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PubMed2001

Lateral magnocellular nucleus of the anterior neostriatum (LMAN) in the zebra finch: neuronal connectivity and the emergence of sex differences in cell morphology.

The song system of birds provides a model system to study basic mechanisms of neuronal plasticity and development underlying learned behavior. Song learning and production involve discrete sets of interconnected nuclei in the avian brain. One of these nuclei, the lateral magnocellular nucleus of the anterior neostriatum (LMAN), is the output of the so-called anterior forebrain pathway known to be essential for learning and maintenance of song, both processes depending on auditory feedback. In zebra finches, only males sing and this sexually dimorphic behavior is mirrored by sexual dimorphism in neuronal structure that develops during ontogeny. Female zebra finches are not able to sing and nuclei of the song system are strongly reduced in size or even lacking, when compared to male brains. Only LMAN can be delineated as easily in females as in males. Since female zebra finches, despite being unable to sing, recognize song just as males do and form a memory for song (model acquisition) early in life, LMAN is a putative candidate for song acquisition in both sexes. Therefore, development of LMAN was studied at the cellular and ultrastructural level in both male and female zebra finches. Regressive development of dendritic spines, enlargement of neuronal cell body and nuclei size, as well as changes at the nucleolar level are events all occurring exclusively in males, when song learning progresses. The decline in synapse number and the augmentation in synaptic contact length at synapses in LMAN in males are indicative for synaptic plasticity, whereas in females synapse number and synaptic contact length remain unchanged.

Animals↗
PubMed1994

Multiple cholinergic markers are unexpectedly not altered in the rat dentate gyrus following entorhinal cortex lesions.

Since major cholinergic deficits are observed in Alzheimer's disease, the development of models to study possible cholinergic plasticity has generated great interest. In this regard, it has been shown that lesions of the entorhinal cortex, which sends glutamatergic projections to the hippocampus, promote the sprouting and plasticity of presumptive cholinergic septohippocampal fibers in the dentate gyrus, as revealed by AChE histochemistry. This sprouting was reported to be evident at 8 d and up to 30 d postlesion (DPL) and is now widely used as a model of cholinergic neuronal plasticity. In the present study, unilateral lesions of the entorhinal cortex were made in adult rats, and the status of various putative pre- and postsynaptic cholinergic markers was assessed after 2, 4, 8, 14, and 30 DPL. As expected, AChE was increased in the outer molecular layer of the ipsilateral dentate gyrus from 8 to 30 DPL. In contrast, the activity of ChAT, the enzyme responsible for the synthesis of ACh, and the densities of specific binding sites for 3H-AH5 183/vesamicol (blocker of the ACh vesicular transport sites), 3H-hemicholinium-3 (blocker of the high-affinity choline uptake sites), muscarinic-M2 (3H-AF-DX 384 and 3H-ACh), muscarinic-M1 (3H-pirenzepine), and nicotinic (3H-N-methylcarbamylcholine) cholinergic receptors were not increased on the ipsilateral molecular layer of the dentate gyrus, as compared to their contralateral controls. We conclude that the increase in AChE staining in the molecular layer of the dentate gyrus following entorhinal cortex lesions may be due to changes in noncholinergic neurons.

Acetylcholine↗
PubMedDate not supplied

Use of tissue culture models to study neuronal regulatory trophic and toxic factors in the aged brain.

Dementia is believed to result from the loss of selective neurons within the brain, but approaches for systematic study of that degenerative process are hampered by the complexity of the neuronal milieu. Tissue culture models provide a means to reduce dramatically the variables inherent in the study of neuronal plasticity. Three levels of complexity can be described: cellular and molecular diversity; primary and secondary interconnections; and finally, the dynamics influenced by age. The following review discusses the advantages and disadvantages of tissue culture models for the detailed study of neuronal trophic and toxic factors. Our selection of factors is broadened to include ions, intermediate metabolites, antioxidants, steroids, neuropeptides, gangliosides, metals, neurotransmitters, brain extracts, and protein molecules. Most of these factors have been shown to be altered in the aged brain, to have a significant effect on cultured neurons, or both. This multilevel analysis provides the reader with an overview of the events regulating neuronal survival, differentiation and death. An understanding of these basic questions is necessary to sequence the molecular events resulting in neuronal death.

Aging↗
PubMed1992

Role of monoamine systems in activation of zif268 by cocaine.

Rapid activation of transcription factor genes is thought to play a key role in stimulus-induced neuronal plasticity. To help understand the genomic response that may underlie long-term effects of cocaine and amphetamine, we have investigated the effect of these agents on Zif268, a transcription regulatory factor that is expressed at high levels in brain neurons. Like c-fos, zif268 is markedly activated in striatum by cocaine and amphetamine. This response appears to involve the dopamine system, since it is abolished by SCH23390, a selective D1 dopamine receptor antagonist, or by 6-hydroxydopamine lesions. To assess the role of other monoamine systems in regulating the expression of these transcription factors, we have examined the effects of selective monoamine uptake blockers as well as agents that lesion the norepinephrine and serotonin systems. These studies indicate that, in addition to the dopamine system, the norepinephrine and serotonin systems also play prominent roles in the activation of zif268 and c-fos by cocaine and amphetamine.

Amphetamine↗
PubMed2004

Reelin immunoreactivity in the adult sea lamprey brain.

The expression of reelin, a large extracellular matrix glycoprotein, was studied in the brain of pre-spawning adult sea lampreys by immunohistochemistry using two monoclonal antibodies against this protein. Reelin immunoreactive (reln-ir) neurons were observed in the olfactory bulb, and pallial and subpallial regions in the telencephalon. In the diencephalon, reln-ir cells were observed in some hypothalamic nuclei, in the nucleus of Bellonci, and in the habenula. In the mesencephalon, this protein was detected in several nuclei related with the centrifugal visual system, although the optic tectum was devoid of immunoreactivity. The hindbrain showed several nuclei with immunopositive neurons, including the branchiomeric nerve motor nuclei and also some groups of non-giant cells of the reticular formation. The rostral spinal cord showed some immunopositive neurons mainly located in lateral and ventral positions. Overall, the pattern of distribution of reelin in the adult sea lamprey correlates with the previously reported in other adult vertebrates. Furthermore, the wide distribution of reelin in the adult lamprey brain is consistent with a possible existence of different roles for this protein not related with development in the central nervous system (CNS) of vertebrates (i.e. neuronal plasticity and/or maintenance).

Animals↗
PubMed1991

Activity of spinal trigeminal pars oralis and adjacent reticular formation units during differential conditioning of the rabbit nictitating membrane response.

Spinal trigeminal nucleus pars oralis (SpoV) is anatomically linked to brain circuitry thought to subserve unconditioned and conditioned nictitating membrane responses in rabbit. Single-unit recording from SpoV and adjacent reticular formation obtained during conditioning from awake, behaving animals revealed modulation of unit firing related to CS, US, and CR occurrence. SpoV participates directly in the unconditioned response and probably relays US information to other brain areas subserving conditioning. The presence of CR-related activity suggests that SpoV may participate in the CR motor output pathway, and may also provide CR-related information to cerebellum. Sensory convergence and CR-related activity in reticular formation mark this structure as a candidate locus of primary neuronal plasticity in this example of conditioning.

Acoustic Stimulation↗
PubMed1989

Evolutionary expression of the neuronal form of the src protein in the brain.

The protooncogene src encodes two proteins, designated pp60c-src+ and pp60c-src.pp60c-src+ is expressed only in neurons, whereas pp60c-src is expressed in neuronal and nonneuronal cells. pp60c-src+ differs from pp60c-src in that it contains an insert of 6 amino acids. To study the evolutionary conservation of the 6-amino acid insert, the expression of pp60c-src+ in the brain of animals from different classes was assayed by using pp60c-src+-specific antibodies raised against a synthetic peptide corresponding to the insert. pp60c-src+ was detected only in the brain of mammals, birds, and reptiles, but not amphibians and fish, whereas pp60c-src was present in the brain of all animals tested, including lobster (invertebrate). These findings indicate that pp60c-src+ may play a role in events associated with higher brain function, such as neuronal plasticity.

Amino Acid Sequence↗
PubMed1989

[Neurohistological study of the dendrites of lamina V-pyramidal neurons of the rat following recovery from postnatal malnutrition].

By means of the GOLGI technique the influence of unspecific early postnatal undernourishment (from day 1 till day 20 of postnatal life followed by 40 days of recovery) on the spine morphology was investigated in the brain cortex of young adult animals, 60 days old. It was found that in experimental animals the three main spine types (thin spines, mushroom spines and stubby spines) had developed on apical lateral dendrites of cingulate pyramidal neurons, indicating the realization of the morphological characteristics of pyramidal neurons during starvation and recovery. However, in 60 days old control animals 65-70% of the spines belonged to the thin spine type, but in undernourished and rehabilitated animals the mushroom type is dominating and its percentage was found to have increased from 25-30% (controls) to 50% of all spines. Additionally, a significant enlargement of the stalked spines, especially of their synaptic end-knobs bearing spine heads was demonstrated in experimental animals. In undisturbed animals the short thin stem spine is considered to be necessary in a certain percentage to secure an optimum of resting activity in the neuron. The enhancement in the total spine number of 40-50% between day 20 (end of starvation) and day 60 (end of recovery), found earlier by us, taken together with the present results (increase in mushroom spines and spine head enlargement) point to a real new formation by division of previously enlarged mushroom spines as well as to transformations and shifts in the spine population during the recovery time. In the formation, development and maturation of the spines a change in their morphology from the filopodium-like type over the mushroom type and finally the thin stalked type may occur. Our results are discussed as being the expression of the neuronal plasticity persisting far into adulthood in order to enable the organism to react adaptive against changed living conditions.

Animals↗
PubMed2005

Nucleus retroambiguus-spinal pathway in the mouse: Localization, gender differences, and effects of estrogen treatment.

Nucleus retroambiguus (NRA)-motoneuronal projections are species-specific and serve expiration, Valsalva maneuvers, vocalization, and sexual behavior. In cat and monkey, estrogen induces sprouting of NRA-spinal axons. This pathway may thus serve as a model to study mechanisms through which estrogen induces neuronal plasticity. In this study, NRA-spinal projections are described in adult mice by using anterograde and retrograde tracing techniques, with attention to gender, strain (CD-1 and C57BL/6), and estrogen-induced changes (in ovariectomized females). Labeled NRA-spinal neurons at the level of the decussation of the corticospinal tract were most numerous after tracer injections into the thoracic and upper lumbar cord. They were medium-sized and had axons that descended through the contralateral cord. A group of small neurons was labeled in the NRA immediately rostral to the decussation of the corticospinal tract after cervical and thoracic, but not after lumbar injections. This group projected mainly via an ipsilateral pathway. The main projections from the caudal NRA involved motoneurons in the thoracic and upper-lumbar cord that supply abdominal wall and cremaster muscles. Pelvic floor motoneurons did not receive substantial input. NRA-spinal projections, especially those involving the upper lumbar cord, were sexually dimorphic, being more extensive in males than in females. Moreover, they were more distinct in estrogen-treated females than in control females. Strain differences were not observed. The unique features of the caudal NRA-spinal pathway in the mouse are discussed in the framework of possible functions of this system, such as mating behavior and related social behaviors, parturition, thermoregulation, and control of balance.

Animals↗
PubMed2005

Monitoring of intercellular messengers released from neuron networks cultured in a microchip.

A cellular biochemistry analysis system was integrated on a quartz glass microchip with a microchamber for cell culture followed by a microchannel for detecting with a thermal lens microscope (TLM). Nerve cells from rat hippocampus were successfully cultured to form neural networks in the microchip. An aqueous solution of glutamate, which is known as a neurotransmitter, was introduced to stimulate the cultured neuron to release a retrograde messenger, arachidonate which is considered to be critical for neuronal plasticity, especially for long-term potentiation (LTP). After the introduction, the solution that flowed through the culture chamber was analyzed using the UV-TLM (excitation wavelength, 244 nm). The measured signal intensity was dependent on glutamate solution concentration, and the neurons were considered to release the retrograde messenger according to the glutamate concentration. This system is suitable for time-course monitoring of ultra trace amounts of chemicals released from very small amount of cultured cells.

Animals↗
PubMed1997

Involvement of three glutamate receptor epsilon subunits in the formation of N-methyl-D-aspartate receptors mediating excitotoxicity in primary cultures of mouse cerebellar granule cells.

The N-methyl-D-aspartate receptors have been implicated in neuronal plasticity and their overactivation leads to neurotoxicity. Molecular cloning and co-expression of various glutamate receptor zeta and epsilon complementary DNAs support a heteromeric structural organization for N-methyl-D-aspartate receptors. In this study, we show that cerebellar granular neurons in primary culture of mouse express glutamate receptor zeta1 and at least three glutamate receptor epsilon (epsilon1, epsilon2, and epsilon3) protein subunits. In vitro, the temporal patterns of glutamate receptor epsilon1, epsilon2, and epsilon3 subunit expression depend on culture stages. By day 9, a somatic and neuritic immunolocalization for all N-methyl-D-aspartate subunits was clearly identified in most neuronal, but not glial cells. The role of particular subunits in N-methyl-D-aspartate-mediated excitotoxicity was probed by exposing the cerebellar granule cells to antisense oligodeoxynucleotides generated against specific N-methyl-D-aspartate receptor subunits. Antisense oligodeoxynucleotide treatments significantly down-regulated the amounts of the corresponding N-methyl-D-aspartate subunits. The decrease in N-methyl-D-aspartate subunit protein correlated with a reduction in N-methyl-D-aspartate-induced calcium influx and N-methyl-D-aspartate-mediated excitotoxicity in cerebellar cultures. In contrast, antisense oligodeoxynucleotide treatment failed to protect neurons from 1-methyl-4-phenylpyridinium-induced metabolic cell toxicity. Antisense oligodeoxynucleotide treatment targeted at N-methyl-D-aspartate glutamate receptor epsilon subunits demonstrate that glutamate receptor epsilon1, epsilon2, and epsilon3 proteins form N-methyl-D-aspartate receptors responsible for neurotoxic effects on cerebellar neurons. This study provides direct evidence for the existence of distinct N-methyl-D-aspartate receptor subunit proteins in cerebellar granule cells developing in vitro that may trigger N-methyl-D-aspartate-dependent excitotoxicity.

Animals↗
PubMed1998

Calcitonin gene-related peptide increase in the rat spinal dorsal horn and dorsal column nucleus following peripheral nerve injury: up-regulation in a subpopulation of primary afferent sensory neurons.

Calcitonin gene-related peptide in sensory primary afferent neurons has an excitatory effect on postsynaptic neurons and potentiates the effect of substance P in the rat spinal dorsal horn. It has been established that calcitonin gene-related peptide expression in dorsal root ganglion neurons is depressed, and the effect of calcitonin gene-related peptide on dorsal horn neurons is attenuated, following peripheral nerve injury. We report here that a subpopulation of injured dorsal root ganglion neurons show increased expression of calcitonin gene-related peptide. Using in situ hybridization and the retrograde tracer, FluoroGold, we detected an increased number of medium- to large-sized rat dorsal root ganglion neurons projecting to the gracile nucleus that expressed alpha-calcitonin gene-related peptide messenger RNA following spinal nerve transection. Immunohistochemistry revealed a significant increase in calcitonin gene-related peptide immunoreactivity in the gracile nucleus and in laminae III-IV of the spinal dorsal horn. These results indicate that a subpopulation of dorsal root ganglion neurons express alpha-calcitonin gene-related peptide messenger RNA in response to peripheral nerve injury, and transport this peptide to the gracile nucleus and to laminae III-IV of the spinal dorsal horn. The increase of the excitatory neuropeptide, calcitonin gene-related peptide, in sites of primary afferent termination may affect the excitability of postsynaptic neurons, and have a role in neuronal plasticity following peripheral nerve injury.

Animals↗
PubMed1998

Adrenal steroid regulation of neurotrophic factor expression in the rat hippocampus.

Adrenal steroids and neurotrophic factors are important modulators of neuronal plasticity, function, and survival in the rat hippocampus. Adrenal steroids act through two receptor subtypes, the glucocorticoid receptor (GR) and the mineralocorticoid receptor, and activation of each receptor subtype has distinct biochemical and physiological consequences. Adrenal steroids may exert their effects on neuronal structure and function through the regulation of expression of neurotrophic and growth-associated factors. We have examined adrenal steroid regulation of the neurotrophins brain-derived neurotrophic factor, neurotrophin-3, and basic fibroblast growth factor, as well as the growth associated protein GAP-43, through activation of GR or mineralocorticoid receptor with selective agonists. Our findings indicated that in CA2 pyramidal cells, adrenalectomy resulted in decreases in the levels of basic fibroblast growth factor and neurotrophin-3 messenger RNA, which were prevented by activation of mineralocorticoid but not glucocorticoid receptors. Adrenalectomy-induced increases in GAP-43 and brain-derived neurotrophic factor messenger RNA levels could be blocked by activation of glucocorticoid receptors in CA1, but not in CA3, pyramidal cells. Thus the extent to which adrenal steroids regulate hippocampal neurotrophic and growth-associated factors, appears to be dependent both on the adrenal steroid receptor subtype activated and on the hippocampal subregion examined.

Adrenalectomy↗
PubMed2002

Effect of plantar local anesthetic injection on dorsal horn neuron activity and pain behaviors caused by incision.

Hypersensitivity after tissue injury is an expression of neuronal plasticity in the central nervous system. This has been explored most extensively using in vitro preparations and animal models of inflammatory pain and chemical irritation. For pain after surgery, a similar process has been proposed. In the present study, we examined dorsal horn neuron (DHN) sensitization using the plantar incision model for post-operative pain. In behavioral experiments, the effect of a local anesthetic injection (or saline vehicle) 15 min before plantar incision on pain behaviors several days after incision was studied. Bupivacaine injection before incision prevented pain behaviors until 4 h afterwards; injection after incision produced the same effect. One day after incision, pain behaviors were not different between rats injected with saline or bupivacaine. In neurophysiologic experiments, however, bupivacaine injection blocked activation of DHNs during incision. One hour after incision, expansion of receptive fields (RFs) to pinch and increased background activity occurred in 14 of 16 neurons in the saline group but only in two of 22 neurons in the bupivacaine group. The difference was not due to a systemic effect of bupivacaine. Ten sensitized neurons were studied using the injection of bupivacaine 90 min after incision. Increased background activity (n=7) and expanded RFs (n=7) were reversed by bupivacaine. Sensitization was re-established in seven of eight neurons 2 h after injection as the local anesthetic dissipated. These results indicate that activation of DHNs during plantar incision and sensitization 1 h later are not necessary for subsequent pain behaviors. Because sensitization was reversed 90 min after plantar incision and then re-established as the local anesthetic effect diminished, enhanced responsiveness of DHN requires ongoing afferent input during the first day after incision.

Anesthetics, Local↗
PubMedDate not supplied

[The amiridin and tacrine modulation of the cholinoreceptor activity and plasticity of snail neurons: the phenomenology and mechanisms].

The effects of amiridine and tacrine on the membrane potential, activity and plasticity of cholinoreceptors have been studied using the recording of intracellular and transmembrane currents in identified neurons of Helix lucorum. Amiridine and tacrine (1-100 mcM) have no noticeable effects on the membrane potential of the cells. Both compounds modulate the activity of cholinoreceptors to judge from their influence on the inward current induced by the local acetylcholine (ACh) application: they increase the duration of the current with a two-phase effect on the amplitude (a short-latent intensification with a following decrease). Amiridine and tacrine intensify ACh current extinction induced by repeated ACh application to the soma. Acetylcholinesterase inhibitor physostigmine has a similar modulating effect on ACh current and its extinction. It impedes the modulating effects of amiridine and tacrine. Amiridine and physostigmine directly affect cholinoreceptors and ion channels controlled by them changing in a similar way the current-voltage curves of ACh-current and approximating it to the equilibrium potential of chloride ions. Modulating effects of amiridine, tacrine and physostigmine on the activity and plasticity of cholinoreceptors may be supposed to be caused by their direct membrane-cytoplasmic action.

Acetylcholine↗
PubMed2002

Synaptic plasticity and tianeptine: structural regulation.

Stress-induced structural and cellular alterations in the hippocampus can contribute to the pathophysiology of depression. The reversal of these alterations may be a mechanism by which antidepressants achieve their therapeutic effect. The aim of the present study was therefore to investigate the effect of tianeptine on stress-induced structural changes and alterations in cerebral metabolites. To this end, psychosocially stressed male tree shrews were treated with tianeptine. A combination of in vivo and postmortem methods was used to evaluate the antidepressant treatment on the preservation of neuronal plasticity. It was found that all stress-induced effects were prevented by the administration of tianeptine. It is concluded that these findings provide experimental evidence for recent theories that impairment of neuronal viability and neuroplasticity might be important causal factors in mood disorders, suggesting tianeptine as a potential stimulator of neural resilience.

Administration, Oral↗
PubMed1991

Actions of noradrenaline on neocortical neurons in vitro.

The effects of noradrenaline (NA) and alpha- and beta-adrenergic agonists on neocortical neurons in rat brain slices were studied by intracellular recording. NA added to the perfusion medium decreased the orthodromically evoked excitatory postsynaptic potential (EPSP) and increased the neuronal excitability on current injection. The decrease of the EPSP by NA was mimicked by alpha-adrenoceptor activation. The beta-adrenergic agonist, isoprenaline, increased the neuronal excitability to current injections similarly to NA. In addition, isoprenaline markedly increased the amplitude of a late component of the EPSP (I-EPSP). The increase of the I-EPSP was long-lasting (up to 90 min). Since this late component of the EPSP is blocked by the NMDA (N-methyl-D-aspartate)-antagonist APV (D-2-amino-5-phosphonovalerate), an enhancement of this excitatory synaptic transient via beta-adrenoceptors may be relevant for the facilitatory effect of NA on neuronal plasticity.

2-Amino-5-phosphonovalerate↗
PubMed2006

GABAmimetic intravenous anaesthetics inhibit spontaneous Ca2+ -oscillations in cultured hippocampal neurons.

BACKGROUND: Spontaneous Ca2+ -oscillations are a possible mechanism of Ca2+ -mediated signal transduction in neurons. They develop by a periodical interplay of Ca2+, which enters the neuron from the extracellular medium and triggers Ca2+ release from the endoplasmic reticulum (ER). Ca2+ -oscillations are terminated by reuptake into the ER or plasmalemmal extrusion. Spontaneous Ca2+ -oscillations are glutamate dependent and appear to be responsible for neuronal plasticity and integration of information. Here, we examined the role of the gamma-aminobutyric acid (GABAA) receptor on spontaneous Ca2+ -oscillations and studied the effects of the anaesthetics midazolam, thiopental and the non-anesthetic barbituric acid on spontaneous Ca2+ -oscillations. METHODS: Hippocampal neuronal cell cultures of 19-day-old embryonic Wistar rats 17-18 days in culture were loaded with the Ca2+ -sensitive dye Fura-2AM. Experiments were performed using dual wave-length excitation fluorescence microscopy and calibration constants were obtained from in situ calibration. RESULTS: Spontaneous Ca2+ -oscillations are influenced by the GABAA receptor. The intravenous anaesthetics midazolam and thiopental suppressed the amplitude and frequency reversibly in a dose-dependent manner with EC50 in clinically relevant concentrations. This effect was mediated via the GABAA receptor as it could be reversed by the GABAA receptor antagonist bicuculline. In contrast, the application of barbituric acid had no effects on the spontaneous Ca2+ -oscillations. CONCLUSION: Spontaneous Ca2+ -oscillations are influenced by the GABAA receptor. Spontaneous Ca2+ -oscillations might represent an interesting model system to study anaesthetic mechanisms on neuronal information processing.

Anesthetics, Intravenous↗