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PubMed1988

Effect of auditory deafferentation on the synaptic connectivity of a pair of identified interneurons in adult field crickets.

In adult crickets, Teleogryllus oceanicus, unilateral auditory deafferentation causes the medial dendrites of an afferent-deprived, identified auditory interneuron (Int-1) in the prothoracic ganglion to sprout and form new functional connections in the contralateral auditory neuropil. The establishment of these new functional connections by the deafferented Int-1, however, does not appear to affect the physiological responses of Int-1's homolog on the intact side of the prothoracic ganglion which also innervates this auditory neuropil. Thus it appears that the sprouting dendrites of the deafferented Int-1 are not functionally competing with those of the intact Int-1 for synaptic connections in the remaining auditory neuropil following unilateral deafferentation in adult crickets. Moreover, we demonstrate that auditory function is restored to the afferent-deprived Int-1 within 4-6 days following deafferentation, when few branches of Int-1's medial dendrites can be seen to have sprouted. The strength of the physiological responses and extent of dendritic sprouting in the deafferented Int-1 progressively increase with time following deafferentation. By 28 days following deafferentation, most of the normal physiological responses of Int-1 to auditory stimuli have been restored in the deafferented Int-1, and the medial dendrites of the deafferented Int-1 have clearly sprouted and grown across into the contralateral auditory afferent field. The strength of the physiological responses of the deafferented Int-1 to auditory stimuli and extent of dendritic sprouting in the deafferented Int-1 are greater in crickets deafferented as juveniles than as adults. Thus, neuronal plasticity persists in Int-1 following sensory deprivation from the earliest juvenile stages through adulthood.

Acoustic Stimulation↗

PubMed2001

The impact of inflammation on bronchial neuronal networks.

It is well-recognized that the activities of airway neuronal systems can be modulated by various agonist molecules. This brief review examines some of the evidence that inflammation and some of the mediators relevant to the expression of inflammatory processes can also significantly alter the function and activities of airway nerves. The concept of neuronal plasticity and phenotype switching induced by inflammation is also examined, with particular emphasis on sensory airway nerves.

Animals↗

PubMed1997

Developmental expression of 5-HT7 receptor mRNA in rat brain visual structures after neonatal enucleation.

Binocular enucleation is a useful experimental tool for studying mechanisms of neuronal plasticity. Serotonin (5-HT) is a neuromodulator that mediates a wide range of physiological functions by activating multiple receptors. We have performed an in situ hybridization study to analyse in detail the regional distribution of 5-HT7 receptor mRNA expression during postnatal development in different brain visual areas following neonatal binocular enucleation. We found that eye removal clearly induced 5-HT7 receptor mRNA expression in the stratum opticum of superior colliculus, this effect being especially evident at postnatal day 21 (P21). Similarly, there was a clear lesion-induced up-regulation of receptor mRNA expression in the primary visual cortex from P15 through P21. These results suggest a plastic role of 5-HT7 receptor during neurogenesis triggered by eye removal.

Animals↗

PubMed2001

Changes in vesicular monoamine transporter (VMAT2) and synaptophysin in rat Substantia nigra and prefrontal cortex induced by psychotropic drugs.

We investigated the regulatory effect of the dopaminergic agent L-dopa, the mood stabilizer lithium and the nonselective monoamine oxidase inhibitor phenelzine on brain vesicular monoamine transporter (VMAT2) expression. Rats were treated chronically (21 days) with the three psychoactive drugs. VMAT2 gene expression at the protein level was assessed in the prefrontal cortex and striatum by autoradiography with high-affinity [(3)H]dihydrotetrabenazine ([(3)H]TBZOH) binding and at the mRNA level in the substantia nigra pars compacta by in situ hybridization. In addition, the effect of various treatments on the synaptophysin mRNA level was determined in the substantia nigra by in situ hybridization. Chronic administration of L-dopa resulted in a significant decrease (28%, p < 0.05) in the density of [(3)H]TBZOH binding in the prefrontal cortex but had no effect on VMAT2 and synaptophysin mRNA levels in the substantia nigra. Lithium treatment increased [(3)H]TBZOH-specific binding in the prefrontal cortex (23%, p < 0.05) but had no effect on VMAT2 and synaptophysin mRNA levels. Phenelzine did not modulate VMAT2 gene expression but reduced the synaptophysin mRNA level (19%, p < 0.05). The modulatory activities of these drugs, although relatively weak, may be relevant to the drug-induced synaptic and neuronal plasticity as well as to the molecular and cellular pathophysiology of monoamine-related neuropsychiatric disorders.

Animals↗

PubMed2004

Attentional cueing improves vision restoration therapy in patients with visual field defects.

BACKGROUND: In patients with postgenicular lesions of the visual system, areas of residual vision (ARVs) are the main predictor of recovery induced by vision restoration therapy (VRT). In these partially defective regions, the elevated perceptual thresholds can be acutely reduced by attentional cueing. OBJECTIVE: To examine whether directing attention to ARVs using a visuospatial cue also increases long-term neural plasticity and thus enhances permanent training outcome. METHODS: In a prospective, randomized clinical trial, treatment outcome was compared in patients with postgenicular visual system lesions who received either standard VRT (control group [CG]; n = 10) or VRT with attentional cueing (experimental group [EG]; n = 9). Visual field size was determined before and after a 6-month treatment period using Tubingen Automated Perimetry and computer-based high-resolution perimetry (HRP) and in regular intervals throughout this period by HRP and detection performance in VRT. RESULTS: In the area of the cue, restoration of vision was significantly greater than during VRT without cueing: cued patients showed a much more pronounced shift of the visual field border toward the blind area than that observed in the CG or in uncued regions of the EG. Focusing attention at ARVs during treatment changed topographic and temporal patterns of recovery as compared with uncued regions of the visual field. CONCLUSIONS: Use of a visuospatial cue to focus attention at areas of residual vision amplifies long-term neuronal plasticity. The authors propose that top-down signals preactivate partially damaged areas of V1, thus linking visual and attentional neuronal networks, with the effect of permanently increasing conscious visual perception.

Adult↗

PubMed1996

Inhibition of TEA-induced LTP by aluminum.

Brief application of tetraethylammonium (TEA) to hippocampal slices causes long-term potentiation (TEA LTP) at synapses of CA1 pyramidal neurons characterized by a long-lasting increase of field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude. Since this kind of potentiation requires the activation of voltage-dependent calcium channels, we examined the effect of the inorganic calcium channel blocker aluminum, which has been shown to impair tetanus-induced LTP (eLTP). We found that Al inhibited in a concentration-dependent manner both fEPSP slope and PS amplitude potentiation by TEA; 0.68 microgram/ml A1 attenuated TEA LTP, while a complete block of long-lasting potentiation was obtained for 2.7 micrograms/ml Al. Occlusion experiments revealed that both concentrations of Al allowed the induction of eLTP 60 min after TEA/Al exposure. However, longer application (15 min) of 2.7 micrograms/ml Al before the induction of TEA LTP prevented the subsequent induction of eLTP although no significant differences concerning the action on TEA LTP were observed. This indicates a general loss of neuronal plasticity which might be due to progressive neuronal cell damage. Since the effective concentration range of Al is directly comparable to the action of Al on eLTP, our data provide evidence for shared mechanisms of both potentiations. Although based on different induction mechanisms, Ca2+ is assumed to be a general intracellular trigger for both forms of LTP and thus it can be hypothesized that the neurotoxic action of Al is due to interference with Ca(2+)-dependent processes by inhibition of calcium conductances.

Aluminum↗

PubMed2002

The significance of action potential bursting in the brain reward circuit.

The brain reward circuit consists of specialized cortical and subcortical structural components that code for various cognitive aspects of goal-directed behavior. These components include the prefrontal cortex (PFC), amygdala (AMY), nucleus accumbens (Nac), subiculum (SUB) of the hippocampal formation, and the dopamine (DA) neurons in the ventral tegmental area (VTA). Both serial and parallel processing in the different components of the circuit code the various aspects of reward-related behavior. Individual neurons within each component have developed specialized intrinsic membrane properties that have led them to be typically defined as either single spiking or high frequency burst-firing neurons. However, a strict definition based on the output mode may not be appropriate. Under the right conditions, neurons can switch between bursting and single-spiking modes, therefore providing a conditional output state. The preferred mode of each individual neuron depends on a combination of different plastic neuronal properties such as, dendritic architecture, neuromodulation, intracellular calcium (Ca(++)) buffering, excitatory and inhibitory synaptic strength, and the spatial distribution and density of voltage and ligand-gated channels. It is likely that, in vivo, most neurons in the circuit, despite variations in intrinsic membrane properties, are conditional output neurons equipped with the versatility of switching between output modes under appropriate conditions. Bursting mode may be used to boost the gain of neural signaling of important or novel events by enhancing transmitter release and enhancing dendritic depolarization, thereby increasing synaptic potentiation. Conversely, single spiking mode may be used to dampen neuronal signaling and may be associated with habituation to unimportant events. Mode switching may provide flexibility to the circuit allowing different sets of neurons to conditionally code for the various aspects of reward-related memory and behavior.

Action Potentials↗

PubMed2000

Pain: molecular mechanisms.

Our understanding of chronic inflammatory and neuropathic pain at the molecular and cellular level has developed at an extraordinary rate in recent years. Inflammatory, or neuropathic, neuronal plasticity describes the process by which the neurons involved in pain transmission are converted from a state of normosensitivity to one in which they are hypersensitive. Here we summarize current theories on somatosensory neuroplasticity in a molecular context, highlighting key receptors, ion channels, and signal molecules involved. We also suggest new possibilities for drug design, based on the rational targeting of these molecular players.

Journal Article↗

PubMed1998

Changes in mRNA abundance of microtubule-associated proteins in the rat brain following electroconvulsive shock.

Microtubule-associated proteins (MAPs) are involved in the maintenance of mature neuronal morphology, neurite outgrowth and neuronal plasticity. Alteration in MAP expression may underlie neuronal structural changes in response to seizure activity. The aim of the present study was to investigate whether electroconvulsive shock (ECS), an animal model of electroconvulsive therapy (ECT) in clinical treatment of depression, affected gene expression of MAPs in the rat brain. Using in situ hybridization, we studied the expression of encoding mRNA for MAPs in the brains of rats treated with ECS 5 times over 10 days. The abundance of mRNA encoding microtubule-associated protein 2 (MAP2), a dendritic MAP, was significantly increased (142% compared with controls) in the dentate gyrus 6 and 24 h after the last shock, and had returned to baseline levels within 48 h. These changes were confined to the dentate gyrus no significant changes were observed in CA1 and CA3 of the hippocampus. The increase in MAP2 expression was accompanied by an increase in MAP2 immunoreactivity in the molecular layer of the dentate gyrus. The abundance of mRNA encoding for tau, an axon-specific MAP, and MAP1B, an embryonic MAP, was unaffected by ECS. These data demonstrate that ECS specifically altered the mRNA and protein expression of MAP2 but had no effect on tau or MAP1B, and suggest that changes in MAP2 expression may be related to morphological changes in the dentate gyrus, particularly in the dendrites.

Animals↗

PubMed2005

Section 3: The nature of pain: pathophysiology.

An understanding of the pathophysiology of pain involves the concepts of neuronal plasticity at the levels of the nociceptor neurons, spinal cord, and brain. Neuroplasticity allows the neurons in the brain to compensate for injury and adjust their activity in response to new situations or changes in their environment. This is an important physiologic event in the development of central sensitization. Other concepts include modulatory effects at the nociceptor, sympathetically mediated pain, the "wind-up" phenomenon, central sensitization, and descending and ascending central modulatory mechanisms for the perception of pain, as well as the related pain motivations and behaviors. Numerous modulatory mechanisms for pain have been postulated that control the degree of pain perceived and the emotional and behavioral phenomena associated with a patient's pain experience. These numerous mechanisms take place at all levels of the nervous system: peripheral nerves, spinal cord, and brain. Despite great advances in unraveling the complexities of the pathophysiology of pain, much remains to be discovered. It is hoped that further research into this critical area will lead to better therapies.

Acute Disease↗

PubMed1999

Perinatal supplementation of low doses of ethanol enhances 5-HT restoration in the central nervous system.

It has been reported that long-term administration of ethanol has deleterious effects on the central nervous system; the alterations are particularly evident if the exposure occurs during development. Our study shows that rat perinatal administration of 3% and 6% ethanol does not alter development of serotonin (5-HT) pathways in the central nervous system, while their reactive changes triggered by neonatal lesioning are greatly altered. The administration of 5, 7-dihydroxytriptamine (5,7-DHT) within 6 hours from birth causes 5-HT fiber degeneration throughout the central nervous system. The loss of 5-HT is particularly relevant in lumbar spinal cord, occipital cortex, and hippocampus. This early decrease in 5-HT content is followed by a slow and partial recovery. If animals are exposed to 3% ethanol during the perinatal period, there is an enhancement of the 5,7-DHT-induced degeneration that is, however, followed by a faster and greater recovery throughout the central nervous system. Conversely, perinatal exposure to 6% ethanol and 5, 7-DHT administration lead to an irreversible 5-HT loss with no subsequent recovery. The deleterious effects of 6% ethanol are accompanied by a reduced expression of neurotrophin. Thus, our study suggests that chronic exposure to ethanol can influence central nervous system plasticity during development. Low doses may enhance neuronal plasticity and repair perhaps via an increased efficacy of neurotrophic factors, whereas higher doses may negatively affect neural development also by means of the impairment of the expression of neurotrophic factors.

5,7-Dihydroxytryptamine↗

PubMed2001

Acetylcholine becomes the major excitatory neurotransmitter in the hypothalamus in vitro in the absence of glutamate excitation.

Glutamate and GABA are two major fast neurotransmitters (excitatory and inhibitory, respectively) in the CNS, including the hypothalamus. They play a key role in the control of excitation/inhibition balance and determine the activity and excitability of neurons in many neuronal circuits. Using neuronal cultures, whole-cell recording, Ca(2+) imaging, and Northern blots, we studied the compensatory regulation of neuronal activity during a prolonged decrease in glutamate excitation. We report here that after a chronic (6-17 d) blockade of ionotropic glutamate receptors, neurons in hypothalamic cultures revealed excitatory electrical and Ca(2+) synaptic activity, which was not elicited in the control cultures that were not subjected to glutamate blockade. This activity was suppressed with acetylcholine (ACh) receptor antagonists and was potentiated by eserine, an inhibitor of acetylcholinesterase, suggesting its cholinergic nature. The upregulation of ACh receptors and the contribution of ACh to the control of the excitation/inhibition balance in cultures after a prolonged decrease in glutamate activity were also demonstrated. Enhanced ACh transmission was also found in chronically blocked cerebellar but not cortical cultures, suggesting the region-specific character of glutamate-ACh interactions in the brain. We believe that in the absence of glutamate excitation in the hypothalamus in vitro, ACh, a neurotransmitter normally exhibiting only weak activity in the hypothalamus, becomes the major excitatory neurotransmitter and supports the excitation/inhibition balance. The increase in excitatory ACh transmission during a decrease in glutamate excitation may represent a novel form of neuronal plasticity that regulates activity and excitability of neurons during the glutamate/GABA imbalance.

Acetylcholine↗

PubMed1996

[Calcium, neuronal death and neurological disease].

Calcium ion (Ca2+) plays a role in several important functions in the central nervous system such as production of action potentials, neurotransmitter release, or neuronal plasticity, etc. However, its excessive influx to neurons due to failure of the mechanisms implicated in the regulation of its intracellular concentration (Ca(2+)-channels, calcium binding proteins), leads to a cascade of events which causes cytotoxicity and neuronal death. Ca2+ mediated toxicity has been implicated in the pathogenesis of neurodegenerative diseases (Parkinson's, Alzheimer's, amyotrophic lateral sclerosis, Huntington's), brain ischemia, epilepsy, cranial trauma, and AIDS-dementia complex. In this article we review the current status of this topic.

Alzheimer Disease↗

PubMed1990

Robust synaptic plasticity of striatal cells following partial deafferentation.

Partial ablation of the cerebral cortical input to the neostriatum generates a rapid lasting effect on the size of remaining synaptic sites. The neocortex was lesioned in adult rats and the neostriatum was analyzed for effects on remaining spines of principal cells during the period from 2 to 40 days. There was an increase in the size of spine heads, boutons and synaptic contact sites. The spine heads became very complex and a corresponding bouton enlargement was accompanied by an increase in the number of synaptic vesicles. By two days, the average profile length of postsynaptic membrane densities (PSDs) had increased by 25% representing an equivalent 50% increase in synaptic contact area. The number of synaptic sites was reduced on each principal neuron of the lesioned group. Comparison of the number of sites per unit volume to their average contact area revealed a reciprocal relationship indicating a conservation in the total synaptic contact area on each neuron. This effect was consistent for all postsurgical days. The lack of a significant return of synaptic number by 40 days indicates that axonal sprouting is not a major factor in neuronal plasticity in the adult striatum. The rapid increase in the size of spines, boutons and synaptic sites at remaining connections suggests that dendrites are the first to initiate the plasticity response in adult neurons through postsynaptic attachments and their corresponding receptor structure. The underlying mechanism of this plasticity may be through a conservation of macromolecules forming postsynaptic membrane specializations on target neurons. Remaining axons appear to follow the dendritic response with a plasticity generating presynaptic appositional specializations to match the contact area of the postsynaptic site.

Animals↗

PubMed2006

Additive effect of dextromethorphan on the inhibitory effect of anti-NT4 on morphine tolerance.

It has been proposed that opioid tolerance is a model of neuronal plasticity similar to learning and memory. Recent evidence suggests that neurotrophins may be involved in synaptic development and plasticity. Observations indicate that neurotrophin 4 (NT4) is required for the synaptic plasticity mediating both tolerance and memory. Also there are lines of evidence to indicate that NMDA receptors are involved in the neural plasticity underlying the development of opiate tolerance. Neurotrophins affect central transmission postsynaptically by enhancing NMDA receptor responsiveness. So we used the clinically available NMDA receptor antagonist, dextromethorphan, and the neurotrophin 4 antibody, anti-NT4, concomitantly and alone to investigate their effects on morphine tolerance. Tolerance was induced by injecting morphine (7 and 10 mg/kg i.p.) once per day for 4 days. Anti-NT4 (1 microg/rat i.c.v.) was administered 15 min before morphine. Results showed that chronic concomitant treatment of anti-NT4 with morphine in both doses inhibited the development of morphine tolerance. Also acute treatment of anti-NT4 significantly reversed the tolerance that was induced by morphine 7 mg/kg but failed to reverse the tolerance of morphine 10 mg/kg. Dextromethorphan in both doses (10 or 30 mg/kg) has an additive effect on the inhibitory effect of anti-NT4 on the reversal of morphine tolerance (7 mg/kg). These findings provide additional support for the hypothesis that NMDA receptor and NT4 may be involved in neural plasticity underlying opiate tolerance.

Analgesics, Opioid↗

PubMed2003

Roles of protein kinase A and protein kinase G in synaptic plasticity in the visual cortex.

Monocular deprivation leads to clear physiological and anatomical changes in the visual cortex known as ocular dominance plasticity. Protein kinase A (PKA) is necessary for ocular dominance plasticity, while protein kinase G (PKG) is not. We have now tested the role of PKA and PKG in long-term potentiation (LTP) and long-term depression (LTD). We have shown that PKA inhibitors have a major effect on both LTP and LTD in the visual cortical slices, whereas a PKG inhibitor affects LTP but not LTD. The PKA activator, 8-chloroadenosine-3',5'-monophosphorothioate, Sp-isomer (Sp-8-Cl-cAMPS), by itself induces a slowly rising form of LTP, which is occluded by theta-burst stimulation (TBS)-induced LTP. These results support the point that the PKA signaling pathway is crucial for neuronal plasticity in visual cortex, and the dissociation of the role of PKA and PKG in long-term synaptic plasticity in the visual cortex suggests that LTP alone is not sufficient to support ocular dominance plasticity, or LTD plays a more fundamental role than LTP in ocular dominance plasticity.

Animals↗

PubMed2006

Motor fluctuations and dyskinesias in advanced/end stage Parkinson's disease: a study from a population of brain donors.

Treatment-related motor fluctuations (MFs) and dyskinesias are considered one of the most important problems in the long-term management of Parkinson's disease (PD). However, only a few studies have focused on their characteristics during advanced and end stages of the disease. We therefore assessed MFs and dyskinesias in a cohort of 61 late/end stage patients with a clinical and pathological diagnosis of PD and investigated the influence of disease- and treatment-related variables on their occurrence. A total of 62.3% of our patients experienced "wearing-off" phenomena, 68.9% "on-off" motor fluctuations and 60.7% dyskinesias at advanced/end stage disease. Age at disease onset and disease duration were significantly associated with dyskinesias. A substantial number of patients experienced spontaneous resolution of their motor complications during the last two years of their disease without treatment modifications. The clinical heterogeneity of treatment-related motor complications in PD points towards a complex mechanism for their etiopathogenesis. Although advanced disease and L-dopa administration are closely tied to their development, other mechanisms involving synaptic aging, altered neuronal plasticity and post-synaptic degeneration may be involved.

Age of Onset↗

PubMed1999

The impact of brain imaging technology on our understanding of motor function and dysfunction.

Brain imaging techniques have demonstrated functional specialisation of multiple areas within the motor system. They have also defined the patterns of interactions between these regions during normal motor function and in motor disorders. Functional imaging makes visible the changes in cortical activity that take place over time during motor functions, from the activations a fraction of a second before voluntary action to cortical neuronal plasticity several weeks after injury. Recently, the functional abnormalities underlying various acquired and developmental motor disorders have been described, as well as the effects of therapeutic intervention.

Brain↗