the SFSTs are not a sensitive measure for detecting the presence of low levels of amphetamine.

Accidents, Traffic↗
PubMed2005

Effects of methylphenidate on EEG coherence in attention-deficit/hyperactivity disorder.

This study investigated the effects of methylphenidate on intrahemispheric and interhemispheric EEG coherence in children with Attention-Deficit/Hyperactivity Disorder (AD/HD). Twenty boys with AD/HD Combined type and 20 age- and sex-matched control subjects, aged 8 to 13 years, participated in this study. EEG was recorded from 21 sites during an eyes-closed resting condition. Wave-shape coherence was calculated for eight intrahemispheric electrode pairs (four in each hemisphere), and eight interhemispheric electrode pairs, within each of the delta, theta, alpha and beta bands. AD/HD children were tested both off and, 6 months later, on a therapeutic dose of methylphenidate. In intrahemispheric comparisons, AD/HD children had lower theta coherences at long inter-electrode distances, and reduced lateralisation at both long and short-medium inter-electrode distances than controls. For interhemispheric comparisons, AD/HD children showed increased coherences in the frontal regions for the low frequency bands (delta and theta), and reduced coherences in the alpha bands in all other regions. These EEG coherences suggest reduced cortical differentiation and specialisation in AD/HD, particularly in the frontal regions. Methylphenidate did not produce any changes in coherence values. The lack of sensitivity of coherence measures to methylphenidate in the present study suggests that eyes-closed resting EEG coherence measures are associated with structural connectivity of the underlying regions of the brain rather than the degree of functionality of these regions. These results suggest the existence of structural as well as functional brain dysfunction in AD/HD.

Adolescent↗
PubMed2005

Muscarinic and nicotinic receptor modulation of object and spatial n-back working memory in humans.

Working memory impairments in the n-back task in schizophrenia have been linked to sustained deficiency in mesocortical dopamine function. More recently, abnormalities in the cholinergic system have also been documented in schizophrenia, with cortical reductions in both nicotinic and muscarinic receptors. While the cholinergic hypothesis of memory is well established, the role of cholinergic receptors in modulating n-back working memory is not known. We investigated the effects of selective and simultaneous muscarinic and nicotinic antagonism on spatial and object n-back working memory performance. The study was a double-blind, placebo-controlled repeated-measures design in which 12 healthy subjects were tested under four acute treatment conditions; placebo (P), mecamylamine (M), scopolamine (S) and mecamylamine+scopolamine (MS). Muscarinic antagonism with scopolamine significantly impaired both object and spatial n-back working memory, whereas nicotinic antagonism with mecamylamine had little effect. Simultaneous antagonism of both muscarinic and nicotinic receptors produced greater impairments in both object and spatial n-back working memory performance than muscarinic or nicotinic antagonism alone. These results suggest that: (1) both muscarinic and nicotinic receptors may functionally interact to synergistically modulate n-back working memory, and (2) that n-back working memory impairments in schizophrenia may in part be due to reductions in both muscarinic and nicotinic receptors.

Adult↗
PubMed2005

EOG correction: a comparison of four methods.

EOG correction is a class of techniques that account for ocular artifact in the electroencephalogram (EEG) by subtracting electrooculographic data from the EEG. The purpose of this study was to evaluate four of these correction techniques (Verleger, Gasser, & Mocks, 1982 [VGM]; Gratton, Coles, & Donchin, 1983 [GCD]; Semlitsch, Presslich, Schuster, & Anderer, 1986 [SPSA]; Croft & Barry, 2000 [CB]). Blinks, vertical eye movements (VEM), and horizontal eye movements (HEM) from 26 subjects were corrected using these techniques, and eye movement event-related potentials computed to aid validation. HEMs were corrected better by CB, VGM/GCD then SPSA, VEMs by CB, VGM/GCD then SPSA, and blinks by CB, SPSA, GCD and then VGM, with the advantage of CB substantial for blinks (eta2>.72), VEMs (eta2>.60), and HEMs (eta2>.27). It is argued that the CB procedure adequately accounts for ocular artifact in the EEG. Reasons for the limitations of the other procedures are discussed.

Blinking↗
PubMed2004

Suppression of P50 evoked potential component, schizotypal beliefs and smoking.

Suppression of the P50 component of the evoked potential is an electrophysiological index of sensory gating that is blunted in schizophrenia spectrum disorders. Although P50 suppression is thought to be related to symptomatology, this is yet to be shown. The failure to demonstrate this relation has led some to argue that P50 suppression and symptomatology are not related. However, a possible confound has recently been corroborated [i.e., chronic smoking is related to superior P50 suppression [Crawford et al., Neuroscience Letters 317 (2002) 151]], and a relation has been found in questionnaire-defined individuals with indications of schizotypy [i.e., psychometric schizotypy is related to poor P50 suppression [Croft et al., Biological Psychiatry 50 (2001) 441]]. The present study attempted to replicate and extend both studies by examining P50 suppression, smoking histories, psychometric schizotypy and NEO Five-Factor Inventory (NEO-V) scores in 37 healthy participants. Replicating Crawford et al., P50 suppression was better in the heavier smokers. Providing a partial replication of Croft et al., P50 suppression was inversely related to schizotypy scores in participants who smoked little or not at all; however, P50 suppression was positively related to schizotypy in heavier smokers. Covarying for age and NEO-V scale scores had little effect on these relations. The findings provide evidence of important confounds that would limit our ability to detect P50 suppression/symptom relations in schizophrenia.

Adolescent↗
PubMed2004

Mismatch negativity in schizophrenia: a family study.

BACKGROUND: Mismatch negativity (MMN) is a measure of cortical activity that occurs in response to a change in auditory stimuli. We investigated whether MMN is a potential marker of genetic vulnerability to schizophrenia by comparing MMN in a group of patients with schizophrenia, their unaffected relatives, and controls. METHOD: There are 25 schizophrenic patients, 37 of their unaffected first-degree relatives, and 20 unrelated controls that performed the MMN task. Linear regression with robust standard errors, and accounting for correlations within families, was employed to test for differences in MMN amplitude between the groups. RESULTS: Patients had significantly smaller MMN amplitudes compared to both their unaffected relatives and controls at FZ (P<0.01) and at F3 (P=0.01), whereas relatives and controls did not differ at FZ or at F3. No differences were found between any of the groups at F4. Furthermore, we found no strong evidence that the MMN amplitude is a familial trait. CONCLUSIONS: Our results confirm that the MMN amplitude is reduced in schizophrenia. However, the MMN does not show a significant familial influence and is normal among the unaffected relatives. We conclude that while the MMN is abnormal in patients with schizophrenia, it is a weak or unreliable marker of vulnerability when applied to subclinical populations, and therefore is unlikely to be an endophenotype for the disorder.

Acoustic Stimulation↗