The presence of Matthew effects in Dutch primary education, development of language skills over a six-year period.

Using a nationally representative sample of 5,150 Dutch students who have been followed over a 6-year period, the presence of the Matthew effect was investigated for general language skills. The analyses do not reveal unmistakable evidence for the supposition that the rich get richer and the poor poorer. On the contrary, in schools with low starting levels students make more progress than in schools with higher starting levels.

Evaluation of a new mental health liaison role in a rural health centre in Rocky Mountain House, Alberta: a Canadian story.

This paper describes the evaluation of a mental health liaison (MHL) role in a rural community in Alberta, Canada. The role provides advocacy, education, indirect and direct client intervention, and follow up. It was developed to eliminate gaps in mental health care and build collaborative cultures between the local hospital, physicians' offices, mental health clinics, and community agencies.

Induction of activin A is essential for the neuroprotective action of basic fibroblast growth factor in vivo.

Exogenous application of neurotrophic growth factors has emerged as a new and particularly promising approach not only to promote functional recovery after acute brain injury but also to protect neurons against the immediate effect of the injury. Among the various growth factors and cytokines studied so far, the neuroprotective and neurotrophic profile of basic fibroblast growth factor (bFGF) is the best documented. Using an animal model of acute excitotoxic brain injury, we report here that the neuroprotective action of bFGF, which is now being tested in stroke patients, depends on the induction of activin A, a member of the transforming growth factor-beta superfamily.

Local disinhibition of neocortical neuronal circuits causes augmentation of glutamatergic and GABAergic synaptic transmission in the rat neostriatum in vitro.

Intra- and extracellular recordings were performed to investigate the influence of local disinhibition of neocortical circuits on corticostriatal synaptic transmission. In rat brain slices with preserved corticostriatal connections, electrical stimulation of the neocortex elicited composed postsynaptic responses in neostriatal neurons consisting of glutamatergic excitatory postsynaptic potentials (EPSPs) and weakly expressed GABAA receptor-mediated inhibitory postsynaptic potentials (IPSPs). Following local application of the GABAA receptor antagonist bicuculline to the neocortex, neocortical neurons responded to intracortical stimulation with transient paroxysmal depolarizations.

Postnatal development of calretinin- and parvalbumin-positive interneurons in the rat neostriatum: an immunohistochemical study.

On the basis of cytochemical and morphologic differences, two classes of gamma-aminobutyric acidergic (GABAergic) interneurons expressing calcium-binding proteins have been identified in the striatum of adult animals: neurons expressing either parvalbumin (PV) or calretinin (CR). The function of these calcium-binding proteins is not clear, however, they are associated with distinct classes of inhibitory interneurons within the adult neostriatum. By using immunocytochemical techniques, we analyzed the postnatal maturation and the spatiotemporal distribution of PV- and CR-positive neurons in the rat neostriatum compared with a third class of interneurons characterized by the expression of the acetylcholine-synthesizing enzyme, choline acetyltransferase (ChAT).

Spread of excitation in chronically lesioned mouse hippocampus determined by laser scanning microscopy.

Fast optical recordings by means of laser scanning microscopy in conjunction with a voltage-sensitive dye (RH 414) were performed to monitor the spatio-temporal spread of neuronal activity in CA3/CA4-lesioned C57BL6 mouse hippocampal slices prepared approximately 3 months after intracerebroventricular kainic acid (KA) injection. The aim of our study was to assess the effects of a circumscribed neuronal loss on the propagation of electrical activity along the trisynaptic hippocampal circuit. Both in physiological bathing solution and in bicuculline (10 microM), hilar stimulation failed to activate the downstream pathway, so that, under these conditions, the chronically disinhibited CA1 region appeared to be effectively isolated from burst activity arising upstream; however, epileptiform discharges evoked in zero Mg2+ solution were reliably transmitted from the dentate gyrus to the CA1 region.

The intracellular tracer Neurobiotin alters electrophysiological properties of rat neostriatal neurons.

During whole-cell recordings from rat neostriatal neurons with Neurobiotin-filled patch-clamp electrodes, we observed markedly prolonged action potentials. Similar long-lasting action potentials were not detected when the tracer was omitted from the pipette solution. Resting membrane potential and input resistance remained unchanged in the presence of the tracer.

Changes in quantal size distributions upon experimental variations in the probability of release at striatal inhibitory synapses.

Postsynaptic inhibitory gamma-aminobutyric acid-A (GABAA)-receptor-mediated current responses were measured using simultaneous pre- and postsynaptic whole cell recordings in primary cell cultures of rat striatum. Substitution of Sr2+ for extracellular Ca2+ strongly desynchronized the inhibitory postsynaptic currents (IPSCs), resulting in a succession of asynchronous IPSCs (asIPSCs). The rise times and decay time constants of individual evoked asIPSCs were not significantly different from those of miniature IPSCs that are the result of spontaneous vesicular release of GABA.

Spatial pattern of evoked synaptic excitation in the mouse neostriatum in vitro.

The spatial distribution of stimulus-evoked excitation in the mouse neostriatum was investigated in vitro by using voltage-sensitive dyes and an optical multi-site recording system (laser scanning microscopy). The scanning area (880 x 830 microns) was positioned in the center of coronal neostriatal slices and records were taken simultaneously from up to 20 detection sites. Stimulus-induced optical signals were blocked by tetrodotoxin (TTX) and disappeared following removal of Ca2+ from the extracellular medium.

Chronic clozapine versus chronic haloperidol treatment: differential effects on electrically evoked dopamine efflux in the rat caudate putamen, but not in the nucleus accumbens.

Fast cyclic voltammetry at carbon-fibre micro-electrodes was used to investigate the effects of chronic clozapine or haloperidol administration on electrically evoked dopamine efflux in the nucleus accumbens and caudate putamen of the anaesthetized rat. Stimulation trains were delivered to the median forebrain bundle (60 pulses, 350 microns duration) every 5 min, and the evoked dopamine efflux measured as a function of a) the applied stimulus intensity (range 0.2 mA-1.

Strong induction of activin expression after hippocampal lesion.

We studied the temporal and spatial mRNA expression pattern of activin/inhibin beta A, beta B and alpha subunits after unilateral kainic acid lesions of the hippocampal CA3 region. We found a strikingly increased expression of beta A mRNA in the ipsilateral hippocampus 6-24 h after injury. By contrast, the beta B and alpha mRNAs were expressed at equally low levels in normal and injured hippocampi, suggesting that the beta A transcripts give rise to activin A, but not to activin AB or inhibin.

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced dopaminergic denervation potentiates gabaergic inhibition in the mouse neostriatum in vitro.

Using the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease, we investigated the long-term effects of dopaminergic denervation on synaptic transmission in an in vitro slice preparation of the mouse neostriatum. In control mice, electrical stimulation elicited an antidromic potential (N1) followed by a synaptically mediated field potential (N2). In many slices, a third component (N3) was observed.

Dopamine autoreceptor sensitivity is unchanged in rat nucleus accumbens after chronic haloperidol treatment: an in vivo and in vitro voltammetric study.

Fast cyclic voltammetry was used to assess the effects of chronic oral haloperidol treatment (0.7 mg/kg/day for 21 days) on the sensitivity of dopamine autoreceptors in the rat nucleus accumbens both in vivo and in vitro. Evoked dopamine overflow was significantly reduced after chronic haloperidol treatment, but the sensitivity of dopamine overflow to sulpiride, an antagonist at release-inhibiting dopamine autoreceptors, and quinpirole, an agonist at these receptors, was unchanged.

Delta, mu and kappa opioid receptor agonists inhibit dopamine overflow in rat neostriatal slices.

The actions of opioid receptor agonists on stimulus evoked dopamine overflow in rat neostriatal slices were investigated using fast cyclic voltammetry. Activation of delta and mu receptors reversibly depressed striatal dopamine efflux induced by intrastriatal stimulation. The inhibitory effect of DADLE (D-Ala2, D-Leu5-enkephalin, delta/mu agonist), DPDPE (D-Pen2,5-enkephalin, delta selective) and DALDA (D-Arg2, Lys4-dermorphin-(1,4)-amide, mu selective), respectively, were concentration dependent and could be blocked by application of receptor subtype selective antagonists.

Stimulus-evoked dopamine overflow in the rat nucleus accumbens is decreased following chronic haloperidol administration: an in vivo voltammetric study.

Fast cyclic voltammetry was used to investigate the effects of chronic haloperidol (HAL) treatment on electrically evoked dopamine (DA) overflow in the nucleus accumbens of the anaesthetized rat in vivo. Evoked DA efflux was significantly reduced in rats treated with 1.0 mg/kg per day HAL for 21 days.

Spread of epileptiform activity in the immature rat neocortex studied with voltage-sensitive dyes and laser scanning microscopy.

1. Adult rats and rats with a postnatal age of 3-29 days (PN 3-29) were used for the preparation of in vitro slices of the frontal neocortex. Epileptiform activity was induced by bath application of the gamma-aminobutyric acid-A (GABAA) receptor antagonists bicuculline or picrotoxin.

The NMDA receptor antagonist CPP suppresses long-term potentiation in the rat hippocampal-accumbens pathway in vivo.

Excitation of afferent fibres originating in the ventral subiculum of the hippocampus through stimulation of the fimbria elicits field potentials in the nucleus accumbens. When recorded in the dorsomedial aspect of the nucleus accumbens, the evoked field responses consisted of an early, negative-going component (N1) with a peak latency of 8-10 ms, followed by a second negative-going peak (N2) with a latency of 22-24 ms. The N1 response reflects monosynaptic activation of nucleus accumbens neurons; the N2 component appears to be polysynaptic in origin.

Disinhibition of hippocampal CA3 neurons induced by suppression of an adenosine A1 receptor-mediated inhibitory tonus: pre- and postsynaptic components.

Intracellular recordings were performed on hippocampal CA3 neurons in vitro to investigate the inhibitory tonus generated by endogenously produced adenosine in this brain region. Bath application of the highly selective adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine at concentrations up to 100 nM induced both spontaneous and stimulus-evoked epileptiform burst discharges. Once induced, the 1,3-dipropyl-8-cyclopentylxanthine-evoked epileptiform activity was apparently irreversible even after prolonged superfusion with drug-free solution.

Differential effects of dentate kindling on working and reference spatial memory in the rat.

An 8-arm radial maze was used to examine the effects of dentate kindling on the performance of a task which requires both working (short-term) and reference (long-term) memory. During the 4-week post-operative training period, control and experimental rats performed both components of the task equally well. Performance of the reference memory component, but not the working memory component of the task was significantly impaired during kindling stimulation.

Cholinergic modulation of synaptic inhibition in the guinea pig hippocampus in vitro: excitation of GABAergic interneurons and inhibition of GABA-release.

1. The effect of cholinergic receptor activation on gamma-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission was investigated in voltage-clamped CA1 pyramidal neurons (HPNs) in the guinea pig hippocampal slice preparation. 2.

Do NMDA receptor antagonists protect against MPTP-toxicity? Biochemical and immunocytochemical analyses in black mice.

We investigated whether excitatory amino acids acting at the N-methyl-D-aspartate (NMDA) subtype of the L-glutamate receptor contribute to the dopaminergic neurotoxicity induced by systemic administration of the Parkinson's syndrome-inducing toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57Bl/6 mice. The MPTP-regimen chosen (30-40 mg/kg body weight subcutaneously) resulted a 60-70% depletion of striatal dopamine (DA) content and a 20% reduction of tyrosine hydroxylase immunoreactive (TH-IR) cells in the substantia nigra pars compacta 20 days after administration. Repeated systemic coadministration of the non-competitive NMDA receptor antagonist MK-801 or of the novel competitive NMDA receptor antagonist CGP 40116 did not protect against MPTP-induced striatal DA depletion 20 days after toxin administration.

Lesions of the medial septum which produce deficits in working/spatial memory do not impair long-term potentiation in the CA3 region of the rat hippocampus in vivo.

The effects of removing the septohippocampal pathway on the ability to induce long-term potentiation (LTP) in the CA3 region of the hippocampus was examined in vivo in rats. The septal input to the hippocampus was destroyed by electrolytic lesioning of the medial septum (MS). Prior to electrophysiological investigation, working/spatial memory of lesioned and control rats was tested using an 8-arm radial maze task.

Cryopreservation, survival and function of intrastriatal fetal mesencephalic grafts in a rat model of Parkinson's disease.

In the present study we quantitatively assessed to what extent freeze-storage at liquid nitrogen temperature influences the survival and function of fetal mesencephalic grafts in the dopamine-depleted rat striatum. Ventral mesencephalic (VM) tissue was dissected from rat fetuses and stored overnight in a preservative medium at 4 degrees C (hibernation). It was grafted intrastriatally either as a fresh cell suspension or was frozen as tissue fragments or as a cell suspension after stepwise incubation in ascending concentrations of dimethyl-sulphoxide.

Postsynaptic inhibition by adenosine in hippocampal CA3 neurons: Co(2+)-sensitive activation of an inwardly rectifying K+ conductance.

The properties of the current underlying the membrane hyperpolarization evoked by adenosine (50-100 microM) were investigated in hippocampal CA3 neurons in vitro using current-clamp and single-electrode voltage-clamp techniques. In voltage-clamp measurements, the adenosine-induced current (IAdo) was outward at rest and reversed at membrane potentials close to the equilibrium potential of K+ (EK), indicating that IAdo was carried by K+ ions. Determination of IAdo at several membrane potentials revealed a nonlinear current/voltage (I/V) relationship of the current displaying inward rectification in the hyperpolarizing direction.

Adenosinergic inhibition in hippocampus is mediated by adenosine A1 receptors very similar to those of peripheral tissues.

The amplitude of the orthodromically evoked population spike (PS) of CA1 neurons was used to investigate quantitatively adenosine receptor antagonism in guinea pig hippocampal slices. Increasing concentrations of the highly selective adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 3-100 nM) produced parallel, rightward shifts of the dose-response curve for the N6-cyclopentyladenosine (CPA)-induced decrease in PS amplitude. Schild plot analyses of the respective antagonism data obtained in both the presence and virtual absence of endogenous adenosine yielded apparent dissociation constants (KD) of DPCPX at the hippocampal A1 receptor of 3.