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PubMedDate not supplied

Comparing fluctuations of synaptic responses mediated via AMPA and NMDA receptor channels--implications for synaptic plasticity.

Glutamate-releasing synapses are essential in fast neuronal signalling. Plasticity at these synapses is important for learning and memory as well as for the activity-dependent control of neuronal development. We have evaluated the trial-to-trial fluctuations of excitatory postsynaptic currents mediated by glutamate receptors of the AMPA and NMDA types in CA1 pyramidal cells. By using the whole cell patch clamp technique in brain slices from young rats, we have demonstrated that the relative variability of AMPA and NMDA receptor mediated responses, expressed as the coefficient of variation, is similar for these two types of responses [Brain Res. 800 (1998) 253-259]. The present paper summarizes and discusses these results in relation to current theories on hippocampal synaptic plasticity, especially with regard to the ideas of glutamate spillover and silent synapses. Our finding of a correspondence between AMPA and NMDA responses with respect to fluctuations is compatible with our previous finding of equal relative changes of the two during activity induced synaptic plasticity. However, the results argue against the glutamate spillover model according to which the effect of glutamate--and hence the induction of plasticity--may spread unspecifically between synapses. But how can silent synapses become functional if no spread of glutamate occurs and no initial signal is present to trigger the functionalization? Is it necessary that NMDA responses are present at these synapses, which are then silent merely with respect to AMPA receptors, or do other alternatives exist? Our discussion aims to elucidate these questions.

Animals↗
PubMed1996

Enhancement of mRNA expression of tissue-type plasminogen activator by L-threo-3,4-dihydroxyphenylserine in association with ocular dominance plasticity.

Tissue-type plasminogen activator (tPA) plays important roles in the regulation of synaptic plasticity in the hippocampus and cerebellum. We found that the expression of tPA mRNA in the visual cortex was increased significantly by the peripheral administration of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS; 100 mg/kg, i.p.), which we had previously shown to have a promotive effect on ocular dominance (OD) plasticity. When plasminogen activator inhibitor-1 (PAI-1; 100 muM in an osmotic minipump) was infused into the kitten visual cortex, OD plasticity was suppressed; i.e. a significantly large number of binocular cells was recorded in the PAI-1 infused cortex following monocular deprivation. These results, therefore, suggest that the PA system is involved in the promotive effect of L-threo-DOPS in OD plasticity.

Animals↗
PubMed2001

Infusion of nerve growth factor (NGF) into kitten visual cortex increases immunoreactivity for NGF, NGF receptors, and choline acetyltransferase in basal forebrain without affecting ocular dominance plasticity or column development.

Intracerebroventricular or intracortical administration of nerve growth factor (NGF) has been shown to block or attenuate visual cortical plasticity in the rat. In cats and ferrets, the effects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF affects ocular dominance column formation or the plasticity produced by monocular deprivation in cats at the height of the critical period, we infused recombinant human NGF into the primary visual cortex of kittens using an implanted cannula minipump. NGF had no effect on the normal developmental segregation of geniculocortical afferents into ocular dominance columns as determined both physiologically and anatomically. The plasticity of binocular visual cortical responses induced by monocular deprivation was also normal in regions of immunohistochemically detectable NGF infusion, as measured using intrinsic signal optical imaging and single-unit electrophysiology. Immunohistochemical analysis of the basal forebrain regions of the same animals demonstrated that the NGF infused into cortex was biologically active, producing an increase in the number of NGF-, TrkA-, p75(NTR)-, and choline acetyltransferase-positive neurons in basal forebrain nuclei in the hemisphere ipsilateral to the NGF minipump compared to the contralateral basal forebrain neurons. We conclude that NGF delivered locally to axon terminals of cholinergic basal forebrain neurons resulted in increases in protein expression at the cell body through retrograde signaling.

Animals↗
PubMed2002

Testing the role of the cell-surface molecule Thy-1 in regeneration and plasticity of connectivity in the CNS.

Thy-1 is a cell-surface signaling molecule of the Ig superfamily implicated in the regulation of neurite outgrowth, synaptic function and plasticity. There is, however, no consensus as to its precise function in the nervous system, and it remains unclear or untested as to what its role is in the development, maintenance and plasticity of neuronal connectivity in the intact brain and whether it is essential for any of the purported functions which have been attributed to it based largely on in vitro bioassays. Here, we have engineered transgenic mice with a targeted deletion of the Thy-1 gene and, after characterizing the development of their corticospinal and thalamocortical pathways, subjected them at adulthood to paradigms of axonal regeneration and plasticity which can be readily induced during development. Quantitative analyses of the brains and spinal cords of adult null mutants showed normal cellular organization, normal anatomical features of the corticospinal and thalamocortical pathways, and basic neurophysiological properties of thalamocortical synaptic transmission which were quantitatively indistinguishable from wild-type mice. Despite the absence of Thy-1, corticospinal axons in adult mutants failed to exhibit overt regeneration following spinal cord lesion; likewise, the terminal arbors of ventrobasal thalamocortical axons also failed to reorganize in adult barrel cortex in response to whisker cautery, although they did so during a developmental critical period identical to that displayed by wild-type mice.Taken together, these results suggest that Thy-1 is not essential for the normal development and maintenance of major axon pathways and functional synaptic connections, nor would it appear to be critically important for inhibiting or promoting axonal growth, regeneration and plasticity in the developing and mature CNS.

Afferent Pathways↗
PubMed2002

Neuromodulatory transmitter systems in the cortex and their role in cortical plasticity.

Cortical neuromodulatory transmitter systems refer to those classical neurotransmitters such as acetylcholine and monoamines, which share a number of common features. For instance, their centers are located in subcortical regions and send long projection axons to innervate the cortex. The same transmitter can either excite or inhibit cortical neurons depending on the composition of postsynaptic transmitter receptor subtypes. The overall functions of these transmitters are believed to serve as chemical bases of arousal, attention and motivation. The anatomy and physiology of neuromodulatory transmitter systems and their innervations in the cerebral cortex have been well characterized. In addition, ample evidence is available indicating that neuromodulatory transmitters also play roles in development and plasticity of the cortex. In this article, the anatomical organization and physiological function of each of the following neuromodulatory transmitters, acetylcholine, noradrenaline, serotonin, dopamine, and histamine, in the cortex will be described. The involvement of these transmitters in cortical plasticity will then be discussed. Available data suggest that neuromodulatory transmitters can modulate the excitability of cortical neurons, enhance the signal-to-noise ratio of cortical responses, and modify the threshold for activity-dependent synaptic modifications. Synaptic transmissions of these neuromodulatory transmitters are mediated via numerous subtype receptors, which are linked to multiple signal transduction mechanisms. Among the neuromodulatory transmitter receptor subtypes, cholinergic M(1), noradrenergic beta(1) and serotonergic 5-HT(2C) receptors appear to be more important than other receptor subtypes for cortical plasticity. In general, the contribution of neuromodulatory transmitter systems to cortical plasticity may be made through a facilitation of NMDA receptor-gated processes.

Acetylcholine↗
PubMed2002

The influence of developmental period of aluminum exposure on synaptic plasticity in the adult rat dentate gyrus in vivo.

Previous studies from our group have demonstrated that chronic aluminum exposure from parturition throughout life impairs both long-term potentiation (LTP) and long-term depression (LTD) of the excitatory postsynaptic potential (EPSP) slope and reduces the population spike (PS) amplitude in the rat dentate gyrus in vivo. The present study sought to extend these findings by evaluating the developmental periods critical for aluminum-induced impairment of synaptic plasticity. Rats were exposed to aluminum (gestational, lactational and postlactational) through drinking 0.3% aluminum chloride in water over different developmental intervals: (1) prenatal exposure; (2) beginning from birth and terminating at weaning; (3) beginning at weaning throughout life; (4) beginning at birth and continuing throughout life. As adults (postnatal day 80-100), field potentials were measured in the dentate gyrus of hippocampus in response to stimulation applied to the lateral perforant path. The results showed: (1) Prenatal aluminum exposure had no effect on the magnitude of LTP as measured by the EPSP slope and LTD as measured for the PS amplitude, while it had a small effect on the magnitude of LTP as measured for the PS amplitude and LTD as measured by the EPSP slope. (2) Lactational, postlactational and throughout life exposure to aluminum impaired both LTP and LTD of the EPSP slope and PS amplitude, except that LTD of PS amplitude was not significantly changed in animals postlactationally exposed. (3) Aluminum exposure from parturition throughout life caused the greatest impairment of the range of synaptic plasticity, while prenatal aluminum exposure caused the least. From these results we conclude that the lactational period was the most susceptible to aluminum-induced impairment of synaptic plasticity and that chronic aluminum exposure from parturition throughout life is extremely disruptive to synaptic plasticity and should be avoided.

Aluminum↗
PubMed1999

A new form of synaptic plasticity is transiently expressed in the developing rat visual cortex: a modulatory role for visual experience and brain-derived neurotrophic factor.

Synaptic plasticity has been implicated in the mechanisms contributing to the shaping of the cortical circuits responsible for the transmission of the visual input in the rat primary visual cortex. However, the degree of plasticity of the thalamocortical synapse may change during development, perhaps reflecting the degree of stabilization of the circuitry subserving it. We have chosen the ability of this synapse to be first depressed and then potentiated as a specific indicator of its plasticity. In this study we have investigated how this parameter changes during development and the factors controlling it. Extracellular field potentials in cortical layers 2/3 were evoked by stimulation of the white matter in rat primary visual cortex slices prepared at different postnatal ages. Low-frequency stimulation (900 pulses at 1 Hz) of the white matter was used to induce long-term depression of field potential amplitude, whereas long-term potentiation was evoked by high-frequency stimulation consisting of three trains at 100 Hz. We provide evidence that while it is possible to potentiate previously depressed synapses soon after eye opening (postnatal day 17) this synaptic characteristic decreases rapidly thereafter. The decrease in this form of cortical synaptic plasticity closely matches the stabilization of the cortical circuitry towards an adult pattern of connectivity and function. Depressed cortical synapses cannot be potentiated in normal rats at postnatal 23, but they can be potentiated in rats reared in the dark from postnatal days 17 to 29. Moreover, application of brain-derived neurotrophic factor, known to be expressed in an activity-dependent manner, was able to restore the ability of synapses to be potentiated after long-term depression, thus indicating its important modulatory role in brain development.

Animals↗
PubMed2000

Surprises from Drosophila: genetic mechanisms of synaptic development and plasticity.

Drosophila are excellent models for the study of synaptic development and plasticity, thanks to the availability and applicability of a wide variety of powerful molecular, genetic, and cell-biology techniques. Three decades of study have led to an intimate understanding of the sequence of events leading to a functional and plastic synapse, yet many of the molecular mechanisms underlying these events are still poorly understood. Here, we provide a review of synaptogenesis at the Drosophila glutamatergic neuromuscular junction (NMJ). Next, we discuss the role of two proteins that forward genetic screens in Drosophila have revealed to play crucial-and completely unexpected-roles in NMJ development and plasticity: the origin of replication complex protein Latheo, and the enzyme glutamate decarboxylase. The requirement for these proteins at the NMJ highlights the fact that synaptic development and plasticity involves intense inter- and intracellular signaling about which we know almost nothing.

Animals↗
PubMed2003

Prenatal morphine exposure suppresses mineralocorticoid receptor-dependent basal synaptic transmission and synaptic plasticity in the lateral perforant path in adult male rats.

The effects of prenatal morphine exposure (E11-18) on mineralocorticoid receptor (MR) modulation of synaptic plasticity were investigated in the lateral perforant path (LPP)-dentate gyrus granule cell synaptic system. Hippocampal slices were prepared from adult, prenatally saline- or morphine-exposed male rats. One hour prior to decapitation, some adult male rats were injected subcutaneously with saline or the MR antagonist, canrenoic acid (50 mg/kg). LPP was stimulated with high-frequency (2x100 Hz/0.5 s) and short-term plasticity (STP) and long-term potentiation (LTP) were evaluated at 5 and 30 min poststimulation, respectively. Prenatally saline-exposed male rats injected with saline 1 h prior to decapitation showed significantly higher levels of baseline, STP, and LTP than prenatally saline-exposed, canrenoic acid-treated males. In contrast, prenatally morphine-exposed male rats regardless of saline or canrenoic acid injection 1 h prior to decapitation were comparable in their baseline, STP, and LTP activities. Thus, the results demonstrate that canrenoic acid decreases the efficacy of the basal synaptic transmission in the LPP as well as suppresses synaptic plasticity in saline-exposed males. However, in adult morphine-exposed male rats, canrenoic acid has no other or further effects than a saline treatment suggesting that prenatal morphine exposure suppresses MR-dependent basal synaptic transmission as well as synaptic plasticity.

Animals↗
PubMed2001

Drug release from and mechanical properties of press-coated tablets with hydroxypropylmethylcellulose acetate succinate and plasticizers in the outer shell.

Dissolution profiles of diltiazem hydrochloride (DIL) contained in core tablets from press-coated (PC) tablets with hydroxypropylmethylcellulose acetate succinate (HPMCAS) and plasticizers-adsorbent in the outer shell were investigated. Although, on the addition of triethyl citrate (TEC), triacetin (TA), and acetyltriethy citrate (ATEC) as plasticizers, DIL release was suppressed completely in first fluid (pH 1.2) for 10 h, it was not suppressed in HPMCAS on the addition of dibutyl sebacate (DBS) and acetylated monoglyceride. On the other hand, DIL in second fluid (pH 6.8) was released rapidly after a lag time in all the PC tablets. Water-soluble plasticizers such as TEC, TA, and ATEC showed greater compatibility to HPMCAS, and the results were consistent with suppression of DIL release in first fluid. Furthermore, as to PC tablets with HPMCAS and TEC-adsorbent, the DIL release in second fluid did not change after pretreatment in first fluid by the paddle-beads methods. To evaluate the resistance of the outer shell against such a mechanical impact, tablets with HPMCAS, HPMCAS and TEC- or DBS-adsorbent (H, HT, or HD tablets, respectively) were prepared. In compressive load-strain curves after immersion in first fluid, wet crushing strength was lower in the order of HT > H > HD tablets. Also, the curves of HT tablets at 3 and 21 h after immersion were quite different from those of other tablets, and it was hard to find crushing points. These results suggested that the resistance of the outer shell was due to plastic deformation properties involving some interaction between HPMCAS and TEC.

Cardiovascular Agents↗
PubMed2003

Enhanced stability of rubbery amylose-rich maize starch films plasticized with a combination of sorbitol and glycerol.

Well known aging problems with rubbery starch films are the migration of plasticizer and increased crystallinity leading to embrittlement. The effects of a combination of sorbitol and glycerol used as plasticizers on mechanical, moisture permeability and solid-state properties of rubbery amylose maize starch (Hylon VII) films were studied. The films were prepared by casting and were exposed to conditions of 25 degrees C/60% relative humidity (RH) and 40 degrees C/75% RH for 9 months. The starch films plasticized with a combination of sorbitol and glycerol (1:1) at equal amount to the polymer weight, were shown to be the most stable alternative of the studied films during the 9 months storage period. The water vapor transmission (WVTR) of the films did not change during the period of storage and neither did the elongation at break, but the tensile strength increased. X-ray diffraction (XRD) results showed that during storage no crystallization had occurred. The combination of sorbitol and glycerol prevented the migration of the plasticizer molecules out of the film.

Amylose↗
PubMed2000

Reversed phase HPLC of Met58 oxidized rhIL-11: oxidation enhanced by plastic tubes.

The hydrophobicity of human recombinant interleukin 11 (rhIL-11) with an oxidized Met58 residue is nearly identical to the hydrophobicity of native rhIL-11. Consequently, separation of these species using standard gradient elution or isocratic elution is very difficult. Using an optimized, shallow gradient RP-HPLC method. Met58 oxidized rhIL-11 could be separated sufficiently from native rhIL-11. The identity of the oxidized form detected with this method was confirmed by peptide mapping with trypsin and endoproteinase Asp-N, N-terminal sequencing and mass spectrometric analysis. This method was employed to determine the effect of disposable laboratory plastic tubes for the oxidation. The amounts of Met58 oxidized rhIL-11 were increased when rhIL-11 samples were stored in plastic tubes at 37 degrees C in the dark. Samples stored in polypropylene tubes were oxidized much more than samples stored in polystyrene tubes. Additionally, the oxidation was greatly enhanced when samples were stored in polypropylene tubes exposed to light before rhIL-11 sample storage. The extent of the oxidation was also affected by the sources of polypropylene tubes. A maximum increase in Met58 oxidized rhIL-11 was more than 30% when samples were stored at 37 degrees C for 14 days in polypropylene tubes exposed to a daylight fluorescent lamp for 25 days. Consequently, these results indicate that attention should be paid for selection of suitable plastic tubes used for storage of protein samples, and for protection of the plastic tubes themselves from extended exposure to light while in storage.

Amino Acid Sequence↗
PubMed2002

Neonatal electrolytic lesions of the basal forebrain stunt plasticity in mouse barrel field cortex.

Previous studies have shown that neonatal electrolytic lesions of basal forebrain cholinergic projections in mice lead to a transient cholinergic depletion of neocortex and to permanent alterations in cortical cytoarchitecture and in cognitive performance. The present study examines whether neonatal electrolytic lesions of the basal forebrain modify neocortical plasticity. Using cytochrome oxidase histochemistry, we compared cross-sectional areas of individual barrels in the barrel field of four groups of postnatal day 8 (P8) old mice that on P1 received either (1) right electrolytic lesions of the basal forebrain, (2) left C row 1-4 whisker follicle ablations, (3) combined lesion treatments or (4) ice anesthesia only. The size of barrels in basal forebrain lesioned animals was not significantly different from controls. However, the plastic response to whisker removal was compromised in basal forebrain lesioned animals. An index of plasticity, the ratio of row D/row C areas, was reduced significantly in the combined nBM lesioned/follicle ablation group. Compared to whisker-lesioned mice, the expansion in rows B and D and the shrinkage in the lesioned row C area were diminished in the combined treatment group. The present findings correspond to those from a study of rats injected with a cholinergic immunotoxin [Cereb. Cortex 8 (1998) 63]. These results suggest that cholinergic inputs play a role in regulating plasticity as well as in the morphogenesis of mouse sensory-motor cortex.

Acetylcholine↗
PubMed1998

Appearance and maturation of synaptic plasticity during juvenile development in Aplysia.

In the present study we examine the developmental appearance and maturation of synaptic plasticity at the A-B neuron synapse in the cerebral ganglion of Aplysia. In the CNS of juvenile Aplysia 120 days after hatching, the excitatory synaptic connection between A and B cluster neurons is essentially the same as in the adult cerebral ganglion. No differences were observed between the amplitudes of the initial EPSPs in the cerebral ganglia of juveniles and adults. One form of plasticity, low frequency synaptic depression, is also present in juveniles. Another form of activity-dependent plasticity, slow developing potentiation (SDP) appears and matures during the late juvenile stage of development. At 120 days posthatching SDP, evoked by tetanic stimulation, is largely absent. Potentiated EPSPs have a significantly smaller amplitude than in adults. Over the next 80 days SDP undergoes a maturation process. The peak potentiation increases linearly with age from 135 +/- 12% at 125 days to 275 +/- 20% at 188 days. The duration of the potentiation, as measured by the time-constant its decay, also increases linearly from 12.7 +/- 3.4 min to 27.9 +/- 3.9 min. From 120-170 days, < 50% of the A neurons tested exhibited SDP. After 170 days, > 85% exhibited SDP. Changes in the rising phase of the A neuron action potential have been implicated in mediating SDP. At 120 days, the A neuron action potential has a significantly shorter duration (half-width) than in the adult. Between 120 and 200 days, both the duration and rise-time of the A neuron action potential increase linearly. These results confirm findings by other investigators, that different forms of synaptic plasticity develop independently, with depression appearing before potentiation.

Action Potentials↗
PubMed2001

Stimulus timing-dependent plasticity in cortical processing of orientation.

The relative timing of presynaptic and postsynaptic spikes plays a critical role in activity-induced synaptic modification. Here we examined whether plasticity of orientation selectivity in the visual cortex depends on stimulus timing. Repetitive pairing of visual stimuli at two orientations induced a shift in orientation tuning of cat cortical neurons, with the direction of the shift depending on the temporal order of the pair. Induction of a significant shift required that the interval between the pair fall within +/-40 ms, reminiscent of the temporal window for spike timing-dependent synaptic plasticity. Mirroring the plasticity found in cat visual cortex, similar conditioning also induced a shift in perceived orientation by human subjects, further suggesting functional relevance of this phenomenon. Thus, relative timing of visual stimuli can play a critical role in dynamic modulation of adult cortical function, perhaps through spike timing-dependent synaptic plasticity.

Animals↗
PubMed2001

Barrel cortex critical period plasticity is independent of changes in NMDA receptor subunit composition.

The regulation of NMDA receptor (NMDAR) subunit composition and expression during development is thought to control the process of thalamocortical afferent innervation, segregation, and plasticity. Thalamocortical synaptic plasticity in the mouse is dependent on NMDARs containing the NR2B subunit, which are the dominant form during the "critical period" window for plasticity. Near the end of the critical period there is a gradual increase in the contribution of NR2A subunits that happens in parallel to changes in NMDAR-mediated current kinetics. However, no extension of the critical period occurs in NR2A knockout mice, despite the fact that NMDA subunit composition and current kinetics remain immature past the end of the critical period. These data suggest that regulation of NMDAR subunit composition is not essential for closing the critical period plasticity window in mouse somatosensory barrel cortex.

Animals↗
PubMed2001

Rate, timing, and cooperativity jointly determine cortical synaptic plasticity.

Cortical long-term plasticity depends on firing rate, spike timing, and cooperativity among inputs, but how these factors interact during realistic patterns of activity is unknown. Here we monitored plasticity while systematically varying the rate, spike timing, and number of coincident afferents. These experiments demonstrate a novel form of cooperativity operating even when postsynaptic firing is evoked by current injection, and reveal a complex dependence of LTP and LTD on rate and timing. Based on these data, we constructed and tested three quantitative models of cortical plasticity. One of these models, in which spike-timing relationships causing LTP "win" out over those favoring LTD, closely fits the data and accurately predicts the build-up of plasticity during random firing. This provides a quantitative framework for predicting the impact of in vivo firing patterns on synaptic strength.

Action Potentials↗
PubMed2002

Cholinergic modulation of experience-dependent plasticity in human auditory cortex.

The factors that influence experience-dependent plasticity in the human brain are unknown. We used event-related functional magnetic resonance imaging (fMRI) and a pharmacological manipulation to measure cholinergic modulation of experience-dependent plasticity in human auditory cortex. In a differential aversive conditioning paradigm, subjects were presented with high (1600 Hz) and low tones (400 Hz), one of which was conditioned by pairing with an electrical shock. Prior to presentation, subjects were given either a placebo or an anticholinergic drug (0.4 mg iv scopolamine). Experience-dependent plasticity, expressed as a conditioning-specific enhanced BOLD response, was evident in auditory cortex in the placebo group, but not with scopolamine. This study provides in vivo evidence that experience-dependent plasticity, evident in hemodynamic changes in human auditory cortex, is modulated by acetylcholine.

Acetylcholine↗