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At least 91 records · Page 5Linked to original sources
PubMed2006

Restoration of neuronal plasticity by a phosphodiesterase type 1 inhibitor in a model of fetal alcohol exposure.

Although some studies showed the efficacy of phosphodiesterase (PDE) inhibitors as neuronal plasticity enhancers, little is known about the effectiveness of these drugs to improve plasticity in cases of mental retardation. Fetal alcohol syndrome (FAS) is the leading cause of mental retardation in the western world. Using a combination of electrophysiological and optical imaging techniques, we show here that vinpocetine, a PDE type I inhibitor, restores ocular dominance plasticity in the ferret model of fetal alcohol exposure. Our finding should contribute to a better understanding and treatment of cognitive deficits associated with mental disorders, such as FAS.

Animals↗
PubMed1978

Neuronal plasticity in the limbic system during classical conditioning of the rabbit nictitating membrane response. II: Septum and mammillary bodies.

Neuronal unit activity was recorded from several limbic system structures during classical conditioning of the rabbit nictiating membrane response to a tone CS. Air puff to cornea was used as a UCS. The present and past investigations of hippocampal activity using this paradigm show a neuronal plasticity which develops early in training, increases rapidly and shifts forward in time as behavioral conditioning develops. Recordings from the lateral septal region demonstrate the same within-trial pattern of unit discharge seen in hippocampus, indicating a projection of hippocampal plasticity over precommissural fornix pathways. Medial septal neurons, on the other hand, respond in an excitatory manner to the onsets of tone and air puff stimulation. While unit discharges seen in hippocampus and lateral septum occur only during the paired (learning) paradigm, medial septal activity is identical under both paired and unpaired (control) conditions. The latter fact lends support for a sensory interpretation of medial septal responses, and is consistent with anatomical evidence of a major septohippocampal projection originating from this region. In contrast to results for lateral septum, recordings from medial and lateral mammillary nuclei indicate only small, diffuse excitation that exhibits no consistent changes over training, and is not related to activity seen in hippocampal or septal regions. The apparent lack of correspondence between learning dependent unit measures obtained from pre- and postcommissural fornix structures is entirely consistent with current modified descriptions of limbic system anatomy.

Action Potentials↗
PubMed1999

Comparative study of the neuronal plasticity along the neuraxis of the vibrissal sensory system of adult rat following unilateral infraorbital nerve damage and subsequent regeneration.

The aim of the present study was to examine the physiological consequences of a unilateral infraorbital nerve lesion and its regeneration at different levels of the somatosensory neuraxis. In animals whose right infraorbital nerve had been crushed, a large unresponsive area was found in the main brainstem trigeminal nucleus (Pr5). Responses evoked by ipsilateral vibrissal deflection in the middle of Pr5 reappeared only on days 22-35 after the nerve had been transected, whereas recovery from the nerve crush took only 7-9 days. However, no sign of short-term neuronal plasticity was observed in Pr5 after peripheral nerve injury. An enlargement of the receptive fields in two-thirds of the units and a lengthening in the delay of the evoked responses were observed as long-term plastic changes in Pr5 neurons after peripheral-nerve regeneration. In the ventral posteromedial nucleus of the thalamus (VPM) of partly denervated animals, however, only minutes or hours after the nerve crush, certain units were found to respond in some cases not only to the vibrissae, but also to mechanical stimulation of the face over the eye (two units), the nose (one unit), and the midline (one unit). Apart from the experiments involving incomplete denervation, the vibrissal representation areas of the VPM were unresponsive to stimulation of both the vibrissae and other parts of the face until nerve regeneration had occurred. In the somatosensory cortex, an infraorbital nerve crush immediately resulted in a large cortical area being unresponsive to vibrissal deflection. It was noteworthy, however, that shortly after the nerve crush, this large unresponsive whisker representation cortical area was invaded from the rostromedial direction by responses evoked by stimulation of the forepaw digits. In spite of the reappearance of vibrissa-evoked responses 7-10 days after the nerve crush, an expanded digital representation could still be observed 3 weeks after the nerve crush, resulting in an overlapping area of digital and vibrissal representations. The withdrawal of the expanded representation of forepaw digits was completed by 60 days after the nerve crush. The results obtained in Pr5, the VPM, and the cortex strongly suggest that the higher the station in the neuraxis, the greater the degree of plasticity after infraorbital nerve injury.

Animals↗
PubMed1996

Evidence of neuronal plasticity within the inferior colliculus after noise exposure: a study of evoked potentials in the rat.

Recent investigations have implicated that the central nervous system has a role in the changes that occur in auditory function following acoustic trauma caused by noise exposure. These investigations indicate that the inferior colliculus may be the primary anatomical location in the ascending auditory pathway where noise-induced neuronal plasticity occurs, thereby resulting in changes in the neuronal processing of auditory information. In the present investigation, we show that the amplitudes of all peaks in the click-evoked response from the external nucleus of the inferior colliculus decrease during a 30 min exposure to a tone (104 dB sound pressure level (SPL) at 4 kHz and 8 kHz). After tone exposure, the amplitudes of two of the peaks of the response from the external nucleus of the inferior colliculus that reflect the input from more caudal structures slowly returned to baseline levels, whereas the amplitudes of the two peaks reflecting neuronal activity in the inferior colliculus increased above baseline levels and remained at the increased levels for at least 90 min following exposure to the tone. We also show that exposure to a 4 kHz tone at 104 dB SPL causes changes in the neuronal processing of tonebursts in the form of changes in the temporal integration function for one of the peaks of the response from the external nucleus of the inferior colliculus that originates in the inferior colliculus. Before tone exposure the amplitude of this peak decreased with increasing stimulus duration, but after tone exposure the amplitude of this peak was independent of the duration of the toneburst stimulus. We interpret these changes as evidence that noise exposure (tone exposure) causes changes in the excitability of the inferior colliculus that are not seen in more caudal structures, and these changes are probably a result of a change in the balance between inhibition and excitation in the inferior colliculus.

Acoustic Stimulation↗
PubMed1982

Enhancement of neuronal plasticity by activating the norepinephrine system in the brain: a remedy for amblyopia.

The norepinephrine hypothesis claims that an increase in the local availability of norepinephrine necessarily enhances neuronal plasticity in a given brain region. This claim had been successfully tested, and reviewed here briefly, in two experimental paradigms: 1) restoration of cortical plasticity by localized and continuous perfusion of the catecholamine-terminal-depleted visual cortex with exogenous norepinephrine and dibutyryl adenosine cyclic monophosphate, and 2) acceleration of cortical recovery from the effects of prior monocular lid suture by direct perfusion of the cortex with norepinephrine. Activation of the norepinephrine-beta-adrenergic receptor system in the visual cortex was discussed as a potential remedy for amblyopia.

Amblyopia↗
PubMed1992

Neuronal plasticity and ageing processes in the frame of the 'Red Queen Theory'.

On the basis of the morphofunctional evidence obtained in old brains of humans and mammals the present hypothesis has been introduced. This hypothesis states that neuronal plasticity can be used either to compensate for neuronal degeneration or to store new information. Thus, in pathological ageing the marked rate of degeneration has fully exhausted the already reduced plasticity capability of neural networks. In this way marked impairments of memory trace formation take place in pathological ageing conditions such as Alzheimer's disease. The essence of this hypothesis is that a competition for the available plasticity exists between the compensatory responses to ageing-induced degeneration and the processes necessary for memory trace formation. We have called this hypothesis the 'Red Queen Theory', an analogy borrowed from Lewis Carroll's book Through the Looking Glass. Thus, in ageing, processes responsible for plasticity must be forced to run at the highest possible rate to maintain the morphofunctional substrate of the existing networks as well as to allow the formation of new memory traces.

Aging↗
PubMed2002

Pathophysiology of depression: the concept of synaptic plasticity.

Neuronal plasticity or remodeling is most often discussed with regard to cellular and behavioral models of learning and memory. However, neuronal plasticity is a fundamental process by which the brain acquires information and makes the appropriate adaptive responses in future-related settings. Dysfunction of these fundamental processes could thereby contribute to the pathophysiology of mood disorders, and recovery could occur by induction of the appropriate plasticity or remodeling. These possibilities are supported by preclinical and clinical studies demonstrating that there are structural alterations that occur in response to stress and in patients with mood disorders. Moreover, antidepressant treatment may oppose these effects by regulation of signal transduction and gene expression pathways linked to neuronal plasticity. These findings comprise a novel conceptual framework for future studies of the etiology of mood disorders and for the development of novel therapeutic interventions.

Antidepressive Agents↗
PubMed2002

Different modes of pitch perception and learning-induced neuronal plasticity of the human auditory cortex.

We designed a melody perception experiment involving eight harmonic complex tones of missing fundamental frequencies (hidden auditory object) to study the short-term neuronal plasticity of the auditory cortex. In this experiment, the fundamental frequencies of the complex tones followed the beginning of the virtual melody of the tune "Frère Jacques". The harmonics of the complex tones were chosen so that the spectral melody had an inverse contour when compared with the virtual one. Evoked magnetic fields were recorded contralaterally to the ear of stimulation from both hemispheres. After a base line measurement, the subjects were exposed repeatedly to the experimental stimuli for 1 hour a day. All subjects reported a sudden change in the perceived melody, indicating possible reorganization of the cortical processes involved in the virtual pitch formation. After this switch in perception, a second measurement was performed. Cortical sources of the evoked gamma-band activity were significantly stronger and located more medially after a switch in perception. Independent Component Analysis revealed enhanced synchronization in the gamma-band frequency range. Comparing the gamma-band activation of both hemispheres, no laterality effects were observed. The results indicate that the primary auditory cortices are involved in the process of virtual pitch perception and that their function is modifiable by laboratory manipulation.

Adult↗
PubMed1994

Neuronal plasticity that underlies improvement in perceptual performance.

The electrophysiological properties of sensory neurons in the adult cortex are not immutable but can change in response to alterations of sensory input caused by manipulation of afferent pathways in the nervous system or by manipulation of the sensory environment. Such plasticity creates great potential for flexible processing of sensory information, but the actual effects of neuronal plasticity on perceptual performance are poorly understood. The link between neuronal plasticity and performance was explored here by recording the responses of directionally selective neurons in the visual cortex while rhesus monkeys practiced a familiar task involving discrimination of motion direction. Each animal experienced a short-term improvement in perceptual sensitivity during daily experiments; sensitivity increased by an average of 19 percent over a few hundred trials. The increase in perceptual sensitivity was accompanied by a short-term improvement in neuronal sensitivity that mirrored the perceptual effect both in magnitude and in time course, which suggests that improved psychophysical performance can result directly from increased neuronal sensitivity within a sensory pathway.

Animals↗
PubMed1998

Neuronal plasticity: adaptation and readaptation to the environment of space.

While there have been few documented permanent neurological changes resulting from space travel, there is a growing literature which suggests that neural plasticity sometimes occurs within peripheral and central vestibular pathways during and following spaceflight. This plasticity probably has adaptive value within the context of the space environment, but it can be maladaptive upon return to the terrestrial environment. Fortunately, the maladaptive responses resulting from neuronal plasticity diminish following return to earth. However, the literature suggests that the longer the space travel, the more difficult the readaptation. With the possibility of extended space voyages and extended stays on board the international space station, it seems worthwhile to review examples of plastic vestibular responses and changes in the underlying neural substrates. Studies and facilities needed for space station investigation of plastic changes in the neural substrates are suggested.

Adaptation, Physiological↗
PubMed2003

Partial arousal deficiency in SIDS victims and noradrenergic neuronal plasticity.

Sudden infant death syndrome (SIDS) victims had exhibited during sleep a reduction in cortical arousals despite an increase in subcortical activation. Arousal deficiency in SIDS victims was partial. We could suggest the latent existence of inadequate noradrenergic neuronal plasticity as the background of this partial arousal deficiency of SIDS victims.

Humans↗
PubMed1991

Maintenance of neuronal plasticity in the reticular core and changes in trophic activity in Alzheimer's disease.

1. Neuronal loss in Alzheimer's disease (AD) is accompanied by a proliferative response of the remaining neurons. 2. Different cell types are differently involved in the process of degeneration and proliferation in AD. 3. The extent of dendritic growth in AD is related to the formation of amyloid, not preamyloid. 4. Proliferative changes similar to those observed in AD can be induced in an animal model as a response to neuronal death. 5. The processes of degeneration and proliferation in AD are probably associated with an increase in trophic activity.

Aged↗
PubMed1987

The cAMP cascade in the nervous system: molecular sites of action and possible relevance to neuronal plasticity.

Many intercellular messages regulate the activity of their target cells by altering the intracellular level of cAMP and, as a consequence, the phosphorylation state of proteins which serve as substrates for cAMP-dependent protein kinase. Such regulation plays a crucial role in neuronal development, neuronal function, and neuronal plasticity (e.g., elementary learning mechanisms). Ample information has been accumulated in recent years on the enzymes that regulate the level of cAMP or respond to it, on the regulation of cAMP synthesis by neurohormones, neurotransmitters, ions, and toxins, on neuronal-specific substrate proteins that are phosphorylated by the cAMP-dependent kinase, and on the interaction of the cAMP-cascade with other second-messenger systems within neurons. Such data, obtained by a combination of molecular-biological, biochemical, and cellular approaches, shed light on the detailed mechanisms by which modulation of a ubiquitous molecular cascade leads to a great variety of short-term as well as long-term specific neuronal responses and alterations.

Animals↗
PubMed2004

[Psychosomatics, psychotherapy and neuronal plasticity--how words change our mind].

Certain psychosomatic disorders such as chronic psychosomatic pain, phobias and other anxiety disorders as well as depression are often stress-related but may also be acquired by learning associated with traumatic experience. As learning is based on changes in neuronal networks, the brain will be altered in these diseases. In turn, brain structure and function may also be influenced and even changed by effective psychotherapy as well as by other (behavioural) cognitive interventions--words and thoughts--when leading to cognitive restructuring. Due to their neuronal plasticity our brains are capable of constantly rewiring themselves so that we can--in Andreasen's words--"literally change our mind".

Anxiety Disorders↗
PubMed1991

Kindling-induced neuronal plasticity in the dorsal hippocampus CA1 in acutely prepared rabbits: unit activity analysis.

To elucidate kindling-induced neuronal plasticity single cell discharge analysis, responses consisting of action potentials orthodromically elicited in the dorsal hippocampus CA1 by a single electric shock to the neighboring region were serially observed before, during and after kindling i.e. the repetition of stimulus trains applied to the same hippocampal region in acutely prepared rabbits. Eventually, the orthodromic unit response with identical amplitudes, which were regarded as a single cell origin, gradually increased in the firing rate at the interictal stages during and after the kindling. Further, an inhibitory period following the unit responses, during which no spontaneous unit activity appeared, was remarkably prolonged during and after the kindling. Both the increase of the unit responses and the prolongation of the inhibitory period irreversibly lasted for hours once they occurred. Such unit activity analysis confirms kindling-induced excitatory and inhibitory synaptic plasticity.

Action Potentials↗
PubMed2003

The prefrontal cortex regulates lateral amygdala neuronal plasticity and responses to previously conditioned stimuli.

The amygdala plays a role in learning and memory processes that involve an emotional component. However, neural structures that regulate these amygdala-dependent processes are unknown. Previous studies indicate that regulation of affect may be imposed by the prefrontal cortex (PFC) and its efferents to the amygdala. The presentation of conditioned affective stimuli enhances activity of neurons in the lateral nucleus of the amygdala (LAT), which is thought to drive conditioned affective responses. Moreover, plasticity of LAT neuronal responses to stimuli during the course of conditioning is believed to underlie affective learning. This study examines the role of the PFC in the regulation of affective behaviors by evaluating how the PFC affects LAT neuronal plasticity and activity that is evoked by previously conditioned stimuli. In vivo intracellular recordings were performed from the LAT of anesthetized rats during pavlovian conditioning and during the presentation of stimuli that were conditioned in the awake rat before recording. Train stimulation of the PFC suppressed LAT neuronal activity that was evoked by both previously conditioned and neutral stimuli. In addition, PFC stimulation blocked LAT neuronal plasticity associated with an affective conditioning procedure. These results indicate that the PFC has the potential to regulate affective processes by inhibition of the LAT. Patients with disruptions of the PFC-LAT interaction often display an inability to regulate affective responses. This may be attributable to the loss of PFC-imposed inhibition of the emotional response to a stimulus but may also include the formation or diminished extinction of inappropriate associations.

Amygdala↗
PubMed1990

[The importance of neuronal plasticity for regeneration and transplantation in the CNS].

In the CA3 area of the hippocampus the pyramidal neurons were destroyed by intraventricular application of kainic acid. After transplantation of a suspension of embryonic hippocampal cells agglomerations of cells at the site of injection were observed. Some of them were in the layer of the destroyed neuronal population. These neurons formed dendritic branches and dendritic spines. As compared with control areas with a normal neuronal population, the neurons at the site of transplantation had less regular branching of dendrites and some of the branches were quite chaotic.

Animals↗