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Environmental alteration and phenotypic regulation of Candida albicans adhesion to plastic.

The adhesion of Candida albicans to plastic was examined after growth in two chemically defined media, Lee-Buckley-Campbell (LBC) and yeast nitrogen base (YNB), by binding isotherms, Langmuir isotherms, and Scatchard plots, and the number of binding sites (N) and the affinity constants (K) were calculated. K and N were twofold and fourfold higher, respectively, after growth in LBC compared with that in YNB. A comparison of adhesion in different assay solutions gave similar results, with the solution given to dehydrated patients (5% glucose in 0.45% NaCl [D5.45]) allowing for the highest K and the largest N. Scatchard curves for both LBC- and YNB-grown cells had negative slopes, which is supportive evidence for the view that negative cooperativity is involved in the binding process. Additional experiments to examine the role of cell surface hydrophobicity in adhesion to plastic were conducted with the white and opaque phenotypes of C. albicans. There was no significant difference in the adhesion of these phenotypes to plastic, although the opaque phenotype was significantly more hydrophobic. Adhesion, but not cell surface hydrophobicity, of both phenotypes was significantly greater in D5.45. Moreover, relatively hydrophilic mycelial forms of C. albicans were found to attach only when D5.45 was used as the assay medium and, in contrast to yeast-phase cells, were insensitive to reduced adhesion by nonionic detergents. These results suggest that the adhesion of C. albicans to plastic is regulated by environmental circumstances and the phenotypic state of the organism.

Adhesiveness↗

Controlled clinical comparison of plastic and glass bottles of BacT/ALERT FA medium for culturing organisms from blood of adult patients.

A new, clear-plastic nonvented aerobic FA bottle, designed to prevent breakage, has been developed for the BacT/ALERT blood culture system. We assessed the new plastic FA bottle by comparing its performance with that of the current glass FA bottle for recovery of microorganisms and time to detection of growth in blood samples obtained for culture from adult patients with suspected bloodstream infections. We conclude that the BacT/ALERT plastic and glass FA bottles are comparable for recovery of microorganisms and that the safety advantage of plastic bottles can be achieved without compromising performance.

Adult↗

Stress and hippocampal plasticity.

The hippocampus is a target of stress hormones, and it is an especially plastic and vulnerable region of the brain. It also responds to gonadal, thyroid, and adrenal hormones, which modulate changes in synapse formation and dendritic structure and regulate dentate gyrus volume during development and in adult life. Two forms of structural plasticity are affected by stress: Repeated stress causes atrophy of dendrites in the CA3 region, and both acute and chronic stress suppresses neurogenesis of dentate gyrus granule neurons. Besides glucocorticoids, excitatory amino acids and N-methyl-D-aspartate (NMDA) receptors are involved in these two forms of plasticity as well as in neuronal death that is caused in pyramidal neurons by seizures and by ischemia. The two forms of hippocampal structural plasticity are relevant to the human hippocampus, which undergoes a selective atrophy in a number of disorders, accompanied by deficits in declarative episodic, spatial, and contextual memory performance. It is important, from a therapeutic standpoint, to distinguish between a permanent loss of cells and a reversible atrophy.

Adrenal Glands↗

Plasticity in the nucleus tractus solitarius and its influence on lung and airway reflexes.

The nucleus tractus solitarius (NTS) is the first central nervous system (CNS) site for synaptic contact of the primary afferent fibers from the lungs and airways. The signal processing at these synapses will determine the output of the sensory information from the lungs and airways to all downstream synapses in the reflex pathways. The second-order NTS neurons bring to bear their own intrinsic and synaptic properties to temporally and spatially integrate the sensory information with inputs from local networks, higher brain regions, and circulating mediators, to orchestrate a coherent reflex output. There is growing evidence that NTS neurons share the rich repertoire of forms of plasticity demonstrated throughout the CNS. This review focuses on existing evidence for plasticity in the NTS, potential targets for plasticity in the NTS, and the impact of this plasticity on lung and airway reflexes.

Action Potentials↗

Motor training induces experience-specific patterns of plasticity across motor cortex and spinal cord.

The motor cortex and spinal cord possess the remarkable ability to alter structure and function in response to differential motor training. Here we review the evidence that the corticospinal system is not only plastic but that the nature and locus of this plasticity is dictated by the specifics of the motor experience. Skill training induces synaptogenesis, synaptic potentiation, and reorganization of movement representations within motor cortex. Endurance training induces angiogenesis in motor cortex, but it does not alter motor map organization or synapse number. Strength training alters spinal motoneuron excitability and induces synaptogenesis within spinal cord, but it does not alter motor map organization. All three training experiences induce changes in spinal reflexes that are dependent on the specific behavioral demands of the task. These results demonstrate that the acquisition of skilled movement induces a reorganization of neural circuitry within motor cortex that supports the production and refinement of skilled movement sequences. We present data that suggest increases in strength may be mediated by an increased capacity for activation and/or recruitment of spinal motoneurons while the increased metabolic demands associated with endurance training induce cortical angiogenesis. Together these results show the robust pattern of anatomic and physiological plasticity that occurs within the corticospinal system in response to differential motor experience. The consequences of such distributed, experience-specific plasticity for the encoding of motor experience by the motor system are discussed.

Action Potentials↗

Temporal regulation of the expression locus of homeostatic plasticity.

Homeostatic plasticity of excitatory synapses plays an important role in stabilizing neuronal activity, but the mechanism of this form of plasticity is incompletely understood. In particular, whether the locus of expression is presynaptic or postsynaptic has been controversial. Here we show that the expression locus depends on the time neurons have spent in vitro. In visual cortical cultures < or =14 days in vitro (DIV), 2 days of TTX treatment induced an increase in miniature excitatory postsynaptic current (mEPSC) amplitude onto pyramidal neurons, without affecting mEPSC frequency. However, in cultures > or =18 DIV, the same TTX treatment induced a large increase in mEPSC frequency, whereas the amplitude effect was reduced. The increased mEPSC frequency was associated with an increased density of excitatory synapses and increased presynaptic vesicle release in response to electrical stimulation. This indicates a shift from a predominantly postsynaptic response to TTX in < or =14 DIV cultures, to a coordinated pre- and postsynaptic response in > or =18 DIV cultures. This shift was not specific for cortical cultures because a similar shift was observed in cultured hippocampal neurons. Culturing neurons from older animals showed that the timing of the switch depends on the time the neurons have spent in vitro, rather than their postnatal age. This temporal switch in expression locus can largely reconcile the contradictory literature on the expression locus of homeostatic excitatory synaptic plasticity in central neurons. Furthermore, our results raise the intriguing possibility that the expression mechanism of homeostatic plasticity can be tailored to the needs of the network during different stages of development or in response to different challenges to network function.

Anesthetics, Local↗

Computational studies on acquisition and adaptation of ocular following responses based on cerebellar synaptic plasticity.

To investigate how cerebellar synaptic plasticity guides the acquisition and adaptation of ocular following response (OFR), a large-scale network model was developed. The model includes the cerebral medial superior temporal area (MST), Purkinje cells (P cells) of the ventral paraflocculus, the accessory optic and climbing fiber systems, the brain stem oculomotor network, and the oculomotor plant. The model reconstructed temporal profiles of both firing patterns of MST neurons and P cells and eye movements. Model MST neurons (n = 1,080) were set to be driven by retinal error and exhibited 12 preferred directions, 30 preferred velocities, and 3 firing waveforms. Correspondingly, each model P cell contained 1,080 excitatory synapses from granule cell axons (GCA) and 1,080 inhibitory synapses. P cells (n = 40) were classified into four groups by their laterality (hemisphere) and by preferred directions of their climbing fiber inputs (CF) (contralateral or upward). The brain stem neural circuit and the oculomotor plant were modeled on the work of Yamamoto et al. The initial synaptic weights on the P cells were set randomly. At the beginning, P cell simple spikes were not well modulated by visual motion, and the eye was moved only slightly by the accessory optic system. The synaptic weights were updated according to integral-differential equation models of physiologically demonstrated synaptic plasticity: long-term depression and long-term potentiation for GCA synapses and rebound potentiation for inhibitory synapses. We assumed that maximum plasticity was induced when GCA inputs preceded CF inputs by 200 ms. After more than 10,000 presentations of ramp-step visual motion, the strengths of both the excitatory and inhibitory synapses were modified. Subsequently, the simple spike responses became well developed, and ordinary OFRs were acquired. The preferred directions of simple spikes became the opposite of those of CFs. Although the model MST neurons were set to possess a wide variety of firing characteristics, the model P cells acquired only downward or ipsilateral preferred directions, high preferred velocities and stereotypical firing waveforms. Therefore the drastic transition of the neural representation from the population codes in the MST to the firing-rate codes of simple spikes were learned at the GCA-P cell synapses and inhibitory cells-P cell synapses. Furthermore, the model successfully reproduced the gain- and directional-adaptation of OFR, which was demonstrated by manipulating the velocity and direction of visual motion, respectively. When we assumed that synaptic plasticity could only occur if CF inputs preceded GCA inputs, the ordinary OFR were acquired but neither the gain-adaptation nor the directional adaptation could be reproduced.

Adaptation, Physiological↗

Recovery of cortical binocularity and orientation selectivity after the critical period for ocular dominance plasticity.

Cortical binocularity is abolished by monocular deprivation (MD) during a critical period of development lasting from approximately postnatal day (P) 35 to P70 in ferrets. Although this is one of the best-characterized models of neural plasticity and amblyopia, very few studies have examined the requirements for recovery of cortical binocularity and orientation selectivity of deprived eye responses. Recent studies indicating that different mechanisms regulate loss and recovery of binocularity raise the possibility that different sensitive periods characterize loss and recovery of deprived eye responses. In this report, we have examined whether the potential for recovery of binocularity and orientation selectivity is restricted to the critical period. Quantitative single unit recordings revealed recovery of cortical binocularity and full recovery of orientation selectivity of deprived eye responses following prolonged periods of MD (i.e., >3 wk) starting at P49, near the peak of plasticity. Surprisingly, recovery was present when binocular vision was restored after the end of the critical period for ocular dominance plasticity, as late as P83. In contrast, ferrets that had never received visual experience through the deprived eye failed to recover binocularity even though normal binocular vision was restored at P50, halfway through the critical period. Collectively, these results indicate that there is potential for recovery of cortical binocularity and deprived eye orientation selectivity after the end of the critical period for ocular dominance plasticity.

Animals↗

Cholinergic influences on use-dependent plasticity.

Motor practice elicits use-dependent plasticity in humans as well as in animals. Given the influence of cholinergic neurotransmission on learning and memory processes, we evaluated the effects of scopolamine (a muscarinic receptor antagonist) on use-dependent plasticity and corticomotor excitability in a double-blind placebo-controlled randomized design study. Use-dependent plasticity was substantially attenuated by scopolamine in the absence of global changes in corticomotor excitability. These results identify a facilitatory role for cholinergic influences in use-dependent plasticity in the human motor system.

Administration, Cutaneous↗

Spike-timing-dependent plasticity of inhibitory synapses in the entorhinal cortex.

Actions of inhibitory interneurons organize and modulate many neuronal processes, yet the mechanisms and consequences of plasticity of inhibitory synapses remain poorly understood. We report on spike-timing-dependent plasticity of inhibitory synapses in the entorhinal cortex. After pairing presynaptic stimulations at time t(pre) with evoked postsynaptic spikes at time t(post) under pharmacological blockade of excitation we found, via whole cell recordings, an asymmetrical timing rule for plasticity of the remaining inhibitory responses. Strength of response varied as a function of the time interval Deltat = t(post) - t(pre): for Deltat > 0 inhibitory responses potentiated, peaking at a delay of 10 ms. For Deltat < 0, the synaptic coupling depressed, again with a maximal effect near 10 ms of delay. We also show that changes in synaptic strength depend on changes in intracellular calcium concentrations and demonstrate that the calcium enters the postsynaptic cell through voltage-gated channels. Using network models, we demonstrate how this novel form of plasticity can sculpt network behavior efficiently and with remarkable flexibility.

Animals↗

Local intracortical connections in the cat's visual cortex: postnatal development and plasticity.

1. We have studied the nature, development, and plasticity of local intracortical interactions by examining the visual responses from pairs of cells in the visual cortex of anesthetized and paralyzed adult cats and kittens at postnatal age 4 wk. Simultaneous discharge from nearby cells was analyzed by the cross-correlation method to infer three types of neuronal interactions: monosynaptic excitation, monosynaptic inhibition, and polysynaptic excitation. 2. Among cell pairs that exhibit correlated discharge, the nature of these interactions is similar in kittens and adults. For example, the mean monosynaptic delay is the same for cell pairs in the adult cat and the kitten: 0.8 ms. The primary difference in the distribution of neural interactions is the increased prevalence of inhibitory interactions among adult cat cell pairs compared with kitten cell pairs. However, in both age groups and in nearly all laminae, polysynaptic interactions are the most commonly observed type of interaction. 3. Neural interactions revealed by cross-correlation analysis also were studied with respect to the receptive field properties of the cells. The hierarchical theory proposed by Hubel and Wiesel suggests that monosynaptic excitation should be seen from simple to complex cells. It further suggests that complex cells do not provide monosynaptic excitation either to simple or to other complex cells. However, we find no cases of monosynaptic excitation from simple to complex cells in the adult cat. Moreover, we find explicitly antihierarchical connections, i.e., excitatory connections from complex to simple cells, in both kittens and adults. The excitatory influence of complex cells on simple cell receptive field properties is not incorporated into current models of receptive field structure formation. Our results suggest that complex cells might have an important modulatory role in simple cell discharge. 4. Plasticity of intracortical synaptic connections was studied by examining the dynamics of monosynaptic peaks with cross-correlograms. We examined Hebb's seminal hypothesis regarding synaptic plasticity that the excitatory connections between two neurons should strengthen with simultaneous activity. To test directly whether Hebbian plasticity can be rapidly induced by stimulus-evoked activity, the strength of monosynaptic excitation between pairs of neurons was monitored during periods of visual stimulation lasting < or = 2 h. Synaptic strength was computed by summing the cross-correlogram bins containing the monosynaptic peak. Transient increases in monosynaptic peak area are found among cell pairs linked by monosynaptic excitation after 8-15 min of visual stimulation. The duration and amplitude of these changes are similar in adult cats and kittens.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗

Site of auditory plasticity in the brain stem (VLVp) of the owl revealed by early monaural occlusion.

1. The optic tectum of the barn owl contains a physiological map of interaural level difference (ILD) that underlies, in part, its map of auditory space. Monaural occlusion shifts the range of ILDs experienced by an animal and alters the correspondence of ILDs with source locations. Chronic monaural occlusion during development induces an adaptive shift in the tectal ILD map that compensates for the effects of the earplug. The data presented in this study indicate that one site of plasticity underlying this adaptive adjustment is in the posterior division of the ventral nucleus of the lateral lemniscus (VLVp), the first site of ILD comparison in the auditory pathway. 2. Single and multiple unit sites were recorded in the optic tecta and VLVps of ketamine-anesthetized owls. The owls were raised from 4 wk of age with one ear occluded with an earplug. Auditory testing, using digitally synthesized dichotic stimuli, was carried out 8-16 wk later with the earplug removed. The adaptive adjustment in ILD coding in each bird was quantified as the shift from normal ILD tuning measured in the optic tectum. Evidence of adaptive adjustment in the VLVp was based on statistical differences between the VLVp's ipsilateral and contralateral to the occluded ear in the sensitivity of units to excitatory-ear and inhibitory-ear stimulation. 3. The balance of excitatory to inhibitory influences on VLVp units was shifted in the adaptive direction in six out of eight owls. In three of these owls, adaptive differences in inhibition, but not in excitation, were found. For this group of owls, the patterns of response properties across the two VLVps can only be accounted for by plasticity in the VLVp. For the other three owls, the possibility that the difference between the two VLVps resulted from damage to one of the VLVps could not be eliminated, and for one of these, plasticity at a more peripheral site (in the cochlea or cochlear nucleus) could also explain the data. In the remaining two owls, there was no evidence of adaptive adjustment in the VLVp despite large adaptive adjustments in the optic tectum. 4. The adjustment of ILD coding in the VLVp was always substantially smaller than expected based on the adjustment of ILD tuning in the optic tectum measured in the same animals. This indicates the involvement of at least one additional site of adaptive plasticity in the auditory pathway above the level of the VLVp.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗

Synaptic plasticity of the interpositorubral pathway functionally related to forelimb flexion movements.

1. Some connections from the afferents to the magnocellular red nucleus (RNm), like the corticorubral synapses, have plastic properties that are thought to contribute to long-term changes such as functional readaptation, motor learning, and the establishment of conditioned responses. Because previous studies have focused on corticorubral synaptic reorganization after these events, we attempted to investigate cerebellorubral connections in intact adult cats during associative conditioning by pairing electrical stimulation of interpositus nucleus [the conditional stimulus (CS)] with electrical simulation of the forelimb [the unconditional stimulus (UCS)]. A large increase in the amplitude of the forelimb flexion (conditioned response) induced by the CS was observed after several days of paired CS-UCS presentations. 2. For this purpose, both behavioral and electrophysiological methods were used to correlate synaptic plasticity with changes in the motor responses. The somatotopically organized sensorimotor network functionally related to the control of the elbow joint movements was studied in awake adult cats. This circuit was defined on the basis of sites at which elbow flexions could be evoked both as a CS and a UCS. The CS was applied in the cerebellar interpositus nucleus (IN) site and the UCS was given to the skin on the dorsum of the distal part of the forepaw. Daily classical conditioning consisted of repetitive pairings of CS and UCS with an interstimulus interval (ISI) of 100 ms. 3. The transmission efficacy resulting from the conditioning was tested in various targets of the cerebellar efferent pathway, including the RNm. Electrophysiological responses evoked in these relay structures by the CS and the forelimb angular deviations were simultaneously recorded throughout each daily conditioning session. The surface areas of the rubral responses to CS and the percentage response rate, the angular deviation (amplitude), and the latency of the motor responses were systematically measured throughout the conditioning procedure. Test sessions were also performed before and after each period of conditioning. Quantification and statistical analysis were carried out to determine whether changes observed in interpositorubral synaptic transmission and in the motor responses evoked by the CS were correlated. 4. Daily repetition of paired CS and UCS according to a predefined and fixed temporal schedule led to an increase in the response rate and amplitude of the forelimb flexions. A procedure with repeated presentation of CS preceded by UCS was used to produce extinction of the enhanced motor responses. The associative nature of these changes was confirmed by the fact that the CS given alone for 11 days in a control condition failed to produce any modification of the motor response. 5. The changes in the flexion movements were accompanied by a nearly parallel increase of the amplitude of the "postsynaptic field potentials" evoked in the RNm by the CS (IN stimulation). Changes in the transmission efficacy of the interpositorubral synapses stayed stable even after several days of interruption and remained constant up the extinction period. Changes affecting both the motor and the central responses were significantly correlated, suggesting that modifications in the interpositorubral transmission efficacy might be one of the plastic correlates of forelimb flexion conditioning. 6. Examination of the neuronal excitability within either the IN or the RNm or in the spinal cord failed to show any evidence of facilitation suggesting that the increases in the postsynaptic rubral field potential were attributable to a plasticity of the interpositorubral connections. The long-lasting duration of the increase of cerebellorubral synaptic transmission suggests that structural changes were induced by conditioning in the intact animal. (ABSTRACT TRUNCATED)

Animals↗

Plasticity in an electrosensory system. I. General features of a dynamic sensory filter.

1. In this study we describe changes in neuronal responses within the primary electrosensory processing nucleus of a weakly electric fish that occur when the fish are exposed to repetitive patterns of electrosensory stimuli. Extracellular single-unit recordings show that pyramidal cells within the electrosensory lateral line lobe develop, over a time course of several minutes, an insensitivity to repetitive stimuli applied to a cell's receptive field (local stimulus). The pyramidal cell response cancellation only develops if the local stimulus is applied simultaneously with a diffuse pattern of electrosensory stimulation that affects the entire fish, or with proprioceptive stimuli. 2. The mechanism by which responses to repetitive afferent inputs are canceled relies on the central generation of "negative image inputs" that provide increased inhibitory input to a cell's apical dendrites at times when excitatory afferent input is increased. The negative image input becomes excitatory when afferent excitation is reduced or when input from inhibitory interneurons is predominant. The integration of a specific pattern of receptor afferent input with the complementary negative image input results in strong attenuation of pyramidal cell responses. The negative image inputs are plastic, so that a single pyramidal cell can learn to reject a variety of afferent input patterns. 3. These electric fish commonly experience repetitive electrosensory signals as a result of changes in posture. Because the electric organ is located in the trunk and tail, cyclical movements associated with exploratory behaviors result in amplitude modulations (AMs) of the electric field, and these AMs alter electroreceptor afferent firing frequency but not the firing frequency of second-order pyramidal cells. The adaptive cancellation mechanism described in this study can account for the insensitivity of pyramidal cells to reafferent electrosensory stimulation caused by tail movements and other postural changes. 4. The tail movements generate proprioceptive as well as electrosensory inputs, and either of these signals alone provides sufficient information for the generation of negative image inputs. The size of the negative image is larger, however, if both inputs are active. 5. The synaptic plasticity underlying the development of negative image inputs has a long-term component; under appropriate conditions changes in synaptic efficacy persist for > 30 min. 6. Normally functioning glutamatergic synapses are necessary for the expression of the synaptic plasticity associated with this cancellation mechanism. The development of negative image responses is blocked by micropressure ejection of the glutamate antagonist 6,7-dinitroquinoxaline-2,3-dione into the neighborhood of the pyramidal cell apical dendrites. 7. The adaptive cancellation of repetitive inputs is based on anti-Hebbian mechanisms; that is, correlated pre- and postsynaptic activity lead to a reduction in the excitatory input provided by the plastic synapses. As has been shown for several other systems, the cancellation mechanism reduces the cells responses to reafferent patterns of sensory input. In addition, the results of this study indicate that the mechanism may be more general, enabling the system to also cancel patterns of input resulting from exogenous stimuli.

Adaptation, Physiological↗

Rapid development of synaptic connections and plasticity between sensory neurons and motor neurons of Aplysia in cell culture: implications for learning and regulation of synaptic strength.

We describe here the time course of functional synapse formation and of the development of short-term synaptic plasticity at Aplysia sensorimotor synapses in cell culture, as well as the effects of blocking protein synthesis or postsynaptic receptors on the development of synaptic transmission and plasticity. We find that synaptic responses can be elicited in 50% of sensory neuron-motor neuron pairs by 1 h after cell contact and that short-term homosynaptic depression and synaptic augmentation and restoration by the endogenous facilitatory transmitter serotonin are present at the earliest stages of synapse formation. Neither block of protein synthesis with anisomycin nor block of two types of postsynaptic glutamate receptor has any effect on the development of synaptic transmission or synaptic plasticity. The rapidity of synapse formation and maturation and their independence of protein synthesis suggest that changes in the number of functional synapses could contribute to short- and intermediate-term forms of synaptic plasticity and learning.

Animals↗

In vitro plasticity of the direct feedback pathway in the electrosensory system of Apteronotus leptorhynchus.

We have used field and intracellular recording from pyramidal cells in an in vitro preparation of the electrosensory lateral line lobe (ELL) of Apteronotus leptorhynchus to investigate synaptic plasticity of a direct feedback pathway: the (StF). Tetanic stimulation of the StF enhanced the StF-evoked synaptic response by 145% in field and the excitatory postsynaptic potential (EPSP) 190% in intracellular recordings. Maximal enhancement occurred at 5 s and lasted for approximately 120 s. Tetanic frequencies of 100-300 Hz produced enhancement; lower or higher frequencies failed to produce statistically significant changes in EPSP amplitude. Rates of 100-200 Hz occur in vivo in the cells of origin of the StF, suggesting that this form of plasticity may be operative under natural conditions. We could not elicit either long-term potentiation or depression by any stimulation protocol of the StF; in the case of long-term potentiation, this held even when excitatory transmission was enhanced by application of bicuculline, a gamma-aminobutyric acid-A antagonist. When tetanic stimulation of the StF was paired with hyperpolarization of pyramidal cells, subsequent StF-evoked EPSPs were increased by 146% (5 min posttetanus); this anti-Hebbian synaptic enhancement lasted for approximately 10 min. Neither tetanic stimulation alone, hyperpolarization alone, nor tetanic stimulation paired with pyramidal cell depolarization altered StF-evoked EPSP amplitudes on this time scale. Anti-Hebbian synaptic enhancement was not blocked by the N-methyl--aspartate-receptor antagonist D. L-aminophosphovalerate. The in vitro demonstration of anti-Hebbian plasticity at StF synapses replicates similar in vivo results. Anti-Hebbian synaptic plasticity of the StF may be responsible in part for the ability of gymnotiform fish to reject redundant electrosensory signals.

Animals↗

Priming-induced shift in synaptic plasticity in the rat hippocampus.

The activity history of a given neuron has been suggested to influence its future responses to synaptic input in one prominent model of experience-dependent synaptic plasticity proposed by Bienenstock, Cooper, and Munro (BCM theory). Because plasticity of synaptic plasticity (i.e., metaplasticity) is similar in concept to aspects of the BCM proposal, we have tested the possibility that a form of metaplasticity induced by a priming stimulation protocol might exhibit BCM-like characteristics. CA1 field excitatory postsynaptic potentials (EPSPs) obtained from rat hippocampal slices were used to monitor synaptic responses before and after conditioning stimuli (3-100 Hz) of the Schaffer collateral inputs. A substantial rightward shift (>5-fold) in the frequency threshold between long-term depression (LTD) and long-term potentiation (LTP) was observed <1 h after priming. This change in the LTD/P crossover point occurred at both primed and unprimed synaptic pathways. These results provide new support for the existence of a rapid, heterosynaptic, experience-dependent mechanism that is capable of modifying the synaptic plasticity phenomena that are commonly proposed to be important for developmental and learning/memory processes in the brain.

2-Amino-5-phosphonovalerate↗

Enhancement of cortical plasticity by behavioral training in acetylcholine-depleted adult rats.

Trimming all whiskers except two on one side of an adult rat's face results in cortical plasticity in which the spared whiskers, D2 and one D-row surround whisker (either D1 or D3), evoked responses containing more spikes than the response evoked by the cut whisker (called whisker pairing plasticity). Previously we have reported that acetylcholine (ACh) depletion in cortex prevents surround D-row whisker plasticity from developing within the barrel cortex. In this study we examined whether the animal's active use of its two intact whiskers can restore some aspects of plasticity in the ACh-depleted cortex. To achieve this goal, ACh was depleted from barrel field cortex, and 14 days after the depletion surgery, whiskers were trimmed and animals were trained on a whisker-dependent gap crossing task. After 7 days of training, animals were anesthetized with urethan and prepared for single-unit recording. Training the ACh-depleted, whisker-paired animals resulted in a significant enhancement of responses to paired surround whiskers: the D-paired whisker-evoked response contained more spikes than the D-cut evoked response. We conclude that training whisker paired rats has a positive impact on response properties of neurons in S1 cortex, even in ACh-depleted animals.

Acetylcholine↗