bluuebunny/crossref_metadata_2025_split huggingface dataset:
STRADDLING THE PATHWAY FROM PAEDIATRICIAN TO MAINSTREAM HEALTH CARE: TRANSITION ISSUES EXPERIENCED IN DISABILITY CARE
Authors: O'Connell Bev , Bailey Susan , Pearce Julian 
Published: June 2003

ABSTRACTObjective: To identify the strengths and limitations of health care and related services provided to young adults with a disability during the period of transition from the care of a paediatrician to the mainstream health system.Design: A descriptive design was used to address the study objectives.Setting: Barwon and south‐western region of Victoria.Subjects: Twelve focus group discussions, with young adults with a disability, carers of young adults with a disability and health care service providers. Each focus group involved eight to 10 participants.Results: The findings revealed a number of problems with the transition period. All participants acknowledged the supportive, coordinating role of the paediatrician. In the absence of this type of role, carers felt they lacked the knowledge and support to manage the adolescent with a disability. Communication problems between all service providers were identified as being problematical. The general lack of continuity of care between providers made it difficult for individuals to negotiate the transition period and increased the burden of care on carers.Conclusion: There is a need for policy makers to address these transition problems and develop appropriate services that improve the situation for young adults with a disability and their carers.What is already known: It is well documented that the transition period from paediatrician to adult health care services is problematic for the young adult with a disability and their carer. The difficulties experienced are attributed to poor communication between service providers and a lack of continuity of care.What does this study add: This study provides insights from a number of different consumer and health care professionals’ perspectives. The findings identify service delivery gaps and a need to develop health care services that could assist the young adult with the disability negotiate this transition from the paediatric services to mainstream health care services in rural and regional settings in Victoria.
RURAL ORIGIN MEDICAL STUDENTS: HOW DO THEY COPE WITH THE MEDICAL SCHOOL ENVIRONMENT?
Authors: Durkin Shane R. , Bascomb Angela , Turnbull Deborah , Marley John 
Published: June 2003

ABSTRACT:Australia suffers from a well documented shortage of rural medical practitioners. In an attempt to increase recruitment, it has emerged that rural origin medical students are more than twice as likely as their urban colleagues to become rural practitioners. This has led to a wide range of programs aimed at increasing the number of rural students who apply for and gain entry into medical school. But how do rural students cope with the medical school environment? This paper was based on the results of a survey of senior medical students and looked at how rural students’ fare with the medical school environment compared to their urban counterparts. It was concluded that government initiatives currently supporting rural medical students must be continued into the future and continuously evaluated to ensure that rural students have a positive learning experience in preparation for future rural practice.
Differences in activities of daily living motor skills of persons with and without Alzheimer's disease
Authors: Oakley Frances , Duran Leslie , Fisher Anne , Merritt Brenda 
Published: May 2003

The purpose of this descriptive comparison study is to determine if persons with dementia of the Alzheimer's type differ from well older controls in the motor skills that affect the quality of performance of activities of daily living, and if so, to identify those specific activities of daily living motor skills that are retained or lost. The Assessment of Motor and Process Skills was administered to a proportionally matched sample of 567 persons with dementia of the Alzheimer's type and 378 community‐living non‐disabled controls, all of whom were 60 years or older. We found significant differences in mean activities of daily living motor ability between non‐disabled controls, higher functioning participants with dementia of the Alzheimer's type, and lower functioning participants with dementia of the Alzhemier's type. Thus, diminished motor skills appear to affect the quality of activities of daily living task performance of persons with dementia of the Alzhemier's type, even those who are higher functioning. These findings suggest that motor skills may need to be addressed in intervention planning for persons with dementia of the Alzheimer's type.
Excitotoxic lesions of the prelimbic‐infralimbic areas of the rodent prefrontal cortex disrupt motor preparatory processes
Authors: Risterucci Céline , Terramorsi Denise , Nieoullon André , Amalric Marianne 
Published: May 2003

AbstractThe medial prefrontal cortex (mPFC) is involved in a variety of cognitive and emotional processes; in rodents its implication in motor planning is less known, however. We therefore investigated how the mPFC contributes to the information processes involved in the execution of a reaction time task in rats. Subjects were trained to rapidly release a lever at the onset of a cue light, which was presented after an unpredictable period of variable duration (500, 750, 1000 and 1250 ms). Excitotoxic lesions of the whole mPFC or two mPFC subregions [e.g. the dorsal anterior cingulate and the prelimbic‐infralimbic (PL‐IL) areas] were achieved by intracerebral infusions of ibotenic acid (9.4 µg/µL) at different volumes. Extensive mPFC lesions produced increased premature responding and disrupted motor readiness, e.g. the distribution of preparatory patterns during the variable preparatory periods. The deficits lasted for 3 weeks and could be reinstated 2 months after the lesion by varying the duration of the preparatory periods to increase time uncertainty. Furthermore, lesions restricted to the PL‐IL cortex areas reproduced all the deficits of mPFC lesions, whereas pregenual anterior cingulate cortex lesions had no effect. The results emphasize a critical role of the rat PL‐IL region in motor preparatory processes. Hence, discrete lesions of this area reproduce some deficits such as impairment of time estimation and disinhibitory behaviours observed in humans with frontal hypoactivity.
α2‐Adrenoreceptor activation inhibits LTP and LTD in the basolateral amygdala: involvement of Gi/o‐protein‐mediated modulation of Ca2+‐channels and inwardly rectifying K+‐channels in LTD
Authors: DeBock F. , Kurz J. , Azad S. C. , Parsons C. G. , Hapfelmeier G. , Zieglgänsberger W. , Rammes G. 
Published: May 2003

AbstractActivation of adrenoreceptors modulates synaptic transmission in the basolateral amygdala. Here, we investigated the effects of α2‐adrenoreceptor activation on long‐term depression and long‐term potentiation in an in vitro slice preparation of the mouse basolateral amygdala. Field potentials and excitatory postsynaptic currents were evoked in the basolateral amygdala by stimulating the lateral amygdala. Norepinephrine (20 µm) reduced synaptic transmission and completely blocked the induction of long‐term potentiation and long‐term depression. The α2‐adrenoreceptor antagonist yohimbine (2 µm) reversed this effect. The α2‐adrenoreceptor agonist clonidine (10 µm) mimicked the effects of norepinephrine. The Gi/o‐protein inhibitor pertussis toxin (5 µg/mL) reversed the effect of clonidine. Long‐term depression was blocked in the presence of ω‐conotoxin GVIA, but not ω‐agatoxin IVA. Clonidine inhibited voltage‐activated Ca2+ currents mediated via N‐ or P/Q‐type Ca2+‐channels. The inhibitory action of clonidine on long‐term depression was reversed when inwardly rectifying K+‐channels were blocked by Ba2+ (300 µm). The present data suggest that α2‐adrenoreceptor activation impairs the induction of long‐term depression in the basolateral amygdala by a Gi/o‐protein‐mediated inhibition of presynaptic N‐type Ca2+‐channels and activation of inwardly‐rectifying K+‐channels.
The amygdalar circuit that acquires taste aversion memory differs from the circuit that extinguishes it
Authors: Bahar Amir , Samuel Anat , Hazvi Shoshi , Dudai Yadin 
Published: May 2003

AbstractExperimental extinction is the decline in the frequency or intensity of a conditioned behaviour resulting from repetitive performance of the behaviour in the absence of the unconditioned stimulus or reinforcer (Pavlov, 1927). Ample behavioural evidence indicates that experimental extinction does not reflect unlearning of the original trace, but rather a relearning process, in which the new association of the conditioned stimulus with the absence of the original reinforcer comes to control behaviour (Rescorla, 1996). If experimental extinction is indeed learning rather than forgetting, are the neuronal circuits that subserve learning and extinction identical? We address this question by double dissociation analysis of the role of the central (CeA) and the basolateral (BLA) nuclei of the rat's amygdala in the acquisition and extinction, respectively, of conditioned taste aversion (CTA). Whereas local blockade of protein synthesis or β‐adrenergic receptors in the CeA blocks acquisition but not extinction of CTA, a similar intervention in the BLA blocks extinction but not acquisition. Hence, the amygdalar circuit that acquires taste aversion memory differs functionally from the circuit that extinguishes it.
Differential adaptive properties of accumbens shell dopamine responses to ethanol as a drug and as a motivational stimulus
Authors: Bassareo Valentina , De Luca Maria Antonietta , Aresu Marzia , Aste Alessandra , Ariu Teresa , Di Chiara Gaetano 
Published: May 2003

AbstractNon‐adaptive activation of dopamine transmission in the nucleus accumbens shell by drugs of abuse has been attributed a fundamental role in the mechanism of drug addiction. In order to test this hypothesis, we compared in the same subject the effect of an addictive drug (ethanol) and of taste stimuli, including ethanol's own taste, on dialysate dopamine in the nucleus accumbens shell as an estimate of dopamine transmission and on taste reactivity as an expression of motivational valence. Ethanol was also monitored in the dialysates. In naive rats, intraoral infusion of a 20% sucrose + chocolate solution elicited a monophasic increase of dialysate dopamine immediately after the intraoral infusion. In contrast, intraoral infusion of 10% ethanol, 10% ethanol + 20% sucrose or 10% ethanol + 20% sucrose + chocolate solutions elicited a biphasic increase of nucleus accumbens dopamine with an early taste‐related rise and a late rise related to dialysate ethanol. Pre‐exposure to the ethanol solutions 24 h before resulted in the absence of the early dopamine rise and permanence of the late dopamine rise. This late dopamine rise was actually increased as compared with that of the nonpre‐exposed group when sucrose‐containing ethanol solutions were tested. The results indicate that single trial pre‐exposure to the ethanol solutions differentially affects the responsiveness of nucleus accumbens shell dopamine to the direct intracerebral action of ethanol and to the effect of its taste with potentiation, or no change of the first and abolition of the second. These observations point to the existence of major differences in the adaptive regulation of nucleus accumbens dopamine transmission in the shell after drug as compared with taste reward. These differences, in turn, are consistent with a role of nucleus accumbens shell dopamine in the mechanism of the behavioural effects of addictive drugs.
Effects of nicotine in the dopaminergic system of mice lacking the alpha4 subunit of neuronal nicotinic acetylcholine receptors
Authors: Marubio L. M. , Gardier A. M. , Durier S. , David D. , Klink R. , Arroyo‐Jimenez M. M. , McIntosh J. M. , Rossi F. , Champtiaux N. , Zoli M. , Changeux J‐P. 
Published: May 2003

AbstractThe mesostriatal dopaminergic system influences locomotor activity and the reinforcing properties of many drugs of abuse including nicotine. Here we investigate the role of the α4 nicotinic acetylcholine receptor (nAChR) subunit in mediating the effects of nicotine in the mesolimbic dopamine system in mice lacking the α4 subunit. We show that there are two distinct populations of receptors in the substantia nigra and striatum by using autoradiographic labelling with 125I α‐conotoxin MII. These receptors are comprised of the α4, β2 and α6 nAChR subunits and non‐α4, β2, and α6 nAChR subunits. Non‐α4 subunit‐containing nAChRs are located on dopaminergic neurons, are functional and respond to nicotine as demonstrated by patch clamp recordings. In vivo microdialysis performed in awake, freely moving mice reveal that mutant mice have basal striatal dopamine levels which are twice as high as those observed in wild‐type mice. Despite the fact that both wild‐type and α4 null mutant mice show a similar increase in dopamine release in response to intrastriatal KCl perfusion, a nicotine‐elicited increase in dopamine levels is not observed in mutant mice. Locomotor activity experiments show that there is no difference between wild‐type and mutant mice in basal activity in both habituated and non‐habituated environments. Interestingly, mutant mice sustain an increase in cocaine‐elicited locomotor activity longer than wild‐type mice. In addition, mutant mice recover from depressant locomotor activity in response to nicotine at a faster rate. Our results indicate that α4‐containing nAChRs exert a tonic control on striatal basal dopamine release, which is mediated by a heterogeneous population of nAChRs.
Cellular mechanisms of the trigeminally evoked startle response
Authors: Schmid Susanne , Simons Nadine S. , Schnitzler Hans‐Ulrich 
Published: May 2003

AbstractThe startle response is an important mammalian model for studying the cellular mechanisms of emotions and of learning. It consists of contractions of facial and skeletal muscles in response to sudden acoustic, tactile or vestibular stimuli. Whereas the acoustic startle pathway is well described, only a few recent studies have investigated the tactile startle pathway. It was proposed that there is a direct projection from the principal sensory nucleus to the central sensorimotor interface of the startle response, which is formed by the giant neurons in the caudal pontine reticular formation. We explored this projection in greater detail in vitro. Anterograde tracing in rat brain slices confirmed projections with large axon terminals from the ventral part of the principal sensory nucleus to the lateral caudal pontine reticular formation. Electrophysiological studies revealed a monosynaptic glutamatergic connection between principal sensory nucleus neurons and caudal pontine reticular formation giant neurons. The synapses displayed paired‐pulse facilitation at high‐frequency stimulation, and homosynaptic depression at 1 Hz stimulation. The latter form of plasticity is thought to underlie habituation of the startle response. Furthermore, postsynaptic currents in caudal pontine reticular formation giant neurons evoked by principal sensory nucleus neuron stimulation summed in a linear way with signals evoked by stimulation of auditory afferents. Synaptic plasticity and summation of synaptic currents correspond well with in vivo data previously published by other groups. We thus presume that these synapses mediate trigeminal input to the startle pathway.
Trace eyeblink conditioning in decerebrate guinea pigs
Authors: Kotani Sadaharu , Kawahara Shigenori , Kirino Yutaka 
Published: May 2003

AbstractWe investigated the trace eyeblink conditioning in decerebrate guinea pigs to elucidate the possible role of the cerebellum and brainstem in this hippocampus‐dependent task. A 350‐ms tone conditioned stimulus was paired with a 100‐ms periorbital shock unconditioned stimulus with a trace interval of either 0, 100, 250 or 500 ms. Decerebrate animals readily acquired the conditioned response with a trace interval of 0 or 100 ms. Even in the paradigm with a 500‐ms trace interval, which is known to depend critically on the hippocampus in all animal species examined, the decerebrate guinea pigs acquired the conditioned response, which had adaptive timing as well as in the other paradigms with a shorter trace interval. However, it took many more trials to learn in the 500‐ms trace paradigm than in the shorter trace interval paradigms, and the conditioned response expression was unstable from trial to trial. When decerebrate animals were conditioned step by step with a trace interval of 100, 250 and 500 ms, sequentially, they easily acquired the adaptive conditioned response to a 500‐ms trace interval. However, the frequency of conditioned responses decreased after the trace interval was shifted from 250 ms to 500 ms, which was not observed after the shift from 100 ms to 250 ms. These results suggest that the cerebellum and brainstem could maintain the ‘trace’ of the conditioned stimulus and associate it with the unconditioned stimulus even in the 500‐ms trace paradigm, but that the forebrain might be required for facilitating and stabilizing the association.
Expression of the ecto‐ATPase NTPDase2 in the germinal zones of the developing and adult rat brain
Authors: Braun Norbert , Sévigny Jean , Mishra Santosh K. , Robson Simon C. , Barth Stephan W. , Gerstberger Ruediger , Hammer Klaus , Zimmermann Herbert 
Published: May 2003

AbstractIn the adult nervous system, multipotential stem cells of the subventricular zone of the lateral ventricles generate neuron precursors (type‐A cells) that migrate via the rostral migratory stream to the olfactory bulb where they differentiate into neurons. The migrating neuroblasts are surrounded by a sheath of astrocytes (type‐B cells). Using immunostaining, in situ hybridization and enzyme histochemistry, we demonstrate that the ecto‐ATPase nucleoside triphosphate diphosphohydrolase 2 (NTPDase2) is expressed in the subventricular zone and the rostral migratory stream of the adult rat brain. This enzyme hydrolyses extracellular nucleoside triphosphates to the respective nucleoside diphosphates and is thought to directly modulate ATP receptor‐mediated cell communication. Double labelling for the astrocyte intermediate filament protein GFAP and the glial glutamate transporter GLAST identifies the NTPDase2‐positive cells as type‐B cells. During development the enzyme protein is first detected at E18, long before expression of the astrocyte marker GFAP. It gradually becomes expressed along the ventricular and subventricular zone of the brain, followed by complete retraction to the adult expression pattern at P21. NTPDase2 is transiently expressed in the outer molecular layer of the dentate gyrus and within the cerebellar white matter and is associated with select microvessels, tanycytes of the third ventricle, and subpial astrocytes of the adult brain. Our results suggest that NTPDase2 can serve as a novel marker for specifying subsets of cells during in vivo and in vitro studies of neural development and raise the possibility that ATP‐mediated signalling pathways play a role in neural development and differentiation.
Ionic currents underlying rhythmic bursting of ventral mossy cells in the developing mouse dentate gyrus
Authors: Jinno Shozo , Ishizuka Satoru , Kosaka Toshio 
Published: May 2003

AbstractThe electrophysiological properties of mossy cells were examined in developing mouse hippocampal slices using whole‐cell patch‐clamp techniques, with particular reference to the dorsoventral difference. Dorsal mossy cells exhibited a higher spontaneous excitatory postsynaptic potential (EPSP) frequency and larger maximal EPSP amplitude than ventral mossy cells. On the other hand, the blockade of synaptic inputs with glutamatergic and GABAergic antagonists disclosed a remarkable dorsoventral difference in the intrinsic activity: none (0/27) of the dorsal mossy cells showed intrinsic bursting, whereas the majority (35/47) of the ventral mossy cells exhibited intrinsic rhythmic bursting. To characterize the ionic currents underlying the rhythmic bursting of mossy cells, we used somatic voltage‐clamp recordings in the subthreshold voltage range. Ventral bursting cells possessed both hyperpolarization‐activated current (Ih) and persistent sodium current (INaP), whereas dorsal and ventral nonbursting cells possessed Ih but no INaP. Blockade of Ih with cesium did not affect the intrinsic bursting of ventral mossy cells. In contrast, the blockade of INaP with tetrodotoxin or phenytoin established a stable subthreshold membrane potential in ventral bursting cells. The current–voltage curve of ventral bursting cells showed a region of tetrodotoxin‐sensitive negative slope conductance between −55 mV and a spike threshold (≈ −45 mV). On the other hand, no subthreshold calcium conductances played a significant role in the intrinsic bursting of ventral mossy cells. These observations demonstrate the heterogeneous electrophysiological properties of hilar mossy cells, and suggest that the subthreshold INaP plays a major role in the intrinsic rhythmic bursting of ventral mossy cells.
The parieto‐collicular pathway: anatomical location and contribution to saccade generation
Authors: Gaymard B. , Lynch J. , Ploner C.J. , Condy C. , Rivaud‐Péchoux S. 
Published: May 2003

AbstractThe monkey lateral intraparietal area (LIP), involved in reflexive shifts of visual attention, has two main oculomotor outputs: towards frontal oculomotor areas and towards the superior colliculus. Recent studies suggest that these two outputs do not carry similar information. Direct LIP–collicular neurons would convey visual signals providing the oculomotor system with on‐line visuo‐spatial information. Parietal visuo‐spatial information regarding internal stimuli would access the brainstem oculomotor circuitry through a parieto‐frontal network. Consequently, an interruption of parieto‐tectal neurons should affect reflexive saccades towards unpredictable targets and have little or no effect on saccades towards predictable or memorised stimuli. In order to test this hypothesis in humans, we have determined in rhesus monkeys the location of LIP–tectal fibres in the region of the internal capsule, and found that these neurons travel in the most posterior region of the posterior limb of the internal capsule. We have then tested, in seven patients with a small lesion involving this region, several oculomotor paradigms designed to determine the influence of spatial predictability on saccade accuracy and the ability to withhold reflexive saccades. In all patients, saccade accuracy was affected in unpredictable conditions but was normal when target location could be predicted or memorised. Reflexive saccade inhibition was affected only in the three patients in whom the capsular lesion had the most anterior extent. These results therefore support in humans the hypothesis that parieto‐tectal neurons (i) transmit an on‐line signal that is used by the oculomotor system for reflexive saccade triggering, (ii) are not crucial for the computation of internally guided saccades and (iii) are not crucial for reflexive saccade inhibition.