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PubMed2005

Activity- and BDNF-induced plasticity of miniature synaptic currents in ES cell-derived neurons integrated in a neocortical network.

In vitro differentiated embryonic stem (ES) cells have been proposed as potential donor cells for cell replacement therapies of neurodegenerative diseases. The functional synaptic integration of such cells appears conceivable because ES cell-derived neurons are well known to establish excitatory and inhibitory synapses. However, long-term synaptic plasticity, a prerequisite of memory formation, has not yet been demonstrated at these synapses. After in vitro differentiation and purification by immunoisolation, we co-cultured ES cell-derived neurons with neocortical explants, which strongly innervated the ES cell-derived target neurons. ES cell-derived neurons exhibited action potential firing similar to primary cultured neocortical neurons. The formation of glutamatergic synapses was indicated by AMPA receptor-mediated miniature excitatory postsynaptic currents (AMPA mEPSCs). In addition, a N-methyl-D-aspartate receptor-mediated, D-2-amino-5-phosphonopentanoic acid-sensitive mEPSC component was observed. We first studied activity-dependent homeostatic plasticity (synaptic scaling) of mEPSCs at glutamatergic synapses. Chronic blockade of action potential activity by TTX resulted in an increase in the amplitudes of AMPA mEPSCs. This indicates that ES cell-derived neurons are capable of a homeostatic regulation of postsynaptic AMPA receptors. In addition, we investigated neurotrophin-induced synaptic plasticity of mEPSCs at glutamatergic synapses. Chronic addition of brain-derived neurotrophic factor (BDNF; 100 ng/ml) to the culture medium resulted in an increase in both the frequency and the amplitudes of AMPA mEPSCs. These results suggest that BDNF induces the formation and/or the functional maturation of presynaptic release sites in parallel with an upregulation of postsynaptic AMPA receptors. Thus BDNF represents a potential co-factor that could improve functional synaptic integration of ES cell-derived neurons into neocortical networks.

2-Amino-5-phosphonovalerate↗
PubMed2001

Properties and plasticity of synaptic inputs to rat dorsal column neurones recorded in vitro.

1. The mechanisms regulating the flow of sensory signals and their modification by synaptic interactions in the dorsal column nuclei are incompletely understood. Therefore, we examined the interactions between EPSPs evoked by stimulation of dorsal column and corticofugal fibres in the dorsal column nuclei cells using an in vitro slice technique. 2. Dorsal column EPSPs had briefer durations at depolarised membrane potentials than corticofugal EPSPs. Superfusion of the NMDA receptor antagonist 2D(-)-2-amino-5-phosphonovaleric acid (AP5) did not modify dorsal column EPSPs but reduced corticofugal EPSPs. Application of the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) abolished both dorsal column and corticofugal EPSPs in cells held at the resting potential. Therefore, dorsal column EPSPs were mediated by non-NMDA receptors but corticofugal EPSPs revealed both non-NMDA- and NMDA-dependent components. 3. Paired-pulse stimulation of dorsal column fibres elicited a depression of the second EPSP at pulse intervals of < 50 ms; however, paired-pulse stimulation of corticofugal fibres evoked facilitation of the second EPSP at pulse intervals of < 30 ms. When stimulation of the corticofugal fibres preceded stimulation of the dorsal column fibres, facilitation of the dorsal column EPSP was observed at pulse intervals of < 100 ms. This facilitation was blocked at hyperpolarised membrane potentials or in the presence of AP5, suggesting activation of NMDA receptors. There was a depression of corticofugal EPSPs by previous dorsal column stimulation. 4. Dorsal column EPSPs were gradually depressed during stimulation with barrages at frequencies of > 10 Hz, while corticofugal EPSPs were facilitated and summated at frequencies > 30 Hz. Hyperpolarisation and application of AP5 prevented the facilitation of corticofugal EPSPs. High frequency stimulation of the corticofugal input elicited a short-lasting AP5-sensitive facilitation of both corticofugal and dorsal column EPSPs. Depolarising current facilitated dorsal column EPSPs but not corticofugal EPSPs. 5. These results indicate that synaptic interactions include different forms of activity-dependent synaptic plasticity, with the participation of NMDA receptors and probably Ca(2+) inflow through voltage-gated channels. These complex synaptic interactions may represent the cellular substrate of the integrative function of the dorsal column nuclei observed in vivo.

2-Amino-5-phosphonovalerate↗
PubMed2003

An analysis of synaptic normalization in a general class of Hebbian models.

In standard Hebbian models of developmental synaptic plasticity, synaptic normalization must be introduced in order to constrain synaptic growth and ensure the presence of activity-dependent, competitive dynamics. In such models, multiplicative normalization cannot segregate afferents whose patterns of electrical activity are positively correlated, while subtractive normalization can. It is now widely believed that multiplicative normalization cannot segregate positively correlated afferents in any Hebbian model. However, we recently provided a counterexample to this belief by demonstrating that our own neurotrophic model of synaptic plasticity, which can segregate positively correlated afferents, can be reformulated as a nonlinear Hebbian model with competition implemented through multiplicative normalization. We now perform an analysis of a general class of Hebbian models under general forms of synaptic normalization. In particular, we extract conditions on the forms of these rules that guarantee that such models possess a fixed-point structure permitting the segregation of all but perfectly correlated afferents. We find that the failure of multiplicative normalization to segregate positively correlated afferents in a standard Hebbian model is quite atypical.

Animals↗
PubMed2003

Comparative expression patterns of T-, N-, E-cadherins, beta-catenin, and polysialic acid neural cell adhesion molecule in rat cochlea during development: implications for the nature of Kölliker's organ.

We investigated the expression patterns of several cell adhesion molecules (CAMs) during rat cochlea ontogeny, from embryo day 16 to adulthood, with the use of immunohistochemistry: neural cadherin (N-cad) and polysialic acid neural CAM (PSA-NCAM) as two different neural CAM paradigms; epithelial cadherin (E-cad), which was restricted to the epitheloid phenotype; and the cytoplasmic domain-free truncated-cadherin (T-cad). We made the following observations. (1) T-cad was present in all types of fibrocyte and in subdomains within the pillar cells. (2) E- and N-cad were expressed with mutually exclusive patterns and did not overlap with T-cad. All cochlear epithelial cells, including the sensory outer hair cells (OHCs), were E-cad-positive, except for the negative inner hair cells (IHCs) and the nonsensory Kölliker's organ domain close to the IHCs. N-cad expression appeared first in the developing IHCs and then in the neighboring Kölliker's organ in an increasingly mediolateral gradient in opposition to the E-cad gradient. The OHCs, which are never N-cad positive, intensively expressed E-cad, as did the Hensen cells at the beginning of their differentiation. (3) The cadherin-linked molecule beta-catenin, absent in fibrocytes, was detected in all epithelial cell membranes and was prominent in the E-cad-rich modiolar extremity of Kölliker's organ. (4) Gradual PSA-NCAM expression was observed in the lateral portion of Kölliker's organ, and the intense PSA-NCAM expression was seen surrounding the IHCs. As development proceeded, PSA-NCAM immunoreactivity progressively became restricted to the basal poles of the IHCs, where it remained in the adult rat cochlea, suggesting a synaptic plasticity. Synaptic plasticity in rat cochlea and hypotheses about T-cad functions and neosensory features of the Kölliker's organ are discussed.

Animals↗
PubMed1989

Synaptic structural plasticity: role of synaptic shape.

Recent research has indicated that synaptic curvature is an important and potentially critical plastic feature of the synapse. Alterations in synaptic shape are related to synaptic function, being found both during maturation and in adulthood following neuronal activation. In this paper we review the evidence supporting synaptic shape as a plastic feature of synaptic structure. We also propose several mechanisms which might underlie these changes in shape. Finally, we suggest the possible functional role of alterations in synaptic curvature, including its potential in altering synaptic transmission efficacy.

Aging↗
PubMed2006

Learning the structure of correlated synaptic subgroups using stable and competitive spike-timing-dependent plasticity.

Synaptic plasticity must be both competitive and stable if ongoing learning of the structure of neural inputs is to occur. In this paper, a wide class of spike-timing-dependent plasticity (STDP) models is identified that have both of these desirable properties in the case in which the input consists of subgroups of synapses that are correlated within the subgroup through the occurrence of simultaneous input spikes. The process of synaptic structure formation is studied, illustrating one particular class of these models. When the learning rate is small, multiple alternative synaptic structures are possible given the same inputs, with the outcome depending on the initial weight configuration. For large learning rates, the synaptic structure does not stabilize, resulting in neurons without consistent response properties. For learning rates in between, a unique and stable synaptic structure typically forms. When this synaptic structure exhibits a bimodal distribution, the neuron will respond selectively to one or more of the subgroups. The robustness with which this selectivity develops during learning is largely determined by the ratio of the subgroup correlation strength to the number of subgroups. The fraction of potentiated subgroups is primarily determined by the balance between potentiation and depression.

Action Potentials↗
PubMed1994

Changes in reliability of synaptic function as a mechanism for plasticity.

Synaptic transmission in the hippocampus is rather unreliable, with many presynaptic action potentials failing to release neurotransmitter. How is this unreliability affected by the alterations in synaptic strength seen in long-term potentiation (LTP) and long-term depression (LTD)? We find that LTP increases synaptic reliability, and LTD decreases it, both without a change in the size of those postsynaptic currents that do occur. Thus LTD is a functional inverse of LTP.

Animals↗
PubMed1986

Quantitative investigation of the morphological plasticity of synaptic junctions in rat dentate gyrus during aging.

The morphological plasticity of synaptic junctions was investigated by means of quantitative stereology in the dentate gyrus supragranular layer of young (3 months), adult (12 months) and old (30 months) female Fisher 344 rats. The numerical (Nv) and surface (Sv) density and the average surface area (S) of EPTA-stained synaptic junctions were calculated on 100 EM pictures per age group. We found that Nv significantly increased between the young and adult group and decreased in old animals when compared both to 3 and 12 months of age. Sv was unchanged in young and adult rats, whereas it underwent a significant reduction in the old group. The percentage distribution of S showed that at 3 months of age the majority of the synaptic population had an average size ranging between 0.12 and 0.20 micron 2, whereas during adulthood and aging there was a shift towards smaller and larger synaptic contacts, respectively. Taking into account Nv, Sv and S all together per age group, the present findings demonstrate that the morphological aspect of synaptic plasticity is markedly influenced by time and that during aging it undergoes a serious impairment. The possible involvement in memory and learning processes of these synaptic age-related morphological adaptations and the fact that the investigated junctions are supposed to be cholinergic is discussed.

Aging↗
PubMed2005

The subiculum: what it does, what it might do, and what neuroanatomy has yet to tell us.

The subiculum is a pivotal but under-investigated structure positioned between the hippocampus proper and entorhinal and other cortices, as well as a range of subcortical structures. The subiculum has a range of electrophysiological and functional properties which are quite distinct from its input areas; given the widespread set of cortical and subcortical areas with which it interacts, it is able to influence activity in quite disparate brain regions. The rules governing plasticity of synaptic transmission in the hippocampal-subicular axis are poorly understood; this axis appears to share some properties in common with the hippocampus proper, but behaves quite differently in other respects. Equally, its functional properties are not well understood; it plays an important but ill-defined role in spatial navigation, mnemonic processing and control of the response to stress. Here, I review investigations of synaptic plasticity in the hippocampal-subicular pathway, recordings of subicular neurons in the freely moving behaving animal, the effects of behavioural and other stressors on subicular synaptic plasticity, and anatomical data on the dorso-ventral organization of the subiculum in relation to the hypothalamic-pituitary-adrenal (HPA) axis. I argue that there is a dorso-ventral segregation of function within the subiculum: the dorsal component appears principally concerned with the processing of information about space, movement and memory, whereas the ventral component appears to play a major regulatory role in the inhibition of the HPA axis.

Animals↗
PubMed2000

The activity-dependent plasticity of segmental and intersegmental synaptic connections in the lamprey spinal cord.

Activity-dependent synaptic plasticity has been proposed as a contributory factor in the patterning of rhythmic network activity. However, its role has not been examined in detail. Here, paired or triple intracellular recordings have been made from identified neurons in the lamprey locomotor network to examine the potential relevance of activity-dependent synaptic plasticity in segmental and intersegmental spinal networks. Segmental inputs from glutamatergic excitatory interneurons (EIN) to ipsilateral glycinergic crossed caudal (CC) interneurons were facilitated or depressed during spike trains at 5-20 Hz. Connections between EINs were depressed. Glycinergic inputs from small ipsilateral inhibitory interneurons were depressed in motor neurons, but were facilitated in CC interneurons. Excitatory inputs from small crossing interneurons to motor neurons were depressed, whereas inhibitory inputs were unaffected. With the exception of connections between EINs, significant effects occurred with stimulation that mimicked interneuron spiking during network activity. Intersegmental EIN synaptic properties were also investigated. EIN inputs did not differ significantly when examined from zero to four segments rostral to motor neurons or CC interneurons. However, caudally located EINs evoked greater activity-dependent facilitation than did rostral EINs. Whilst the amplitude or plasticity of EIN inputs in the rostral or mid-trunk regions of the spinal cord did not differ, EINs in the caudal trunk region evoked greater facilitation. Synaptic transmission between locomotor network neurons thus exhibits activity-dependent plasticity in response to physiologically relevant stimulation. Activity-dependent plasticity could thus contribute to the patterning of the rhythmic network output.

Action Potentials↗
PubMed2005

Role of adenosine in the control of homosynaptic plasticity in striatal excitatory synapses.

Long-lasting, activity-dependent changes in synaptic efficacy at excitatory synapses are critical for experience-dependent synaptic plasticity. Synaptic plasticity at excitatory synapses is determined both presynaptically by changes in the probability of neurotransmitter release, and postsynaptically by changes in the availability of functional postsynaptic glutamate receptors. Two kinds of synaptic plasticity have been described. In homosynaptic or Hebbian plasticity, the events responsible for synaptic strengthening occur at the same synapse as is being strengthened. Homosynaptic plasticity is activity-dependent and associative, because it associates the firing of a postsynaptic neuron with that of the presynaptic neuron. Heterosynaptic plasticity, on the other hand, is activity-independent and the synaptic strength is modified as a result of the firing of a third, modulatory neuron. It has been suggested that long-term changes in synaptic strength, which are associated with gene transcription, can only be induced with the involvement of heterosynaptic plasticity. The neuromodulator adenosine plays an elaborated pre- and postsynaptic control of glutamatergic neurotransmission. This paper reviews the evidence suggesting that in some striatal excitatory synapses, adenosine can provide the heterosynaptic-like modulation essential for stabilizing homosynaptic plasticity without the need of a "third, modulatory neuron".

Adenosine↗
PubMed2001

Is LTP in the hippocampus a useful model for learning-related alterations in gene expression?

It is well established that the formation of long-term memory requires de novo protein synthesis. Altered gene expression is therefore critical in the signal transduction cascade activated by the learning experience. Long-term potentiation (LTP) is a mnemonic model in which particular patterns of activation of incoming excitatory fibers (representing the learning experience) may induce long-lasting enhancement of the communication between the involved pre- and post-synapses (representing the memory). Therefore, cellular and molecular mechanisms of LTP have been extensively studied under the assumption that their understanding will contribute to our comprehension of the mechanisms underlying memory formation. In recent years, however, this analogy has been challenged by reports of inconsistency between LTP and memory. Here we assess LTP in the hippocampus as a model system to study spatial memory-related alterations in gene expression. We focus on three molecular families that are likely to play a role in synaptic plasticity: (1) synaptic communication related proteins; (2) signal transduction machinery; and (3) growth factors. Reviewing first the literature on LTP and then behavioral research we found both consistent and inconsistent findings regarding the LTP/memory linkage. The importance of restricting the discussion to both a learning phase and a brain (sub)structure, as well as of incorporating more physiological LTP stimulation protocols, is discussed. We conclude that while LTP is indeed limited as a model of memory, a careful use of it as a model system of synaptic plasticity is fruitful and productive in screening out candidate memory-related genes.

Animals↗
PubMed2002

A decade of molecular studies of fragile X syndrome.

Fragile X syndrome is one of the most common forms of inherited mental retardation. In most cases the disease is caused by the methylation-induced transcriptional silencing of the fragile X mental retardation 1 (FMR1) gene that occurs as a result of the expansion of a CGG repeat in the gene's 5'UTR and leads to the loss of protein product fragile X mental retardation protein (FMRP). FMRP is an RNA binding protein that associates with translating polyribosomes as part of a large messenger ribonucleoprotein (mRNP) and modulates the translation of its RNA ligands. Pathological studies from the brains of patients and from Fmr1 knockout mice show abnormal dendritic spines implicating FMRP in synapse formation and function. Evidence from both in vitro and in vivo neuronal studies indicates that FMRP is located at the synapse and the loss of FMRP alters synaptic plasticity. As synaptic plasticity has been implicated in learning and memory, analysis of synapse abnormalities in patients and Fmr1 knockout mice should prove useful in studying the pathogenesis of fragile X syndrome and understanding learning and cognition in general. If an appreciable portion of the total variance (in IQ) is due to sex linked genes, it is of more importance that a boy should have a clever mother than a clever father. Hogben 1932 (quoted in Lehrke 1974)

Animals↗
PubMed1998

Cortical plasticity: from synapses to maps.

It has been clear for almost two decades that cortical representations in adult animals are not fixed entities, but rather, are dynamic and are continuously modified by experience. The cortex can preferentially allocate area to represent the particular peripheral input sources that are proportionally most used. Alterations in cortical representations appear to underlie learning tasks dependent on the use of the behaviorally important peripheral inputs that they represent. The rules governing this cortical representational plasticity following manipulations of inputs, including learning, are increasingly well understood. In parallel with developments in the field of cortical map plasticity, studies of synaptic plasticity have characterized specific elementary forms of plasticity, including associative long-term potentiation and long-term depression of excitatory postsynaptic potentials. Investigators have made many important strides toward understanding the molecular underpinnings of these fundamental plasticity processes and toward defining the learning rules that govern their induction. The fields of cortical synaptic plasticity and cortical map plasticity have been implicitly linked by the hypothesis that synaptic plasticity underlies cortical map reorganization. Recent experimental and theoretical work has provided increasingly stronger support for this hypothesis. The goal of the current paper is to review the fields of both synaptic and cortical map plasticity with an emphasis on the work that attempts to unite both fields. A second objective is to highlight the gaps in our understanding of synaptic and cellular mechanisms underlying cortical representational plasticity.

Animals↗
PubMed1998

The neuromessenger platelet-activating factor in plasticity and neurodegeneration.

Synaptic activation leads to the formation of arachidonic acid, platelet-activating factor (PAF, 1-O-alkyl-2-acyl-sn-3-phosphocholine) and other lipid messengers. PAF is a potent bioactive phospholipid in synaptic plasticity. PAF enhances presynaptic glutamate release, is a retrograde messenger in long-term potentiation and enhances memory formation. PAF also couples synaptic events with gene expression by stimulating a FOS/JUN/AP-1 transcriptional signaling system, as well as transcription of COX-2 (inducible prostaglandin synthase). Since the COX-2 gene is also involved in synaptic plasticity, the PAF-COX-2 pathway may have physiological significance. Seizures, ischemia and other forms of brain injury promote phospholipase A2 (PLA2) overactivation, resulting in the accumulation of bioactive lipids at the synapse. PAF, under these pathological conditions, behaves as a neuronal injury messenger by at least two mechanisms: (a) enhancing glutamate release; and, (b) by sustained augmentation of COX-2 transcription. These events link PAF with neurodegeneration. The upstream intracellular pathways of signal transduction involved in neuronal or photoreceptor cell apoptosis are not well understood and involve stress sensitive kinases. PAF is a transcriptional activator of the COX-2 gene. BN 50730, a potent intracellular PAF antagonist, blocks COX-2 induction. COX-2 transcription and protein expression are upregulated in the hippocampus in kainic acid induced epileptogenesis. There is a selectively elevated induction of COX-2 (72-fold) by kainic acid preceding neuronal cell death. BN 50730 administered by i.c.v. injection blocks seizure-induced COX-2 induction. Overall, PAF is a dual modulator of neural function and becomes an endogenous neurotoxin when over produced.

Animals↗
PubMed2004

Neurodegeneration and plasticity.

Neurofibrillary degeneration, associated with the formation of paired helical filaments (PHF), is one of the critical neuropathological hallmarks of Alzheimer's disease (AD). Although the microtubule-associated protein tau in a hyperphosphorylated form has been established as primary PHF constituent, the process of tau phosphorylation and its potential link to degeneration is not very well understood, mostly because of the lack of a physiological in vivo model of PHF-like tau phosphorylation. PHF formation in AD follows a hierarchical pattern of development throughout different cortical areas, which closely matches the pattern of neuronal plasticity in the adult brain. Those brain areas are most early and most severely affected which are involved in the regulation of memory, learning, perception, self-awareness, consciousness, and higher brain functions that require a life-long re-fitting of connectivity, a process based on a particularly high degree of plasticity. Failures of synaptic plasticity are, thus, assumed to represent early events in the course of AD that eventually lead to alteration of tau phosphorylation. Recently, we have used the hibernation cycle, a physiological model of adaptation associated with an extraordinary high degree of structural neuronal plasticity, to analyze the potential link between synaptic plasticity, synaptic detachment and the regulation of tau phosphorylation. During torpor, a natural state of hypothermia, synaptic contacts between mossy fibers and hippocampal pyramidal neurons undergo dramatic regressive changes that are fully reversible very rapidly during euthermy. This rapid, reversible, and repeated regression of synaptic and dendritic components on CA3 neurons is associated with a reversible PHF-like phosphorylation of tau at a similar time course. The repeated formation and degradation of PHF-tau might, thus, represent a physiological mechanism not necessarily associated with pathological effects. These findings implicate an essential link between neuronal plasticity and PHF-like phosphorylation of tau, potentially involved in neurofibrillary degeneration.

Aging↗
PubMed1988

Functionally significant plasticity of synaptic morphology: studies on the ribbon synapse of the ampullae of Lorenzini.

Changes in electrophysiological properties measured in vitro were correlated with ultrastructural differences at synapses between sense cells and the primary afferent neurons in electrosensory organs of the thornback ray (the ampullae of Lorenzini). Variation in synaptic structure was classified into four synaptic morphotypes, which appear to represent stages in a cyclic pattern of ultrastructural modification associated with changes in synaptic efficacy. Synapses with deeper postsynaptic troughs, and active zone regions located at the "narrow point" of the presynaptic evagination, and other morphological differences, were associated with greater sensitivity and spontaneous activity. Furthermore, the morphology of synapses was different in organs that had shown increasing, decreasing or stable trends in sensitivity prior to fixation, suggesting that changes in synaptic physiology and morphology are interrelated, and providing evidence for the sequence of ultrastructural modifications represented by the four synaptic morphotypes. These results support the conclusion that synaptic morphology is plastic and that this plasticity has functional significance in terms of the threshold sensitivity and spontaneous activity monitored from the afferent nerves. Plasticity of synaptic morphology which is associated with changes in the efficacy of transmitter release at chemically mediated synapses could be important in relatively long-term phenomena.

Animals↗
PubMedDate not supplied

Models of receptive-field dynamics in visual cortex.

The position, size, and shape of the receptive field (RF) of some cortical neurons change dynamically, in response to artificial scotoma conditioning (Pettet & Gilbert, 1992) and to retinal lesions (Chino et al., 1992; Darian-Smith & Gilbert, 1995) in adult animals. The RF dynamics are of interest because they show how visual systems may adaptively overcome damage (from lesions, scotomas, or other failures), may enhance processing efficiency by altering RF coverage in response to visual demand, and may perform perceptual learning. This paper presents an afferent excitatory synaptic plasticity rule and a lateral inhibitory synaptic plasticity rule--the EXIN rules (Marshall, 1995)--to model persistent RF changes after artificial scotoma conditioning and retinal lesions. The EXIN model is compared to the LISSOM model (Sirosh et al., 1996) and to a neuronal adaptation model (Xing & Gerstein, 1994). The rules within each model are isolated and are analyzed independently, to elucidate their roles in adult cortical RF dynamics. Based on computer simulations, the EXIN lateral inhibitory synaptic plasticity rule and the LISSOM lateral excitatory synaptic plasticity rule produced the best fit with current neurophysiological data on visual cortical plasticity in adult animals (Chino et al., 1992; Pettet & Gilbert, 1992; Darian-Smith & Gilbert, 1995) including (1) the retinal position and shape of the expanding RFs; (2) the corticotopic direction in which responsiveness returns to the silenced cortex; (3) the direction of RF shifts; (4) the amount of change in response to blank stimuli; and (5) the lack of dynamic RF changes during conditioning with a retinal lesion in one eye and the unlesioned eye kept open, in adult animals. The effects of the LISSOM lateral inhibitory synaptic plasticity rule during artificial scotoma conditioning are in conflict with those of the other two LISSOM synaptic plasticity rules. A novel "complementary scotoma" conditioning experiment, in which stimulation of two complementary regions of visual space alternates repeatedly, is proposed to differentiate the predictions of the EXIN and LISSOM rules.

Adaptation, Physiological↗