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PubMed2006

Group I mGluR regulates the polarity of spike-timing dependent plasticity in substantia gelatinosa neurons.

The spinal synaptic plasticity is associated with a central sensitization of nociceptive input, which accounts for the generation of hyperalgesia in chronic pain. However, how group I metabotropic glutamate receptors (mGluRs) may operate spinal plasticity remains essentially unexplored. Here, we have identified spike-timing dependent synaptic plasticity in substantia gelatinosa (SG) neurons, using perforated patch-clamp recordings of SG neuron in a spinal cord slice preparation. In the presence of bicuculline and strychnine, long-term potentiation (LTP) was blocked by AP-5 and Ca2+ chelator BAPTA-AM. The group I mGluR antagonist AIDA, PLC inhibitor U-73122, and IP3 receptor blocker 2-APB shifted LTP to long-term depression (LTD) without affecting acute synaptic transmission. These findings provide a link between postsynaptic group I mGluR/PLC/IP3-gated Ca2+ store regulating the polarity of synaptic plasticity and spinal central sensitization.

2-Amino-5-phosphonovalerate↗
PubMed2004

Regulation of neuromodulator receptor efficacy--implications for whole-neuron and synaptic plasticity.

Membrane receptors for neuromodulators (NM) are highly regulated in their distribution and efficacy-a phenomenon which influences the individual cell's response to central signals of NM release. Even though NM receptor regulation is implicated in the pharmacological action of many drugs, and is also known to be influenced by various environmental factors, its functional consequences and modes of action are not well understood. In this paper we summarize relevant experimental evidence on NM receptor regulation (specifically dopamine D1 and D2 receptors) in order to explore its significance for neural and synaptic plasticity. We identify the relevant components of NM receptor regulation (receptor phosphorylation, receptor trafficking and sensitization of second-messenger pathways) gained from studies on cultured cells. Key principles in the regulation and control of short-term plasticity (sensitization) are identified, and a model is presented which employs direct and indirect feedback regulation of receptor efficacy. We also discuss long-term plasticity which involves shifts in receptor sensitivity and loss of responsivity to NM signals. Finally, we discuss the implications of NM receptor regulation for models of brain plasticity and memorization. We emphasize that a realistic model of brain plasticity will have to go beyond Hebbian models of long-term potentiation and depression. Plasticity in the distribution and efficacy of NM receptors may provide another important source of functional plasticity with implications for learning and memory.

Animals↗
PubMed1998

The cell cycle gene SKP1 is regulated by light in postnatal rat brain.

During the early postnatal phase of high neuronal plasticity, an altered visual input leads to great modifications of visual cortex organization [Y. Frégnac, M. Imbert, Development of neuronal selectivity in primary visual cortex of cat, Physiol. Rev., 64 (1984) 375-434; D.H. Hubel, T.N. Wiesel, S. LeVay, Plasticity of ocular dominance columns in monkey striate cortex, Philos. Trans. R. Soc. London, Ser. B, 278 (1977) 377-409.]. We used refined differential screening of an organized cDNA library to identify the genes that may participate in this plasticity. We isolated a candidate plasticity gene encoding for a 163 aa protein that is closely related to the human and yeast Skp1p, a key factor in cell cycle progression [C. Baï, K. Hofman, L. Ma, M. Goebl, J.W. Harper, S.J. Elledge, SKP1 connects cell cycle regulators to the ubiquitin proteolysis machinery through a novel motif, the F-box, Cell, 86 (1996) 263-274; C. Connelly, P. Hieter, Budding yeast SKP1 encodes an evolutionary conserved kinetochore protein required for cell cycle progression, Cell, 86 (1996) 275-285; H. Zhang, R. Kobayashi, K. Galaktionov, D. Beach, p19Skp1 and p45Skp2 are essential elements of the cyclin A-CDK2 S phase kinase, Cell, 82 (1995) 915-925.]. Northern blot analysis showed that the expression of SKP1 (Skp1p gene) dramatically decreased after 2 h of light stimulation in the visual cortex of young dark-reared rats. This down regulation lasted at least 72 h. It was specific for the critical period as we did not observe any significant regulation of SKP1 mRNA by light in adult dark-reared rat brain. The down regulation was observed in the superior colliculus but also in the frontal cortex and in the hippocampus. The fact that this down regulation was not restricted to the visual system, suggested that it could be produced by dark rearing-induced hormonal changes. The significance of SKP1 expression in the brain and its regulation are discussed.

Animals↗
PubMed2005

Long-term synaptic facilitation in defensive behavior command neurons in the snail during acquisition of sensitization depends on RNA synthesis.

Experiments on defensive behavior command neuron LP11 in semi-intact common snails preparations were performed to study transcription processes underlying the mechanisms of neuronal plasticity during acquisition of nociceptive sensitization. Application of nociceptive stimuli to the heads of control snails led to increases in neuron membrane excitability, along with biphasic changes in responses to tactile and chemical sensory stimulation--with depressed responses at the short-term stage and facilitation in the long-term stage of sensitization. Acquisition of sensitization after application of the RNA synthesis inhibitor actinomycin D (20 microM) to neuron LP11 led to complete suppression of synaptic facilitation in responses to sensory stimulation in the long-term stage of sensitization, but had no effect on the short-term depression of responses. However, the inhibitor had no effect on changes in membrane excitability in these conditions. Application of actinomycin D 30 min after the end of the sensitization acquisition process (1 h after the process started) had no effect on membrane excitability or synaptic facilitation. It is suggested that the induction of long-term synaptic facilitation in neuron LP11 during acquisition of nociceptive sensitization is dependent on RNA synthesis occurring in a narrow time interval, while changes in membrane excitability during the 2-3 h after acquisition of sensitization and short-term synaptic plasticity are independent of transcription processes.

Action Potentials↗
PubMed1998

Age-dependent neurotransmitter plasticity of ciliary ganglion neurons.

We have examined neurotransmitter plasticity in postmitotic cholinergic neurons isolated from 6.5- to 11-day-old embryonic quail ciliary ganglia. Purified neurons were labeled with DiI, transplanted into the trunk of young chick embryos, and assayed for catecholamine content and [3H]thymidine uptake 4 to 5 days later. For ciliary neurons derived from 6.5- to 8-day-old embryos, as many as 25% (average of 9% overall) expressed catecholamines in the host sympathetic ganglia, migratory stream, aortic plexuses, and adrenal medulla. In contrast, neurons from >8-day-old ganglia did not acquire or produce detectable catecholamines, indicating a limited time period over which phenotypic conversion can occur in vivo. As a control, ciliary neurons were also injected into the head mesenchyme of young embryos; no catecholamine expression was observed. Interestingly, after transplantation some DiI-labeled postmitotic ciliary neurons took up [3H]thymidine with or without phenotypic change. These results suggest that phenotypic plasticity in ciliary neurons is age-dependent, is location-dependent, and may involve resumption of DNA replication, a characteristic feature of some differentiating adrenergic sympathetic neurons. Apoptosis of a few proliferating transplanted cells may be induced independently or in association with transmitter change.

Adrenal Medulla↗
PubMed1997

Neuronal loss and plasticity in the supraoptic nucleus in Parkinson's disease.

Disturbed circadian control of renal water excretion and blood pressure adaptation in Parkinson's disease (PD) suggest impaired hypothalamic magnocellular neurosecretion. To test the hypothesis that this may relate to specific hypothalamic pathology in PD, we studied morphometrically the neuronal population of the supraoptic nucleus (SON) in PD patients and controls. Neuronal loss in the SON of PD patients was associated with increased somatic, nuclear, and nucleolar size of remaining neurons, suggesting compensatory response of these cells. We conclude that SON pathology is a feature of PD and may account for specific signs of neurohumoral dysfunction.

Aged↗
PubMed2002

Oxytocin-secreting neurons: A physiological model of morphological neuronal and glial plasticity in the adult hypothalamus.

Oxytocin-secreting neurons of the hypothalamoneurohypophysial system undergo reversible morphological changes whenever they are strongly stimulated. In the hypothalamus, such structural plasticity is represented by modifications in the size and shape of their somata and dendrites, in the extent to which their surfaces are covered by glia, and in the density of their synapses. In the neurohypophysis, there is a parallel reduction in glial (pituicyte) coverage of their axons together, with retraction of pituicyte processes from the perivascular basal lamina and an increase in the number and size of their terminals. These changes occur rapidly, within a few hours. On the other hand, the system returns to its prestimulated condition on arrest of stimulation at a rate that depends on the length of time it has remained activated. Such neuronal-glial changes have several functional consequences. In the hypothalamic nuclei, reduction in astrocytic coverage of oxytocinergic neurons and their synapses modifies extracellular ionic homeostasis and glutamate clearance and, therefore, their overall excitability. Since it results in extensive dendritic bundling, it may also lead to ephaptic interactions and may facilitate dendritic electrotonic coupling. A most important indirect effect may be to permit synaptic remodeling that occurs concomitantly and that results in significant increases in the number of excitatory and inhibitory synapses driving their activity. In the stimulated neurohypophysis, glial retraction results in increased levels of extracellular K+ which can enhance neurohormone release while an enlarged neurovascular contact zone may facilitate diffusion of neurohormone into the circulation. Ongoing work aims to unravel the cell mechanisms and factors underlying such plasticity and has revealed that neurons and glia of the hypothalamoneurohypophysial system continue to express juvenile molecular features associated with similar neuronglial interactions and synaptic events during development and regeneration. They include strong expression of cell surface adhesion molecules like F3/contactin and polysialylated neural cell adhesion molecule, extracellular matrix glycoproteins like tenascin C, and cytoskeletal proteins like vimentin and microtubule-associated protein 1D. Some of these molecules reach the cell surface constitutively while others follow the activity-dependent regulated pathway. We consider many of these molecular features permissive, allowing oxytocin neurons and their glia to undergo morphological remodeling throughout life, provided the proper stimulus intervenes. In the hypothalamic nuclei, one such stimulus is centrally released oxytocin; in the neurohypophysis, an adrenergic, cAMP-mediated mechanism appears responsible.

Animals↗
PubMed2002

SCG10-related neuronal growth-associated proteins in neural development, plasticity, degeneration, and aging.

Neuronal growth-associated proteins (nGAPs) are in general neuron-specific gene products whose expression correlates tightly with neuronal process outgrowth and/or regeneration, and are mostly good downstream targets of neurotrophin stimulation. Expression of genes encoding nGAPs such as GAP-43, SCG10, and stathmin is upregulated following lesioning of cortical and hippocampal regions of the adult rat brain. In the brains of aged animals, however, the magnitude of the response is reduced, whereas the time course of the response is mostly unchanged when compared with that for brains of young ones. Expression of GAP-43 and stathmin is reduced by aging, and is also changed in age-related neurodegenerative conditions such as Alzheimer's disease in humans. Certain nGAPs are induced during long-term potentiation (LTP) and also during critical periods of song-learning and ocular dominance column formation in birds and cats, respectively. Recent evidence further supports the idea that functional synaptic modulation is often associated with remodeling of synaptic structures. These results suggest that neurotrophin-responsive nGAPs serve as molecular markers of neuronal plasticity during development and aging, and that the neuronal plasticity decreases, at least in certain neuronal circuits, in the aged brain and neurodegenerative diseases. Recent findings on the roles of stathmin and SCG10-related proteins in microtubule destabilization and its functional block by phosphorylation further support the importance of the SCG10 family proteins in neuronal cytoskeletal regulation, particularly as to microtubule dynamics. We summarize here a decade of research on SCG10 and its related molecules with special interests to brain aging and disease.

Aging↗
PubMedDate not supplied

Involvement of nerve growth factor in visual cortex plasticity.

The physiological role of nerve growth factor (NGF), the prototype member of the neurotrophin family, has been widely studied. NGF has been shown to promote survival, sprouting and differentiation of sympathetic ganglion cells and sensory neurons in the peripheral nervous system; it has also been shown to support survival and regeneration of cholinergic neurons in the central nervous system. Recent evidence indicates that NGF is also involved in the neuronal plasticity of the visual cortex. Exogenous supplies of NGF have been shown to interfere with normal processes underlying activity- and age-dependent synaptic modifications in both developing and adult visual cortex. In parallel to these physiological effects, numerous neuronal markers in the visual cortex have been found to be influenced by NGF. Several proposals have been introduced to explain the physiological role of NGF in visual cortex plasticity. Although the mechanisms underlying NGF effects in the visual cortex are still under active investigation, current evidence implies that NGF, and perhaps other neurotrophins as well, may be useful for preventing or correcting inappropriate or anomalous connections in the visual cortex, and thus for treating visual dysfunctions such as amblyopia and strabismus.

Animals↗
PubMed2002

Neurotrophins and their receptors in the primary olfactory neuraxis.

The primary olfactory pathway is an elegant and simple system in which to study neurogenesis and neuronal plasticity because of the simple fact that olfactory receptor neurons (ORNs) are continually generated throughout the adult lifetimes of vertebrates. Thus, neuronal birth, differentiation, survival, axon pathfinding, target recognition, synapse formation, and cell death are developmental events that can be examined in the mature olfactory epithelium (OE). Neurotrophins (nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3, and 4/5) are a family of bioactive peptides that exert their effects by interacting with high- and low-affinity receptors on the surfaces of responsive cells, and have been implicated in several stages of neuronal development throughout the central and peripheral nervous system (CNS and PNS). There has been significant interest within the olfactory community as to how these multifunctional peptides might regulate the cycle of degeneration and regeneration of olfactory receptor neurons. The focus of this review is to highlight what is known about the actions of neurotrophins in the primary olfactory pathway, and to pinpoint future directions that will enable us to further understand their role in olfactory receptor neuron development and turnover.

Animals↗
PubMed2003

Effects of patch or gel estrogen therapies on auditory brainstem response in surgically postmenopausal women: a prospective, randomized study.

OBJECTIVE: To study the effects of gonadal steroids on the nongenital audiological target in surgically postmenopausal women treated with patch or gel transdermal estrogen therapy (ET). DESIGN: Prospective randomized study. SETTING: Research Group for Sexology, University of Catania, Italy. PATIENT(S): One hundred twenty-two surgically postmenopausal women. INTERVENTION(S): Transdermal E(2) by patch or gel, and evaluation of auditory brainstem response by auditory-evoked potentials for waves I, III, and V latencies, and for interpeak I-III, I-V, and III-V intervals. MAIN OUTCOME MEASURE(S): Changes in auditory wave latencies and in interpeak intervals during treatment with ET with respect to baseline levels. RESULT(S): One hundred two women completed the study. Forty-eight subjects used E(2) patches and 54 E(2) gel. No significant difference was observed in plasma E(2) improvement and in auditory brainstem response values with the two estrogen (E) formulations. The wave latencies and the interpeak intervals showed lower values during the E treatment than at baseline. CONCLUSION(S): Auditory brainstem response seems to depend on the type of E given. Our data suggest that fluctuating E levels act on waves, even if the exact mechanism of the gonadal steroids is not clear. However, we believe that E could influence neuronal plasticity, the metabolic levels of neurotransmitters, and thus, the neuronal conduction time into the audiological system.

Administration, Cutaneous↗
PubMed2002

N-CAM expression and localization in PC12 cells modulated by extracellular peptides.

The neural cell adhesion molecules (N-CAMs) play an important role in mediating cell-cell interactions in the nervous system. Different isoforms of these membrane proteins are involved in the formation of the neuronal network and in the dynamic phases of neuronal plasticity. We studied the early stages of the pseudo neuronal differentiation of PC12 cells induced by a class of small acidic peptides capable of modulating gene expression in these cells. The data presented here indicate that peptides with specific sequences induce an increase in N-CAM mRNA expression and protein translocation to the plasma membrane to a comparable degree as NGF.

Animals↗
PubMedDate not supplied

Auditory brainstem response in postmenopausal women treated with hormone replacement therapy: a pilot study.

OBJECTIVE: To research the nongenital audiological target for gonadal steroids in postmenopausal women who are treated with hormone replacement therapy. DESIGN: Fifty postmenopausal volunteers were treated with hormone replacement therapy. Women with an intact uterus had sequential weekly transdermal estradiol plus nomegestrole acetate 5 mg orally for 12 days per month or a continuous daily oral dose of conjugated estrogen 0.625 mg and medroxyprogesterone acetate 5 mg tablet. Eighteen surgically postmenopausal women received a weekly transdermal estradiol system. Twenty-five postmenopausal volunteers-5 with a natural menopause and 10 with a surgical menopause-and 20 premenopausal normally cycling women were used as a control group. Each woman performed auditory brainstem response by auditory-evoked potentials for waves I, III, and V and for interpeak I-III, I-V, and III-V intervals. RESULTS: Women who were treated with hormone replacement therapy showed wave latencies and interpeak latencies shorter than those for postmenopausal women in the control group (p < or = 0.05), overlapping those of the premenopausal women (p > 0.05). Women who were treated with estrogen replacement therapy showed shorter time latencies than those treated with combined hormone replacement therapy (p < or = 0.05). CONCLUSIONS: Our data suggest that fluctuating hormone levels cause changes in auditory brain-stem response waves, even if the exact mechanism of activity of the gonadal steroids is not clear. However, we believe that estrogen may influence the neuronal plasticity, the metabolic levels of neurotransmitters, and thus the neuronal conduction time into the audiological system.

Administration, Cutaneous↗
PubMed2003

[Musical hallucinations in the elderly].

Musical hallucinations (MH) are probably more frequent in the elderly than those reported in the literature. We will illustrate the clinical findings of MH with 3 personal cases. The differential diagnosis and the diagnostic tools relevant in clinical practice will be presented as well as the pathogenesis of deafferentiation-induced MH. MH can be considered as a phenomenon of neuronal plasticity and also serve as a model to understand neuronal networks involved in mental representation of music and hallucinations in general.

Aged↗
PubMed1997

[Integrins: their structures, functions and gene expressions in the central nervous system. Acta anat].

More than ten years have passed since integrin was shown to function in cellular attachment. To date integrin research has been one of major fields in cell biology. Integrin, which functions as an integrator of both extra- and intracellular skeletal molecules, is regarded as one of the essential molecules for cellular signal transduction as well. Thus, integrin appears to be essential and indispensable for many cellular phenomena. Although every type of cell is thought to express a few kinds of integrin molecules, their expression and functional roles in neurons remain to be determined. Both intensive and extensive researches should reveal one by one how integrins are involved in the neural network formation in development, neuronal plasticity and regeneration, higher function of CNS, and also neuronal degeneration in both inflammation and degenerative diseases.

Amino Acid Sequence↗
PubMed2006

NF-kappaB regulates spatial memory formation and synaptic plasticity through protein kinase A/CREB signaling.

Synaptic activity-dependent de novo gene transcription is crucial for long-lasting neuronal plasticity and long-term memory. In a forebrain neuronal conditional NF-kappaB-deficient mouse model, we demonstrate here that the transcription factor NF-kappaB regulates spatial memory formation, synaptic transmission, and plasticity. Gene profiling experiments and analysis of regulatory regions identified the alpha catalytic subunit of protein kinase A (PKA), an essential memory regulator, as a new NF-kappaB target gene. Consequently, NF-kappaB inhibition led to a decrease in forskolin-induced CREB phosphorylation. Collectively, these results disclose a novel hierarchical transcriptional network involving NF-kappaB, PKA, and CREB that leads to concerted nuclear transduction of synaptic signals in neurons, accounting for the critical function of NF-kappaB in learning and memory.

Animals↗
PubMed2006

Plasticity compartments in basal dendrites of neocortical pyramidal neurons.

Synaptic plasticity rules widely determine how cortical networks develop and store information. Using confocal imaging and dual site focal synaptic stimulation, we show that basal dendrites, which receive the majority of synapses innervating neocortical pyramidal neurons, contain two compartments with respect to plasticity rules. Synapses innervating the proximal basal tree are easily modified when paired with the global activity of the neuron. In contrast, synapses innervating the distal basal tree fail to change in response to global suprathreshold activity or local dendritic spikes. These synapses can undergo long-term potentiation under unusual conditions when local NMDA spikes, which evoke large calcium transients, are paired with a "gating molecule," BDNF. Moreover, these synapses use a new temporal plasticity rule, which is an order of magnitude longer than spike timing dependent plasticity and prefers reversed presynaptic/postsynaptic activation order. The newly described plasticity compartmentalization of basal dendrites expands the networks plasticity rules and may support different learning and developmental functions.

Action Potentials↗