[Current concepts of general properties and plastic phenomena in hippocampal neurons].
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Animals↗
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Results for “Neuronal Plasticity”
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[The plastic reorganization of the neuronal receptive fields of the auditory cortex and medial geniculate body evoked by microstimulation of the auditory cortex].
The effects of intracortical microstimulation (ICMS) on receptive fields (RFs) of simultaneously recorded auditory cortex (A1) and medial geniculate body (MGB) neurons were examined in rats under ketamine. Three types of neurons were distinguished according to the configuration of their RFs: mono-, be-, and polymodal. It was shown that RFs of adjacent neurons may be different and Rfs of distant (up to 1 mm in rostro-caudal direction) neurons may be similar. ICMS was able to produce changes in RF structure of A1 neurons at and near the stimulation side and also in homotopically related regions of MGB. RFs of homotopically related A1 and MGB neurons mostly changed in a similar way after ICMS. We suggest that the mechanism underlying the observed RF changes of A1 and MGB neurons in related to ICMS-induced long-term changes (LTP and LTD) in synaptic efficacy of the cortex-thalamus-cortex loop.
Acoustic Stimulation↗
Differential distribution of functional receptors for neuromodulators evoking short-term heterosynaptic plasticity in Aplysia sensory neurons.
Synaptic transmission and excitability in Aplysia sensory neurons (SNs) are bidirectionally modulated by 5-HT and FMRFamide. To explore the regional distribution of different functional receptors that modulate SN properties, we examined changes in synaptic efficacy and excitability with brief focal applications of the neuromodulators to different regions of SNs that have established connections with motor cell L7 in culture. Short-term changes in synaptic efficacy were evoked only when 5-HT or FMRFamide was applied to regions with SN varicosities along the surface of L7 axons. Applications to adjacent SN neurites with few varicosities in contact with L7 axons failed to evoke a significant change in synaptic efficacy. The distribution of functional receptors mediating changes in excitability differed for 5-HT and FMRFamide. Whereas excitability increases were evoked only when 5-HT was applied to SN cell bodies, excitability decreases in SNs were evoked only when FMRFamide was applied to regions along the L7 axon with SN varicosities. Without the target cell, cell bodies of SNs expressed both 5-HT and FMRFamide receptors that modulate excitability. These results indicate that functional G-protein-coupled receptors for two neuromodulators are distributed differentially along the surface of a presynaptic neuron that forms chemical connections in vitro. This differential distribution of receptors on the presynaptic neuron is regulated by a target and does not require the physical presence of neurons that release the neuromodulators.
Animals↗
Neural plasticity as studied in neuronal cell lines.
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Animals↗
Microvascular plasticity in aging.
Understanding the bases of aging-related cognitive decline remains a central challenge in neurobiology. Quantitative studies reveal little change in the number of neurons or synapses in most of the brain but their ongoing replacement is reduced, resulting in a significant loss of neuronal plasticity with senescence. Aging also may alter neuronal function and plasticity in ways that are not evident from anatomical studies of neurons and their connections. Since the nervous system is dependent upon a consistent blood supply, any aging-related changes in the microvasculature could affect neuronal function. Several studies suggest that, as the nervous system ages, there is a rarefaction of the microvasculature in some regions of the brain, as well as changes in the structure of the remaining vessels. These changes contribute to a decline in cerebral blood flow (CBF) that reduces metabolic support for neural signaling, particularly when levels of neuronal activity are high. In addition to direct effects on the microvasculature, aging reduces microvascular plasticity and the ability of the vessels to respond appropriately to changes in metabolic demand. This loss of microvascular plasticity has significance beyond metabolic support for neuronal signaling, since neurogenesis in the adult brain is regulated coordinately with capillary growth.
Aging↗
Synaptic plasticity and mood disorders.
Recent studies demonstrate that the molecular elements known to regulate neuronal plasticity in models of learning and memory are also involved in the actions of drugs used for the treatment of depression and bipolar disorder. This includes up-regulation of transcription factors, such as the cAMP response element binding protein and neurotrophic factors, such as brain derived neurotrophic factor. These findings raise the possibility that regulation of neural plasticity in specific neuronal circuits is integrally involved in the therapeutic intervention of mood disorders. Atypical antipsychotic drugs, including clozapine and olanzapine, are also effective for the treatment of bipolar disorder, and are used as add-on medication for unipolar depression. The possibility that these atypical antipsychotic drugs also influence the molecular determinants of synaptic plasticity that are involved in the response to drugs used for the treatment of mood disorders, is discussed.
Antidepressive Agents↗
[Receptive field plasticity of a polyfunctional neuron in mollusks].
Plastic properties of the receptive field of the identified LPa3 neurone were studied on a semi-intact snail preparation. Mantle area representing part of the vast receptive field of the LPa3 neurone of the left parietal ganglion consists of three zones. The right part of the mantle is innervated by the right pallial and anal nerves; the former transmits to the CNS the short latency rapidly extinguishing component of the synaptic response, while the anal nerve--the slowly extinguishing long latency component. The left part of the mantle is innervated by the LPa3 neurone through the left pallial nerve which transmits the multi-component slowly extinguishing excitatory synaptic potential. The pneumostome area is innervated by the right pallial and anal nerves which transmit a non-extinguishing response. Thus, different areas of the mantle are linked to the LPa3 neurone by a system of parallel channels differing by their plastic properties.
Action Potentials↗
Hebbian-like functional plasticity in the auditory cortex of the behaving monkey.
In this study, the necessary conditions, including those related to behavior, for lasting modifications to occur in correlated activity ('functional plasticity') were examined in the behaving monkey. Previously, in-vitro studies of neuronal plasticity yielded important information about possible mechanisms of synaptic plasticity, but could not be used to test their functionality in the intact, behaving brain. In-vivo studies usually focused on analysis of the responsiveness of single cells, but did not examine interactions between pairs of neurons. In this study, we combined the two approaches. This was achieved by recording extracellularly and simultaneously the spike activity of several single cells in the auditory cortex of the behaving monkey. The efficacy of neuronal interactions was estimated by measuring the correlation between firing times of pairs of single neurons. Using acoustic stimuli, a version of cellular conditioning was applied when the monkey performed an auditory discrimination task and when it did not. We found that: (i) functional plasticity is a function of the change in correlation, and not of the correlation or covariance per se, and (ii) functional plasticity depends critically on behavior. During behavior, an increase in the correlation caused a short-lasting strengthening of the neuronal coupling efficacy, and a decrease caused a short-lasting weakening. These findings indicate that neuronal plasticity in the auditory cortex obeys a version of Hebb's associative rule under strong behavioral control, as predicted by Thorndike's "Law of Effect".
Acoustic Stimulation↗
Microelectrode array recordings of cultured hippocampal networks reveal a simple model for transcription and protein synthesis-dependent plasticity.
A simplified cell culture system was developed to study neuronal plasticity. As changes in synaptic strength may alter network activity patterns, we grew hippocampal neurones on a microelectrode array (MEA) and monitored their collective behaviour with 60 electrodes simultaneously. We found that exposure of the network for 15 min to the GABA(A) receptor antagonist bicuculline induced an increase in synaptic efficacy at excitatory synapses that was associated with an increase in the frequency of miniature AMPA receptor-mediated EPSCs and a change in network activity from uncoordinated firing of neurones (lacking any recognizable pattern) to a highly organized, periodic and synchronous burst pattern. Induction of recurrent synchronous bursting was dependent on NMDA receptor activation and required extracellular signal-regulated kinase (ERK)1/2 signalling and translation of pre-existing mRNAs. Once induced, the burst pattern persisted for several days; its maintenance phase (> 4 h) was dependent on gene transcription taking place in a critical period of 120 min following induction. Thus, cultured hippocampal neurones display a simple, transcription and protein synthesis-dependent form of plasticity. The non-invasive nature of MEA recordings provides a significant advantage over traditional assays for synaptic connectivity (i.e. long-term potentiation in brain slices) and facilitates the search for activity-regulated genes critical for late-phase plasticity.
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Neurotransmitter plasticity at the molecular level.
Contrary to long-held assumptions, recent work indicates that neurons may profoundly change transmitter status during development and maturity. For example, sympathetic neurons, classically regarded as exclusively noradrenergic or cholinergic, can also express putative peptide transmitters such as substance P. This neuronal plasticity is directly related to membrane depolarization and sodium ion influx. The same molecular mechanisms and plastic responses occur in mature as well as developing neurons. Further, contrary to traditional teaching, adult primary sensory neurons may express the catecholaminergic phenotype in vivo. Transmitter plasticity is not restricted to the peripheral nervous system: ongoing studies of the brain nucleus locus ceruleus in culture indicate that specific extracellular factors elicit marked transmitter changes. Consequently, neurotransmitter expression and metabolism are dynamic, changing processes, regulated by a variety of defined factors. Transmitter plasticity adds a newly recognized dimension of flexibility to nervous system function.
Adrenal Medulla↗
Cortically induced thalamic plasticity in the primate somatosensory system.
The influence of cortical feedback on receptive field organization in the thalamus was assessed in the primate somatosensory system. Chronic and acute suppression of neuronal activity in primary somatosensory cortex resulted in a striking enlargement of receptive fields in the ventroposterior thalamus. This finding demonstrates a dramatic 'top-down' influence of cortex on receptive field size in the somatosensory thalamus. In addition, this result has important implications for studies of adult neuronal plasticity because it indicates that changes in 'higher-order' areas of the brain can trigger extensive changes in the receptive field characteristics of neurons located earlier in the processing pathway.
2-Amino-5-phosphonovalerate↗
Glutamate receptors in cortical plasticity: molecular and cellular biology.
Glutamate receptors (GluRs) provide the major excitatory input to cortical neurons. Four main subtypes of GluRs are distinguished, namely, N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, kainate, and metabotropic receptors. All of them have been implicated in neuronal plasticity, and this paper reviews data that may be pertinent to the role played by GluRs in neocortical plasticity both in adult animals as well as during postnatal development. Emphasis is given to receptor distribution analyzed by various means, such as physiological responses, ligand binding as revealed by receptor autoradiography, and expression of receptor subunits at both mRNA and protein (immunoreactivity) levels. Possible mechanisms of involvement of GluRs in plastic changes on cortical neuron response are reviewed, and data on up- and downregulation of GluRs in neocortical plasticity are summarized. Functional studies involving either activation or blocking, and effects of such manipulation on cortical plasticity are discussed.
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Postlesional transcriptional regulation of metabotropic glutamate receptors: implications for plasticity and excitotoxicity.
Metabotropic glutamate receptors (mGluRs) seem to be involved both in neuronal excitotoxicity evoked by pathological conditions such as ischemia, and in processes associated with neuronal plasticity and regulation of synaptic strength. Using semiquantitative reverse transcription-polymerase chain reaction, we measured the messenger RNA levels of mGluR2-5, 24 h and 7 days after experimentally induced focal cortical infarcts in rat motor cortex. The mRNA level of mGluR3 was strikingly decreased ipsilaterally after 24 h. On day 7, the expression of mGluR2 was down-regulated both ipsi- and contralaterally. Other receptors of this family showed either a slight or no regulation at both time points. The early changes in the expression pattern of mGluRs might be primarily linked to excitotoxicity processes which occur immediately after an ischemic lesion in cortex, whereas the delayed changes might represent one chain link in the cascade of compensatory mechanisms contributing to functional amelioration.
Animals↗
The effect of norepinephrine on visual cortical neurons in kittens and adult cats.
The responses of visual cortical neurons during iontophoresis of norepinephrine (NE) were compared in kittens and adult cats. One type of neuronal "plasticity" (the ability of visual cortical neurons to have their response properties markedly altered during exposure to a restricted visual environment) normally occurs only in young kittens and has been hypothesized to depend on the presence of NE. We investigated this hypothesis in terms of a model of synaptic plasticity which suggested that NE would selectively enhance the evoked responses of neurons and that this enhancement might exist to a greater extent in kittens than in adult cats. The responses of 72% (43 of 60) of all neurons sampled decreased during NE iontophoresis, while the responses of only a few neurons (3 of 60) increased. Reduced activity occurred in roughly equal percentages of simple and complex cells. We also looked for differences in NE modulation of the "signal-to-noise" ratio of neurons. Most neurons had little spontaneous activity, but, of those that did, the signal-to-noise ratio increased in some instances and decreased in others. No difference in any of the effects of NE was observed between kittens and adult cats. The role of NE in cortical plasticity is discussed.
Animals↗
Effects of age and GDNF on noradrenergic innervation of the hippocampal formation: studies from intraocular grafts.
Recent studies have suggested that factors in the target tissue influence the degree of plasticity and regeneration following aging and/or specific insults. We have investigated whether young or aged targets differ in their noradrenergic innervation from fetal locus coeruleus (LC) neurons, and also if a specific growth factor, glial cell line-derived neurotrophic factor (GDNF) can affect this innervation pattern. Tissue pieces of fetal brainstem and young (3 months) or old (18 months) iris tissue were transplanted simultaneously into the anterior chamber of the eye of adult hosts. We found that aged iris transplants became innervated to a significantly lesser degree by the cografted LC neurons than young iris transplants. Fetal hippocampal tissue was then grafted to adult hosts, and a fetal brainstem graft containing LC neurons was placed adjacent to the first graft, either at 3 or 21 months post-grafting. Thus, old/young chimeras of the noradrenergic coeruleo-hippocampal pathway were created. Aged hippocampal grafts received a much less dense innervation from co-grafted LC neurons than young hippocampal grafts. Tyrosine hydroxylase-positive-immunoreactive innervation was only found in the outskirts of aged grafts, while the young hippocampal grafts contained an even innervation pattern. The innervation density of hippocampal grafts was significantly enhanced by GDNF treatment. These findings demonstrate that target-derived factors may regulate neuronal plasticity, and that the age of the target is more important for innervation properties than the age of the neuron innervating a particular target.
Aging↗
GAP-43 as a plasticity protein in neuronal form and repair.
Neurons exhibit a remarkable plasticity of form, both during neural development and during the subsequent remodelling of synaptic connectivity. Here we review work on GAP-43 and G0, and focus upon the thesis that their interaction may endow neurons with such plasticity. We also present new data on the role of G proteins in neurite growth, and on the interaction of GAP-43 and actin. GAP-43 is a protein induced during periods of axonal extension and highly enriched on the inner surface of the growth cone membrane. Its membrane localization is primarily due to a short amino terminal sequence which is subject to palmitoylation. Binding to actin filaments may also assist in restricting the protein to specific cellular domains. Consistent with its role as a "plasticity protein," there is evidence that GAP-43 can directly alter cell shape and neurite extension, and several theses have been advanced for how it might do so. Two other prominent components of the growth cone membrane are the alpha and beta subunits of G0. GAP-43 regulates their guanine nucleotide exchange, which is an unusual role for an intracellular protein. We speculate that GAP-43 may adjust the "set point" of responsiveness for G0 stimulation by receptors, thereby altering the neuronal propensity to growth, without actually causing growth. To begin to address how G protein activity affects axon growth, we have developed a means to introduce guanine nucleotide analogs into sympathetic neurons. Stimulation of G proteins with GTP-gamma-S retards axon growth, whereas GDP-beta-S enhances it. This is compatible with G protein registration of inhibitory signals.
Actins↗
Regeneration as an application of gastropod neural plasticity.
Gastropod research is providing many insights into mechanisms of neural regeneration. These observations were made possible by the pioneering work of individuals who described the nervous systems of gastropods, mapped prominent neurons and determined their roles and connections, and developed the techniques for culturing them. This information has allowed questions about injury responses, target selection, and pathway cues to be explored at the level of individually identified neurons. Because of gastropod studies, more is known about axon sealing, growth cone formation and behavior, signals that travel from the site of axotomy to the soma, and the second messengers that are activated there. The responses in neurons and non-neuronal cells during neural development and injury are coordinated by chemical messenger systems that are highly conserved, including neurotransmitters, cytokines, and neurotrophins. The nervous system is modified in learning paradigms by some of the same messenger systems activated by injury, because learning and injury both challenge neurons to change. The conservation of basic mechanisms that coordinate neuronal plasticity allows us to approach basic questions in relatively simple nervous systems with reasonable confidence that the findings will be relevant for other nervous systems, including possible applications to the mammalian nervous system.
Animals↗
[Second messengers in the regulation of nerve cell plasticity during learning].
A review of 1972 to 1988 publications is presented, as well the data obtained by the authors on the influence of second messengers and their intracellular receptors on neuron plasticity in the learning experimental models. The emphasis is laid on cyclic 3',5'-adenosine monophosphate; cyclic 3',5'-guanosine monophosphate, calcium ions and their intracellular receptor calmodulin, as well as on the metabolites of phosphoinositide exchange: inositol-1, 4, 5-trisphosphate, 1,2-diacylglycerol and protein kinase C activated by the latter and arachidonic acid.
Animals↗