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PubMed2000

A herpes simplex virus type 1 vector as marker for retrograde neuronal tracing: characterization of lacZ transcription and localization of labelled neuronal cells in sensory and autonomic ganglia after inoculation of the anterior segment of the eye.

Herpes simplex virus type 1 (HSV-1) is a human, neurotropic pathogen which also can infect experimental animals. Much interest has been focused on genetic modification of HSV-1 so that it can be used as a vector for gene delivery and for tracing neuronal connections. For expression of a foreign gene inserted into the HSV-1 genome, both the site of insertion and the promoter activity are important. We have used a previously described HSV-1 vector, KOS/58, to demonstrate that the beta-galactosidase gene inserted together with a neurofilament L promoter into the coding region of the glycoprotein C (gC) gene is under the control of the foreign promoter rather than under that of the gC gene. This was performed by isolation of RNA from infected, neuron-like PC12 cells and Northern blotting using probes from various regions of the modified part of the genome. The vector was then inoculated in the cornea, subconjunctivally, or into the anterior chamber of the mouse eye. Whole mounts of the trigeminal, superior cervical and pterygopalatine ganglions were stained for beta-galactosidase. The localization of labelled neurons was consistent with retrograde axonal transport as the principal way of neuronal infection indicating that KOS/58 could be used as a retrograde tracer. The position of the labelled cells suggests a somatotopic organization of the mouse trigeminal and superior cervical ganglion similar to that of rats and rabbits.

Animals↗
PubMed2006

Metalloprotease-induced ectodomain shedding of neural cell adhesion molecule (NCAM).

Transmembrane forms of neural cell adhesion molecule (NCAM140, NCAM180(1)) are key regulators of neuronal development. The extracellular domain of NCAM can occur as a soluble protein in normal brain, and its levels are elevated in neuropsychiatric disorders, such as schizophrenia; however the mechanism of ectodomain release is obscure. Ectodomain shedding of NCAM140, releasing a fragment of 115 kD, was found to be induced in NCAM-transfected L-fibroblasts by the tyrosine phosphatase inhibitor pervanadate, but not phorbol esters. Pervanadate-induced shedding was mediated by a disintegrin metalloprotease (ADAM), regulated by ERK1/2 MAP kinase. In primary cortical neurons, NCAM was shed at high levels, and the metalloprotease inhibitor GM6001 significantly increased NCAM-dependent neurite branching and outgrowth. Moreover, NCAM-dependent neurite outgrowth and branching were inhibited in neurons isolated from a transgenic mouse model of NCAM shedding. These results suggest that regulated metalloprotease-induced ectodomain shedding of NCAM down-regulates neurite branching and neurite outgrowth. Thus, increased levels of soluble NCAM in schizophrenic brain have the potential to impair neuronal connectivity.

ADAM Proteins↗
PubMed1984

Synaptogenesis in the chick cervical cord and possible initial central pathways from dorsal root fibers to motor neurons--Golgi and electron microscopic studies.

The early formation of neuronal connections in the cervical cord of the chick embryo was studied by observing axonal courses at stages 24 and 27 with Golgi preparations and the distribution of synapses at stages 22, 25 and 27 with electron microscopy. Early developing interneurons sent their axon to the ventral and lateral funiculi. Synapses were observed in the transit part from ventral to lateral funiculus at stage 22, in the ventral funiculus, the ventral part of the lateral funiculus and the dorsal funiculus at stage 25. It was suggested that the neuronal pathways from dorsal root fibers to motor neurons were first formed at stage 25 with the intervention of interneurons.

Animals↗
PubMed2006

Sculpting the nervous system: glial control of neuronal development.

Glial cells are not passive spectators during nervous system assembly, rather they are active participants that exert significant control over neuronal development. Well-established roles for glia in shaping the developing nervous system include providing trophic support to neurons, modulating axon pathfinding, and driving nerve fasciculation. Exciting recent studies have revealed additional ways in which glial cells also modulate neurodevelopment. Glial cells regulate the number of neurons at early developmental stages by dynamically influencing neural precursor divisions, and at later stages by promoting neuronal cell death through engulfment. Glia also participate in the fine sculpting of neuronal connections by pruning excess axonal projections, shaping dendritic spines, and secreting multiple factors that promote synapse formation and functional maturation. These recent insights provide further compelling evidence that glial cells, through their diverse cellular actions, are essential contributors to the construction of a functionally mature nervous system.

Animals↗
PubMed1992

Acute reserpine treatment increases rat brain serotonin synthesis via a nerve impulse-dependent mechanism.

Notwithstanding recent advances in the understanding of central serotonin (5-HT) function, important basic aspects of the control of brain 5-HT neuronal transmission remain incompletely elucidated. The present experiments addressed the putative mechanism(s) by which acute reserpine treatment stimulates cerebral 5-HT synthesis; also, such studies might shed further light on the relation between impulse flow and transmitter synthesis in central 5-HT neurons. Reserpine (5 mg/kg, i.p., 90 min before death) markedly elevated 5-HT synthesis [5-hydroxytryptophan (5-HTP) accumulation after decarboxylase inhibition by means of NSD 1015] in the limbic, striatal, and cortical rat brain parts. Hemitransection of ascending neuronal connections between the brainstem and the forebrain, performed immediately before reserpine injection, did not affect the 5-HT synthesis per se but completely prevented the drug response on the lesioned side. Similarly, systemic administration of the selective 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (0.1 mg/kg, s.c., 60 min before death) blocked the reserpine-induced elevation of brain 5-HT synthesis. These findings indicate that the reserpine-induced rise in axon terminal 5-HTP accumulation is dependent on intact (5-HT) neuronal impulse flow, which may or may not involve a transient impairment of somatodendritic 5-HT release and, in turn, autoreceptor tone.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1989

Ruthenium red selectively prevents capsaicin-induced nociceptor stimulation.

The effect of Ruthenium Red on capsaicin-induced stimulation of polymodal nociceptors was investigated in the isolated perfused rabbit ear with an intact neuronal connection. Ruthenium Red, 20 microM, completely prevented the response to capsaicin but not that to acetylcholine or bradykinin. It is therefore suggested that capsaicin activates sensory nerve terminals by a mechanism which is different from that for bradykinin or acetylcholine, and which can be blocked selectively by Ruthenium Red.

Acetylcholine↗
PubMed2006

Is being plastic fantastic? Mechanisms of altered plasticity after developmental traumatic brain injury.

Traumatic brain injury (TBI) is predominantly a clinical problem of young persons, resulting in chronic cognitive and behavioral deficits. Specifically, the physiological response to a diffuse biomechanical injury in a maturing brain can clearly alter normal neuroplasticity. To properly evaluate and investigate developmental TBI requires an understanding of normal principles of cerebral maturation, as well as a consideration of experience-dependent changes. Changes in neuroplasticity may occur through many age-specific processes, and our understanding of these responses at a basic neuroscience level is only beginning. In this article, we will particularly discuss mechanisms of TBI-induced altered developmental plasticity such as altered neurotransmission, distinct molecular responses, cell death, perturbations in neuronal connectivity, experience-dependent 'good plasticity' enhancements and chronic 'bad plasticity' sequelae. From this summary, we can conclude that 'young is not always better' and that the developing brain manifests several crucial vulnerabilities to TBI.

Aging↗
PubMed1984

Localizing spinal-cord-projecting neurons in neonatal and immature albino rats.

According to results from the horseradish peroxidase (HRP) method of tracing neuronal connections, the spinal cords of neonatal and immature rats receive a large number of descending projections from the first cervical cord segment, various brain-stem nuclei, and deep cerebellar and diencephalic nuclei. All these projections are present at birth, though at this age some of them are not fully established. Thus, only a few cells in the trigeminospinal, solitariospinal, tectospinal, and cerebellospinal groups were labeled after HRP injection in the lumbosacral or cervical cord segments in neonatal animals. They were clearly labeled in older, immature animals. The labeled neurons in other descending pathways appeared to be equal in density in neonatal, immature, and adult rats. This visual impression was stregthened by the counts of neurons in the interstitial nucleus of Cajal, which showed no significant difference in the number of labeled neurons in the three age groups. However, counts of labeled cells in the lateral vestibular nucleus and nucleus of the posterior commissure showed that there is a steady rise in the number of labeled neurons as the animals increase in age.

Animals↗
PubMed1999

Continual remodeling of postsynaptic density and its regulation by synaptic activity.

A postsynaptic density (PSD) protein, PSD-95, was tagged with green fluorescent protein (GFP-PSD-95) and expressed in cultured hippocampal neurons using recombinant adenoviruses. GFP-PSD-95 was selectively localized to excitatory postsynaptic sites. Time-lapse fluorescence imaging of hippocampal neurons revealed that >20% of GFP-PSD-95 clusters turned over within 24 hours. The appearance rate of clusters was higher than the disappearance rate, and this difference accounted for the gradual increase of the cluster density observed in culture. Dynamics of PSD-95 clusters were also inhibited by blockers of excitatory synaptic transmission. Continual PSD turnover and its regulation by synaptic activity may be important in activity-dependent remodeling of neuronal connections.

2-Amino-5-phosphonovalerate↗
PubMed1993

Intracranial injection of Fluoro-Gold results in the degeneration of local but not retrogradely labeled neurons.

Small volumes of either Fluoro-Gold (hydroxy-stilbamidine) or physiological saline were pressure injected into the striatum of adult rats. This paradigm is essentially the same as that used by neuroscientists who inject small quantities of Fluoro-Gold into brain structures to reveal neuronal connections. Using a modified de Olmos' cupric-silver technique, virtually no degeneration could be detected as the result of saline injection at any time point examined. However, comparable injections of Fluoro-Gold resulted in conspicuous cell body and terminal degeneration within the striatum 1-10 days post injection. Terminal degeneration within the substantia nigra pars reticulata could also be seen 2-10 days after injection. Examination of cells of the compacta region revealed conspicuous retrograde uptake of Fluoro-Gold, although none of these cells exhibited any evidence of neuronal degeneration at any postoperative time examined.

Animals↗
PubMed2000

Brain injury: prolonged induction of transcription factors.

A specific temporal order of events at the cellular and molecular level occurs in response to injury to the brain. Injury-compromised neurons degenerate while surviving neurons undergo neuritogenesis and synaptogenesis to establish neuronal connectivity destroyed in the injury. Several genes, such as those coding cytoskeletal proteins and growth factors, have been shown to be regulated by AP-1 and NF-kappa B transcription factors, two of the most studied DNA binding regulatory proteins. Our laboratory has discovered that Fos-related antigen-2 from AP-1 transcription factor family and NF-kappa B p65 and p50 subunits are induced long-term (days to months) in the brain after neurotoxic, excitotoxic or ischemic insult. Fos-related antigen-2 is induced in neurons in several models of injury and its elevated expression lasts days to months, corresponding to the severity. The time-course of FRA-2 induction is abbreviated with less severe insult (terminal damage) relative to the cell death, but the induction occurs during the period of regeneration and repair in both models. NF-kappa B p65 is basally expressed in hippocampal and cortical neurons, but is elevated in reactive astrocytes in hippocampus and entorhinal cortex starting at two days and lasting at least two weeks after kainate treatment. Neurons of the hippocampus surviving ischemic or neurotoxic injury increase expression of NF-kappa B p50 for at least a week after injury, suggesting a function for p50 in neuronal survival and/or repair. The extended expression of these transcription factors implies a role in the activation of genes related to repair and regeneration, such as growth factors and synaptic proteins, after injury to the CNS.

Animals↗
PubMed1988

Interaction among different sensory units within a single fungiform papilla in the frog tongue.

The possible interaction among different sensory units in the frog tongue was studied using several single papillae dually innervated by the medial and lateral branches of the glossopharyngeal (IXth) nerve. The afferent activity in one branch exposed to NaCl stimulation of the papilla revealed marked inhibition after antidromic electrical stimulation (100 Hz, 30 s, and 3 V) of the other branch. The degree of inhibition depended on the number of sensory responses observed in the electrically stimulated branch as well as the nature of the stimulated sensory units. Statistical analysis suggested that antidromic activation of gustatory units conducting the responses to NaCl and quinine and slowly adapting mechanosensitive units produced a large antidromic inhibition amounting to 19-25%, but that of gustatory units conducting the responses to acetic acid and rapidly adapting mechanosensitive units gave rise to only a slight inhibition. To examine the differential effects of these sensory units in antidromic inhibition, antidromic impulses were evoked by chemical stimulation of the adjacent papilla neuronally connected with the dually innervated papilla under study. Antidromic volleys of impulses elicited by NaCl or quinine stimulation produced a large inhibition of the afferent activity in the other branch, as induced by NaCl stimulation of the dually innervated papilla. Plausible mechanisms of synaptic interaction in peripheral gustatory systems are considered.

Acetates↗
PubMed1982

[Study of histoenzymologic signs of selective neuronal hyperactivity].

Injection of kainic acid into the cerebellum leads to a neuroexcitatory and neurotoxic effect on neurons connected with cerebellar granule cells. Observation of the activities of dehydrogenases taking part in glucose metabolism and glutamate dehydrogenase shows that Purkinje cells undergo a rapid destruction. Lesions of small stellate cells come later. But the basket cells present a long period of hyperactivity revealed by an increase of dehydrogenase activity.

Animals↗
PubMed1996

[Psychological stress and neuronal plasticity. An expanded model of the stress reaction process as the basis for understand central nervous system adaptation processes].

A short survey on results and theories in psychosomatic and neurobiologic stress research is presented. Based on a comprehensive definition of the stress-reaction process, the biological and psychological consequences are described which are elicited by either controllable or uncontrollable stress. We conclude that controllable stress triggers the stabilization and facilitation of neuronal networks involved in the generation of appropriate patterns of appraisal and coping, whereas uncontrollable stress favours the extinction of inappropriate patterns and the reorganisation of neuronal connections underlying certain inappropriate behaviors. Both, controllable an uncontrollable stress-reaction-processes are therefore essential prerequisites of, and inherent challenges to, the development and adaptation of an individual in an ever changing external world but may also lead to psychodevelopmental failures and psychosomatic diseases.

Adaptation, Psychological↗
PubMedDate not supplied

Unilateral injection of neuropeptide Y decreases blood flow in the injected testis but may also increase blood flow in the contralateral testis.

Neuropeptide Y (NPY) receptors have recently been described in intratesticular arterioles, but the role of NPY in testicular blood-flow regulation has not been examined. To explore this, we administered NPY in various doses (0.01-10 microg) via intratesticular injections and studied testicular microcirculation using a laser Doppler flow meter. NPY injection shows a dose-response pattern, with 1 microg (the most potent dose) causing a decrease (-42.4 +/- 3.7%, P < 0.00005) in blood flow in the ipsilateral testis of all the animals and an increase in blood flow in the contralateral testis (+17.2 +/- 5.6%, P = 0.03, n = 25 animals). The response in the contralateral testis was variable. A clear-cut increase was seen in 19 of the 25 animals examined, whereas either no response or a slight decrease was seen in the remaining six. The contralateral increase, which was not seen in the hindpaw on the same side, did not occur when the neuronal connections to the testes were blocked by injection of local anesthetics into the spermatic cord, either on the NPY-injected side or on the contralateral side. Our results suggest that NPY may serve as a vasoconstrictor in the testis, probably by acting on the NPY-Y1 receptors present on intratesticular arterioles. Local injection of NPY causes a major decrease in blood flow in the injected testis. This decrease is followed in the majority of animals studied by an increase in blood flow in the contralateral testis, an effect that seems to depend on neuronal mechanisms. This observation suggests that the testes may communicate under certain situations. The functional consequences of this remain to be elucidated.

Animals↗
PubMed2001

Periods of postnatal maturation of hippocampus: synaptic modifications and neuronal disconnection.

The paired-pulse paradigm was used to study the maturation of CA1 population spikes (PS) in the hippocampal slices of Wistar rats. Measurements were taken daily, from postnatal day (PN) 14 to PN27. In the slices from younger animals, inputs exhibit strong paired-pulse profile, which may be associated with low synaptic efficacy. Both responses increased during the third week of life, however, PS1 increased faster so that the PS1/PS2 ratio increased during the early period and remained increased thereafter. This may reflect postnatal modifications of synaptic transmission mediating the increase in hippocampal responses. Modifications of synaptic efficacy are prevailing during early phases while other mechanisms take over at later stages. Partial correlation analysis suggests that the decline of PS amplitude after PN19 may be due to the decrease in the number of connected neurons rather than to modifications of the synaptic efficacy. Thus, the actual direction and magnitude of postnatal PS maturation is suggested to depend on the balance of these two factors. The transient decline of PS amplitude coincided with a period of caspase-3 activation. There was a clear general trend for caspase-3 activity to decrease before PN17, while the inverse trend was observed during next period up to PN21.

Action Potentials↗
PubMed2001

Principles underlying mammalian neocortical scaling.

The neocortex undergoes a complex transformation from mouse to whale. Whereas synapse density remains the same, neuron density decreases as a function of gray matter volume to the power of around -1/3, total convoluted surface area increases as a function of gray matter volume to the power of around 8/9, and white matter volume disproportionately increases as a function of gray matter volume to the power of around 4/3. These phylogenetic scaling relationships (including others such as neuron number, neocortex thickness, soma radius, and number of cortical areas) are clues to understanding the principles driving neocortex organization, but there is currently no theory that can explain why these neocortical quantities scale as they do. Here I present a two-part model that explains these neocortical allometric scaling laws. The first part of the model is a special case of the physico-mathematical model recently put forward to explain the quarter power scaling laws in biology. It states that the neocortex is a space-filling neural network through which materials are efficiently transported, and that synapse sizes do not vary as a function of gray matter volume. The second part of the model states that the neocortex is economically organized into functionally specialized areas whose extent of area-interconnectedness does not vary as a function of gray matter volume. The model predicts, among other things, that the number of areas and the soma radius increase as a function of gray matter volume to the power of 1/3 and 1/9, respectively, and empirical support is demonstrated for each. Also, the scaling relationships imply that, although the percentage of the total number of neurons to which a neuron connects falls as a function of gray matter volume with exponent -1/3, the network diameter of the neocortex is invariant at around two. Finally, I discuss how a similar approach may have promise in explaining the scaling relationships for the brain and other organs as a function of body mass.

Animals↗
PubMed1998

Anatomical distribution of the chemorepellent semaphorin III/collapsin-1 in the adult rat and human brain: predominant expression in structures of the olfactory-hippocampal pathway and the motor system.

Alterations in neuronal connectivity of the mature central nervous system (CNS) appear to depend on a delicate balance between growth-promoting and growth-inhibiting molecules. To begin to address a potential role of the secreted chemorepulsive protein semaphorin(D)III/collapsin-1 (semaIII/coll-1) in structural plasticity during adulthood, we used high-resolution nonradioactive in situ hybridization to identify neural structures that express semaIII/coll-1 mRNA in the mature rat and human brain. SemaIII/coll-1 was expressed in distinct but anatomically and functionally linked structures of the adult nervous system. The olfactory-hippocampal pathway displayed semaIII/coll-1 expression in a continuum of neuronal structures, including mitral and tufted cells of the olfactory bulb, olfactory tubercle, and piriform cortex; and distinct nuclei of the amygdaloid complex, the superficial layers of the entorhinal cortex, and the subiculum of the hippocampal formation. In addition, prominent labeling was found in neuronal components of the motor system, particularly in cerebellar Purkinje cells and in subpopulations of cranial and spinal motoneurons. Retrograde tracing combined with in situ hybridization also revealed that the staining of semaIII/coll-1 within the entorhinal cortex was present in the stellate neurons that project via the perforant path to the molecular layer of the dentate gyrus. Like in the rat, the human brain displayed discrete expression of semaIII/coll-1. Among the structures examined, the most prominent staining was observed in the cellular islands of the superficial layers of the human entorhinal cortex. The constitutive expression of the chemorepellent semaIII/coll-1 in discrete populations of neurons in the mature rat and human CNS raises the possibility that, in addition to its function as repulsive axon guidance cue during development, semaIII/coll-1 might be involved in restricting structural changes that occur in the wiring of the intact CNS.

Adult↗