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Results for “Neuronal Plasticity”

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PubMed1985

Dendritic spines: role of active membrane in modulating synaptic efficacy.

Dendritic spines have been increasingly implicated as sites for neuronal plasticity. Earlier-theoretical studies of dendritic-spine function have assumed passive membrane, and have consequently predicted that postsynaptic potentials in the dendrite are attenuated when the synapse is located on the spine head rather than on the dendritic shaft. Our studies show that active membrane in the spine head (e.g. voltage-dependent Na+ or Ca2+ channels) can produce amplification rather than attenuation of the postsynaptic potential. The presence and amount of amplification depend on the density of active channels and on the spine-neck resistance. For a given type of spine head, there is an optimal spine-neck resistance; a given change in neck resistance can therefore either increase or decrease the amplitude of postsynaptic potentials. These results support the idea that spines mediate synaptic plasticity and suggest a variety of modulatory mechanisms.

Calcium↗

PubMed1990

Identification of injury-induced mitotic cells in adult rat cerebral cortex by neuron-specific markers.

Adult rat brains were injured by partial decortication. Four days later, the brains were examined for mitotic cells that were immunostained for neuronal markers: the neuron-specific enolase (NSE) and neurofilaments (NF). Of the 30 rats stained for NSE, 15 were found to have NSE-positive cells containing mitotic figures; of the 25 rats stained for NF, 12 possessed NF-positive cells in mitosis. Most of the mitotic neurons were granule cells and small- and medium-size pyramidal cells and were located in cortical layer III within 500 microns from the wound margin. Although a rare phenomenon, mitosis of neurons in the neocortex of mature mammalian brains may reflect neuronal plasticity in response to injury.

Animals↗

PubMed2001

Developmental changes in the expression of GABA(A) receptor subunits (alpha(1), alpha(2), alpha(3)) in the cat visual cortex and the effects of dark rearing.

The present study used Western blots and Northern slot blots to determine changes in the level of expression of GABA(A) receptor subunits alpha(1), alpha(2), and alpha(3), in relation to the "critical period" in cat visual cortex. Levels of the GABA(A) alpha(1) subunit were lowest at 1 week, increased four-fold to a maximum at 10 weeks, and declined slightly (35%) into adulthood. Levels of the GABA(A) alpha(2) and alpha(3) subunits were highest at 1 week of age, decreased two-fold by 10 weeks of age and were constant thereafter. Comparison between visual cortex from normal and dark-reared cats at 5 weeks and 20 weeks showed that alpha(1) and alpha(3) subunit expression was elevated in dark-reared animals by approximately 50% at both ages. alpha(2) expression was not affected. These results implicate the importance of a shift from putative immature to mature GABA(A) receptor subunits during the critical period of visual cortex and in conjunction with parallel analysis of NMDA receptor subunit maturation, further support the notion that a changing excitatory/inhibitory balance is critical for neuronal plasticity.

Animals↗

PubMed1993

Molecular characterization of NMDA and metabotropic glutamate receptors.

Our molecular studies have revealed the existence of a large number of different subunits or subtypes for the NMDA and metabotropic glutamate receptors. The individual receptors show functional variabilities and distinct expression patterns in the CNS. The NMDA receptors belong to the ligand-gated ion channel family and consist of a key subunit NMDAR1 and four accessory subunits NMDAR2A-NMDAR2D. The combination of NMDAR1 and NMDAR2 in heteromeric configurations potentiates glutamate response and produces a functional variability. All the NMDAR subunits have an asparagine residue at the corresponding position of the second transmembrane segments, and these residues are thought to be responsible for controlling Ca2+ permeation and the channel blockade by Mg2+ and cationic channel blockers. Individual NMDAR subunit mRNAs are different in their expression patterns during development and in the adult brain. The mGluR family consists of at least six different subtypes. These subtypes are divided into three subgroups according to their sequence similarities, signal transduction mechanisms, and pharmacological properties. Although their physiological roles largely remain to be elucidated, the retinal L-AP4-sensitive mGluR may have a specific function that mediates excitatory neurotransmission in the visual system. It is thus undoubtedly important to investigate specific functions of different combinations of the NMDA receptor subunits and different subtypes of mGluRs and to explore the molecular mechanisms of glutamate receptor-mediated neuronal plasticity and neurotoxicity.

Animals↗

PubMed1992

Neuronal aspects and plasticity of inferior olivary complex and nucleus dentatus.

In primary or physiological ageing, the brain undergoes a 10% weight reduction. This datum was confirmed in vivo by radiological investigation and post mortem by morphological research (Grandi and Coll. 1990, 1990, 1991, 1991), that underscores the same reduction in the medulla oblongata and in the cerebellum. Morphological and cytohistological aspects of primary ageing have been considered for the inferior olivary nucleus and for the dentate nucleus in 41 male subjects, 32 belonging to the decades 7th, 8th, 9th, and 9 to the decades from the 3rd to the 6th. From the two latter structures, separated along standard cut surfaces, serial histological slices were carried out, and histochemical reactions were accomplished, together with immunohistochemistry, for synaptophysin, NF-2F11, NSE, S-100, GFAP, chromogranin. As the weight progressively decreased from the 7th to the 9th decade, it was noted neuronal loss, both in the inferior olivary nucleus, and in the dentate nucleus. Furthermore, the loss appeared to be followed by substitutive astroglial proliferation. Immunocytochemical reaction for synaptophysin revealed peculiar aspects. A consistently regular result of such method concerned the two nuclei studied, in primary ageing, thus allowing the interpretation of the perfect structure of synaptic vesicles as an indirect argument for neuronal plasticity.

Adult↗

PubMed1997

Is activation of the metabotropic glutamate receptors impaired in the hippocampal CA1 area of the aged rat?

The effects of aging on activation of metabotropic glutamate (mGlu) receptors were studied in the CA1 field of hippocampal slices from young (3- to 4-month-old) and aged (24- to 27-month-old) Sprague-Dawley rats with the use of ex vivo electrophysiological recording techniques. The depolarization of membrane potential, the increase in input resistance, and the blockade of the afterhyperpolarization induced in pyramidal cells of young rats by bath application of the mGlu receptor agonist (+/-)-trans-1-aminocyclopentate-1,3-dicarboxylic acid were not altered in aged animals. No age-related changes of the depressive effects of the mGlu receptor agonist were found on either the excitatory glutamatergic postsynaptic potential or the GABA-mediated inhibitory postsynaptic potentials induced by the stimulation of the stratum radiatum. The magnitude of synaptic plasticity involving mGlu receptor activation, although weaker, was not significantly altered in aged rats. This absence of age-related effects on activation of mGlu receptors may be important in understanding the possible origins of the alterations in neuronal plasticity which occur in brain aging.

2-Amino-5-phosphonovalerate↗

PubMed1993

Glial cell functions and activity-dependent plasticity of the mammalian visual cortex.

The presence of highly ordered connectivities is one basic characteristic of the central nervous systems and is believed to be a prerequisite for its proper function. The elaboration of precise, topographic projections has been shown to include two subsequent steps: (1) The formation of exuberant projections with limited topographic accuracy, and (2) the activity-dependent refinement of the appropriate connectivities by synapse elimination and synapse stabilization. Although most current theories on the mechanisms underlying activity-dependent developmental plasticity focus on adaptive changes of the efficacy of synaptic transmission, the present overview deals with possible mechanisms underlying morphologic adaptations in the developing central nervous system. Especially the contribution of glial cells in the activity-dependent selection of neuronal projections in the thalamocortical visual system of higher mammals is elaborated and a unifying hypothesis on the involvement of nonneuronal cells in neuronal plasticity is formulated on the basis of the current knowledge on glial physiology and specific experimental data.

Animals↗

PubMed1998

The distribution of intramural nerves in urinary bladder after partial denervation in the female rat.

We evaluated the degree of neuronal plasticity following a partial denervation of the rat urinary bladder. Using acetylcholinesterase staining we found that the postganglionic nerves from the pelvic ganglion reach the intact bladder as 1-4 nerve trunks on each side, slightly ventral and caudal to the ureteral orifices. Normally a few thinner nerves also reach the bladder posterolateral to the ureterovesical junction. The nerves ventral to the ureters run in the ventral longitudinal muscle layer as well-defined trunks with a pattern that does not differ much from one animal to another. The nerves reaching the bladder dorsolaterally innervate the dorsolateral aspects in a more irregular fashion. Some anastomoses are found across the midline between nerves from either side. This nerve pattern is already in place in newborn rats. After removal of the pelvic ganglion on one side in the adult rat the ipsilateral ventral nerves rapidly degenerate, whereas some dorsolateral nerves usually survive. Axons from the intact ventral nerves can be seen crossing over to the denervated side in the anastomoses. After 13 weeks the surviving ventral nerves, which normally run at some distance from the ventral midline, now run in the midline with equal amounts of ventral longitudinal muscle on either side, and with their branches evenly distributed to both sides. The same pattern is seen after 27 weeks. Unilateral ganglionectomy in 3-week-old rats leads to the same changes in nerve distribution as in the adult rat. We conclude that there is a high degree of plasticity in the bladder innervation following a partial denervation, and that this plasticity includes the distribution of its main intramural nerve trunks.

Acetylcholinesterase↗

PubMed1997

Functions for interneuronal nets in the hippocampus.

Recent advances in the physiology of hippocampal interneurons are summarized in this article. These findings suggest that through their interconnectivity inhibitory interneurons can maintain large-scale oscillations at various frequency ranges (theta, gamma, and 200-Hz bands). We suggest that networks of inhibitory interneurons within the forebrain impose coordinated oscillatory "contexts" for the "content" carried by networks of principal cells. These oscillating inhibitory networks may provide the precise temporal structure necessary for ensembles of neurons to perform specific functions, such as memory trace formation and retrieval. In addition, synaptic inhibition is shown to reduce the somadendritic backpropagation of sodium spikes and to prevent the occurrence of calcium spikes in dendrites. These observations indicate that interneurons are in an excellent position to control neuronal plasticity and allow synaptic transmission either with or without long-term modification of synaptic strength.

Hippocampus↗

PubMed1994

Spinal mediators of hyperalgesia.

Neuronal plasticity associated with altered sensations arising from tissue damage involves both established (e.g. substance P and excitatory amino acids) and novel (e.g. nitric oxide and metabolites of arachidonic acid) mediators released from terminals of primary afferent neurons or synthesised in the spinal cord. These and other mediators lead to activity-dependent synaptic plasticity and enhanced sensitivity to noxious stimuli (hyperalgesia). Activation of the N-methyl-D-aspartate (NMDA) receptor results in a calcium-dependent production of nitric oxide, while activation of alpha-amino-3-hydroxy-5-methylisoxazole-5-propionate (AMPA)-and 1,3- trans-1-amino-cyclopentyl-1,3-dicarboxylate (trans-ACPD)-sensitive glutamate receptors results in a phospholipase A2 (PLA2)-mediated production of different intracellular mediators, including arachidonic acid. Thermal hyperalgesia requires NMDA receptor activation and is primarily mediated by production of nitric oxide. Mechanical hyperalgesia requires AMPA and metabotropic glutamate receptor coactivation, and is primarily mediated by cyclo-oxygenase products of arachidonic acid metabolism.

Animals↗

PubMed2001

Insulin-like growth factor I potentiates kainate receptors through a phosphatidylinositol 3-kinase dependent pathway.

Neurotrophic factors modulate synaptic plasticity through mechanisms that include regulation of membrane ion channels and neurotransmitter receptors. Recently, it was shown that insulin-like growth factor I (IGF-I) induces depression of AMPA-mediated currents without affecting NMDA-receptor function in neurons. We now report that IGF-I markedly potentiates the kainate-preferring ionotropic glutamate receptor in young cerebellar granule neurons expressing functional kainate-, but not AMPA-mediated currents. Potentiation of kainate responses by IGF-I is blocked by wortmannin, a phosphatidylinositol 3-kinase (P13K) inhibitor, indicating a role for this kinase in the effect of IGF-I. These results reinforce the notion that modulation of ionotropic glutamate receptors are involved in the regulatory actions of IGF-I on neuronal plasticity.

Androstadienes↗

PubMed1999

Robust suppression of afferent-induced excitation in the rat spinal dorsal horn after conditioning low-frequency stimulation.

The neuronal plasticity in the spinal dorsal horn induced after conditioning low-frequency stimulation of afferent A fibers, and its relationship with spinal inhibitory networks, was investigated with an optical-imaging method that detects neuronal excitation. High-intensity single-pulse stimulation of the dorsal root activating both A and C fibers evoked an optical response in the dorsal horn in transverse slices of 12- to 25-day-old rat spinal cords stained with a voltage-sensitive dye, RH-482. The optical response, reflecting the net excitation of neuronal elements along the thickness of each slice, was suppressed after a conditioning low-frequency stimulation (0.2-1 Hz for 10 min) to A fibers in the dorsal root. The degree of suppression was largest in the lamina II of the dorsal horn (48% reduction), where the majority of C fibers terminate, and much less in the deeper dorsal horn (5% reduction in laminae III-IV). The onset of suppression was somewhat slow; after the low-frequency stimulation, the magnitude of excitation gradually decreased, reached the maximum effect 30 min after the conditioning, and remained at the suppressed level for >1 h. Suppression was not observed when the low-frequency stimulation was given during a 20-min perfusion with a solution containing an NMDA-receptor antagonist, DL-2-amino-5-phosphonovaleric acid (30 microM). A brief application of an opioid-receptor antagonist, naloxone (0.5 microM), inhibited the induction, but not the maintenance, of low-frequency stimulus-induced suppression. However, treatments with the GABA(A) receptor antagonist bicuculline (1 microM) and the glycine receptor antagonist strychnine (0.3 microM) did not affect suppression induction and maintenance. In conclusion, conditioning low-frequency stimulation to A fibers interferes with the afferent-induced excitation in the dorsal horn. The low-frequency stimulation-induced suppression is maintained by a reduction of glutamatergic excitatory transmissions in the dorsal horn, not by an enhanced inhibition. Activation of the spinal opioid-mediated system by low-frequency stimulation, but not the inhibitory amino acid-mediated system, is necessary to initiate robust suppression. The long-term depression of afferent synaptic efficacy onto excitatory interneurons likely takes the primary role in the robust suppression of neuronal excitation in the dorsal horn.

2-Amino-5-phosphonovalerate↗

PubMed1994

Androgen regulates gene expression of cytoskeletal proteins in adult rat motoneurons.

Expression of beta-actin and beta-tubulin mRNA was examined in androgen-sensitive motoneurons of the spinal nucleus of the bulbocavernosus (SNB) in adult male rats by in situ hybridization histochemistry using complementary DNAs encoding chick beta-actin and mouse beta-tubulin, respectively. Both hybridizable beta-actin and beta-tubulin mRNAs were localized in the somata and proximal dendrites of SNB motoneurons. Removal of androgen by castration significantly reduced the expression levels of both beta-actin and beta-tubulin mRNAs in the SNB motoneurons, whereas the changes were prevented by testosterone treatment. In contrast, castration or testosterone treatment induced little or no change in the expression levels of these mRNAs in the much less androgen-sensitive motoneurons of the retrodorsolateral nucleus (RDLN). These results suggest that androgen regulates the expression of beta-actin and beta-tubulin genes in the SNB motoneurons and may provide evidence for the molecular mechanisms of hormonally induced neuronal plasticity in the SNB motoneurons.

Actins↗

PubMed1992

Depolarization- and agonist-regulated expression of neuronal metabotropic glutamate receptor 1 (mGluR1).

In established 8-12-day-old primary cultures of differentiated rat cerebellar granule neurons the level of metabotropic glutamate receptor 1 (mGluR1) mRNA and the sensitivity of cultures to the agonist-stimulated inositol phosphate (IP) formation was reversibly modified by changing the depolarizing properties of the medium, i.e. the medium KCl concentration. The mGluR1 mRNA content was suppressed by increasing the medium KCl content and elevated by decreasing it. The mGluR agonist quisqualate inhibited the mGluR1 expression. This is the first direct demonstration of a differential expression of neuronal mGluR1 in an established neuronal culture. The model can be used to study the molecular mechanism of neuronal plasticity.

Animals↗

PubMed1999

Central nervous system plasticity and persistent pain.

Nerve signals arising from sites of tissue or nerve injury lead to long-term changes in the central nervous system and contribute to hyperalgesia and the amplification and persistence of pain. These nociceptor activity-induced changes are referred to as central sensitization. Central sensitization involves an increase in the excitability of medullary and spinal dorsal horn neurons brought about by a cascade of events, including neuronal depolarization, removal of the voltage-dependent magnesium block of the N-methyl-D-aspartate (NMDA) receptor, calcium entry into neurons, phosphorylation of the NMDA receptor, a change in the cell's excitability, and an increase in synaptic strength. These changes also include activation of other ionotropic and metabotropic excitatory amino acid receptors, neuropeptides such as substance P, neurotrophins, and kinases involved in the phosphorylation process. Central sensitization occurs in trigeminal nociceptive pathways, and more robust neuronal hyperexcitability occurs following deep tissue stimulation than following cutaneous stimulation. By means of Fos protein immunocytochemistry, researchers have found that 2 distinct regions are activated: the subnucleus interpolaris/caudalis transition zone (Vi/Vc) and the caudal subnucleus caudalis. The latter exhibits changes very similar to those in the spinal dorsal horn, but the Vi/Vc zone likely is involved in autonomic nervous system processing and activation of the pituitary-adrenal axis. Descending systems are also an important component of the central sensitization process and provide the neural networks by which cognitive, attentional, and motivational aspects of the pain experience modulate pain transmission. These findings of nociceptor activity-induced neuronal plasticity have important clinical implications in the development of new approaches to the management of persistent pain.

Chronic Disease↗

PubMed2004

M2 muscarinic acetylcholine receptor knock-out mice show deficits in behavioral flexibility, working memory, and hippocampal plasticity.

Muscarinic acetylcholine receptors are known to play key roles in facilitating cognitive processes. However, the specific roles of the individual muscarinic receptor subtypes (M1-M5) in learning and memory are not well understood at present. In the present study, we used wild-type (M2+/+) and M2 receptor-deficient (M2-/-) mice to examine the potential role of M2 receptors in learning and memory and hippocampal synaptic plasticity. M2-/- mice showed significant deficits in behavioral flexibility and working memory in the Barnes circular maze and the T-maze delayed alternation tests, respectively. The behavioral deficits of M2-/- mice were associated with profound changes in neuronal plasticity studied at the Schaffer-CA1 synapse of hippocampal slices. Strikingly, short-term potentiation (STP) was abolished, and long-term potentiation (LTP) was drastically reduced after high-frequency stimulation of M2-/- hippocampi. Treatment of M2-/- hippocampal slices with the GABA(A) receptor antagonist, bicuculline, restored STP and significantly increased LTP. Whole-cell recordings from CA1 pyramidal cells demonstrated a much stronger disinhibition of GABAergic than glutamatergic transmission in M2-/- hippocampi, which was particularly prominent during stimulus trains. Increased strength of GABAergic inhibition is thus a likely mechanism underlying the impaired synaptic plasticity observed with M2-/- hippocampi. Moreover, the persistent enhancement of excitatory synaptic transmission in CA1 pyramidal cells induced by the transient application of a low concentration of a muscarinic agonist (referred to as LTP(m)) was totally abolished in M2-/- mice. Because impaired muscarinic cholinergic neurotransmission is associated with Alzheimer's disease and normal aging processes, these findings should be of considerable therapeutic relevance.

Amnesia↗

PubMed1998

Neuronal damage and plasticity identified by microtubule-associated protein 2, growth-associated protein 43, and cyclin D1 immunoreactivity after focal cerebral ischemia in rats.

BACKGROUND AND PURPOSE: An objective of therapeutic intervention after cerebral ischemia is to promote improved functional outcome. Improved outcome may be associated with a reduction of the volume of cerebral infarction and the promotion of cerebral plasticity. In the developing brain, neuronal growth is concomitant with expression of particular proteins, including microtubule-associated protein 2 (MAP-2), growth-associated protein 43 (GAP-43), and cyclin D1. In the present study we measured the expression of select proteins associated with neurite damage and plasticity (MAP-2 and GAP-43) as well as cell cycle (cyclin D1) after induction of focal cerebral ischemia in the rat. METHODS: Brains from rats (n=28) subjected to 2 hours of middle cerebral artery occlusion and 6 hours, 12 hours, and 2, 7, 14, 21, and 28 days (n=4 per time point) of reperfusion and control sham-operated (n=3) and normal (n=2) rats were processed by immunohistochemistry with antibodies raised against MAP-2, GAP-43, and cyclin D1. Double staining of these proteins for cellular colocalization was also performed. RESULTS: Loss of immunoreactivity of both MAP-2 and GAP-43 was observed in most damaged neurons in the ischemic core. In contrast, MAP-2, GAP-43, and cyclin D1 were selectively increased in morphologically intact or altered neurons localized to the ischemic core at an early stage (eg, 6 hours) of reperfusion and in the boundary zone to the ischemic core (penumbra) during longer reperfusion times. CONCLUSIONS: The selective expressions of the neuronal structural proteins (MAP-2 in dendrites and GAP-43 in axons) and the cyclin D1 cell cycle protein in neurons observed in the boundary zone to the ischemic core are suggestive of compensatory and repair mechanisms in ischemia-damaged neurons after transient focal cerebral ischemia.

Animals↗

PubMed2006

Adult neurogenesis in a moth brain.

In both vertebrates and invertebrates, neurogenesis not only occurs during development but also persists throughout adult life. So far, adult neurogenesis has been detected in a few insect orders but not in Lepidoptera. In the moth, Agrotis ipsilon, the sensitivity of antennal lobe interneurons of males to sex pheromone is age- and juvenile hormone-dependent in accordance with changes in the behavioral response. As a first step to understand this neuronal plasticity, we tested the hypothesis that adult neurogenesis could occur in the moth brain using 5-bromo-2'-deoxyuridine injections on newly born and sexually mature moths. Our results show that persistent neurogenesis occurs in mushroom bodies of adult males and females of A. ipsilon. Two clusters of one to four neuroblasts in each brain hemisphere continue to divide in adult moths and give rise to small clusters of Kenyon cells in the cortex of the mushroom body calyces. Neurogenesis was observed in both newly born and sexually mature males. There was a clear increase in the number of newly born cells in brains as the time increased after the treatment that was performed soon after emergence. When treatments were performed in mature 3-day-old adults, neurogenesis was still detected in brains dissected 3 hours after treatment but was hardly visible 2 days later. Adult neurogenesis was also detected in the optic lobes but not in the antennal lobes. We hypothesize that the newly born neurons could play a role in the central nervous plasticity of olfactory processing in the adult moth A. ipsilon.

Age Factors↗