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PubMedDate not supplied

[Callosal neurons: monosynaptic connection between them and their descending projections].

Antidromic and monosynaptic unit responses to the stimulation of the corpus callosum and the symmetrical cortical area as well as antidromic responses to pyramidal tract and thalamic nuclei stimulation were recorded in the sensorimotor cortex of unanaesthetized rabbits. Out of 182 callosal neurones 13 exhibited transcallosal monosynaptic responses. 8 out of 56 callosal units responded antidromically to pyramidal tract or thalamic stimulation. Thus callosal neurones may be monosynaptically excited by callosal units via the corpus callosum and by the pyramidal tract units. It was also found that a pyramidal tract neurone may send a collateral through the corpus callosum and at the same time have a transcallosal monosynaptic input. The role of monosynaptic transcallosal excitation of callosal neurones is discussed.

Animals↗
PubMed2002

Directional spread of an alpha-herpesvirus in the nervous system.

Pseudorabies virus (PRV), an alpha-herpesvirus, is capable of spreading between synaptically connected neurons in diverse hosts. In this report, two lines of experimentation are summarized that provide insight into the mechanism of virus spread in neurons. First, techniques were developed to measure the transport dynamics of capsids in infected neurons. Individual viral capsids labeled with green fluorescent protein (GFP) were visualized and tracked as they moved in axons away from infected neuronal cell bodies in culture during egress. Second, the effects of three viral membrane proteins (gE, gI and Us9) on the localization of envelope, tegument, and capsid proteins in infected, cultured sympathetic neurons were determined. These three proteins are necessary for spread of infection from pre-synaptic neurons to post-synaptic neurons in vivo (anterograde spread). Us9 mutants apparently are defective in anterograde spread in neural circuits because essential viral membrane proteins such as gB are not transported to axon terminals to facilitate spread to the connected neuron. By contrast, gE and gI mutants manifest their phenotype because these proteins most likely function at the axon terminal of the infected neuron to promote spread. These two sets of experiments are consistent with a model for herpesvirus spread in neurons first suggested by Cunningham and colleagues where capsids and envelope proteins, but not whole virions, are transported separately into the axon.

Animals↗
PubMed1976

Effects of benzodiazepines and pentobarbital on the evoked potentials in the cat brain.

The sites of action of benzodiazepines, diazepam and ID-540 [7-chloro-5-(o-fluorophenyl)-1-methyl-1,3-dihydro-2H-1,4-benzodiazepin-2-one) on the central nervous system were examined and compared with those of pentobarbital using evoked potentials recorded on the limbic system and hypothalamus in the cat brain. Benzodiazepines affected the various neuronal connections of the intra-limbic, limbic-hypothalamic and midbrain-limbic systems; especially the amygdala (AMYG)-, ventromedial hypothalamus (VMH)- and central gray matter (SGC)-hippocampal (HIPP) evoked potentials were attenuated, whereas the AMYG-VMH, VMH-AMYG and the septum (SP)-VMH evoked potentials were facilitated. Pentobarbital selectively attenuated the SGC-, VMH- and AMYG-HIPP evoked potentials, or facilitated the VMH-AMYG and the SP-HIPP evoked potentials. Both benzodiazepines and pentobarbital affected three afferent hippocampal neuronal connections, areas of the reticulo-hypothalamic systems regulating hippocampal activity, while only benzodiazepines affected the neuronal influence of the amygdaloid and septal areas on the hypothalamus.

Amygdala↗
PubMed1985

Neural plasticity in schizophrenia.

No current biological hypothesis can assimilate the genetic, environmental, and clinical features of schizophrenia. If, as some authors contend, environmental factors have important effects on the course of schizophrenia, then a fruitful research concern may be the adaptation of neuronal circuitry to environmental changes. The plasticity of neuronal connections has been studied by subjecting animals to neurosurgical lesions, brain electro-stimulation, and a variety of rearing environments. The present article approaches the schizophrenia research literature from a theoretical perspective which takes into account the plasticity of neuronal connections. In a speculative manner, it demonstrates how neural plasticity concepts can be invoked to explain the following seemingly disparate features of schizophrenia: the pharmacological support for the dopamine hypothesis, the delayed onset and offset of neuroleptic antipsychotic action, genetic and environmental influences in schizophrenia, the regional alterations in brain structure and function seen in chronic schizophrenic patients, and the various types of behavioral symptoms exhibited by schizophrenic patients. In view of the explanatory potential of neural plasticity concepts, a research program that focuses on these concepts seems warranted.

Animals↗
PubMed1993

Inhibitory commissural connections of neurones in the trigeminal motor nucleus of the rat.

Physiological evidence is presented for the existence of commissural fibres that cross the midsagittal plane in the medulla of the rat at the level of the trigeminal motor nucleus (Mo5). These fibres, which have their origin in the Mo5, terminated in the contralateral Mo5. Small inhibitory postsynaptic potentials were recorded in jaw-closing motoneurones by electrical activation of the commissural fibres; jaw-opening and fusimotor neurones as well as the jaw-closing and jaw-opening reflex were not affected. Electromyographic recordings from jaw-closing and jaw-opening muscles in the unrestrained rat showed that masseter activity was inhibited by the commissural fibres. These trigeminal commissural connections might play a part in the co-ordination of bilateral activity of the jaw-closing musculature during unilateral chewing.

Animals↗
PubMed2003

[Brain central amygdaloid nucleus: cytoarchitechtonics, neuronal organization, connections].

This review describes different aspects of structural and functional organization of amygdaloid central nucleus (CN) in association with the findings indicating its involvement in the development of stress reactions and adaptive behavior in animals. The data on the distribution of neuropeptides, neurotransmitters and neuromodulators in CN are discussed. It is emphasized that CN appears at the earliest stages of amygdaloid formation, undergoes remodeling together with it and reflects the evolution of the whole amygdaloid. The detailed data are presented on the cytoarchitectonic of amygdaloid CN, its heteromorphism and subdivision into zones (subnuclei), based on the different methods of investigation and evaluation criteria. The neuronal organization of CN and its subnuclei is discussed, and the detailed description of neurons of different types is given according to their topography, cell body dimensions and shape, dendrite orientation and branching pattern, organization of spine apparatus and axon structure. The developmental features of amygdaloid CN in mammalian animal and human ontogenesis are considered. The analysis covering the literature data and the results of authors' own investigations indicates that CN functions not only as intraamigdaloid integrative center, but also as one of the major channels providing both afferent and efferent connections of amygdaloid with other brain structures.

Amygdala↗
PubMed2004

The central nucleus of the amygdaloid body of the brain: cytoarchitectonics, neuronal organization, connections.

This review considers the questions of the structural-functional organization of the central nucleus (CN) of the amygdaloid body (AB) of the brain in relation to new data on its involvement in the formation of stress reactions and adaptive behavior in animals. Data are presented on the distribution of neuropeptides, neurotransmitters, and modulators in the CN. It is noted that the CN, appearing at the earliest stages of establishment of the AB, is reorganized with it and reflects the evolution of the whole AB. Detailed data are presented on the cytoarchitectonics of the CN of the AB, its heteromorphousness, and subdivision into zones (subnuclei) based on the use of different study methods and assessment criteria. The neuronal organization of the CN and its subnuclei is considered; detailed descriptions of different types of neurons are provided, with consideration of their topographies, sizes, and shapes and of their perikarya, the orientation and type of branching of their dendrites, the organization of the spine apparatus, and axon structure. The characteristics of the development of the CN of the AB in the ontogenesis of mammals and man are discussed. Analysis of published data and our own results supports the role of the CN not only as an intra-amygdalar integrative center, but also as one of the major channels for the afferent and efferent connections of the AB with the rest of the brain.

Amygdala↗
PubMed1988

Parallel processing of short-term memory for sensitization in Aplysia.

How is the short-term memory for a single form of learning distributed among the various elements of a neuronal circuit? To answer this question, we examined the short-term memory for sensitization, using the siphon component of the defensive gill- and siphon-withdrawal reflex. We found that the memory for short-term sensitization is represented by at least four sites of circuit modification, each involving a different type of plasticity. These include (1) presynaptic facilitation of the sensory neuron connections onto both interneurons and motorneurons; (2) presynaptic inhibition at the connections of the L30 inhibitory neurons onto the excitatory interneuron L29; (3) posttetanic potentiation of the excitatory connections made by L29 onto a specific subclass of siphon motorneurons, the LFS cells; and (4) an increase in the tonic firing rate of the LFS siphon motor neurons, resulting in neuromuscular facilitation. Each of the heterosynaptic changes seems to involve a common modulatory transmitter and to utilize a common second messenger system. Moreover, each of these sites seems capable of encoding a different component of the short-term memory. Facilitation of the connections of sensory neurons should contribute to the increase in amplitude of the response; the disinhibition of the L29 interneurons and the posttetanic potentiation at L29 synapses should contribute to an increase in the duration of the response; and the increase in tonic firing of the LFS subclass of siphon motor neurons seems capable of contributing both to an increase in response amplitude and to changes in response topography.

Animals↗
PubMed2000

Presynaptic protein kinase activity supports long-term potentiation at synapses between individual hippocampal neurons.

Simultaneous microelectrode recording from two individual synaptically connected neurons enables the direct analysis of synaptic transmission and plasticity at a minimal synaptic connection. We have recorded from pairs of CA3 pyramidal neurons in organotypic hippocampal slices to examine the properties of long-term potentiation (LTP) at such minimal connections. LTP in minimal connections was found to be identical to the NMDA-dependent LTP expressed by CA3-CA1 synapses, demonstrating this system provides a good model for the study of the mechanisms of LTP expression. The LTP at minimal synaptic connections does not behave as a simple increase in transmitter release probability, because the amplitude of unitary EPSCs can increase several-fold, unlike what is observed when release probability is increased by raising extracellular calcium. Taking advantage of the relatively short axon connecting neighboring CA3 neurons, we found it feasible to introduce pharmacological agents to the interior of presynaptic terminals by injection into the presynaptic soma and have used this technique to investigate presynaptic effects on basal transmission and LTP. Presynaptic injection of nicotinamide reduced basal transmission, but LTP in these pairs was essentially normal. In contrast, presynaptic injection of H-7 significantly depressed LTP but not basal transmission, indicating a specific role of presynaptic protein kinases in LTP. These results demonstrate that pharmacological agents can be directly introduced into the presynaptic cell and that a purely presynaptic perturbation can alter this plasticity.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2000

[Spatial organizations of projections from area 18 to area 17 in the cat visual cortex].

Spatial distribution of efferent neuronal connections from area 18 to area 17 in the cat was investigated using the microiontophoretic horseradish peroxidase injections in a single cortical columns of area 17. The localization of rertogradely labelled cells in area 18 was determined and plots of labelled cells distribution in the plane of cortical surface, in the sagittal and in the frontal planes were done. It was shown that neuronal connections from area 18 to the single column in area 17 are elongated (in the cortical surface plane) in the same rostrocaudal direction, along the representation of visual field vertical meridian, just as the intrinsic horizontal connections in area 18. This findings demonstrate the spatial correspondence between efferent and intrinsic connections distributions in area 18. Such area 18 connections provide more detailed analysis of the vertical components of visual objects.

Animals↗
PubMed1999

Developmental neuroplasticity: roles in early life seizures and chronic epilepsy.

Both clinical and experimental studies suggest that the immature nervous system is unusually susceptible to seizures during critical periods in postnatal life. A late onset of gamma-aminobutyric acid (GABA)-mediated synaptic inhibition could conceivably play a contributing role in this phenomenon. Numerous studies have shown that neural systems that use GABA in the neonatal brain are different than those of adulthood. GABA is an excitatory neurotransmitter that likely plays a neurotrophic role in neuronal differentiation. Other reports suggest that unique, possibly transient, GABAergic interneuron populations exist in the embryonic and neonatal nervous system. At these early times in development, the immature nervous system is remarkably resistant to seizure generation. However, as the hippocampus and neocortex enter the critical period of enhanced seizure susceptibility, inhibitory GABA systems mature rapidly. At this time, blockade of GABA type A (GABAA) receptors produce unusually severe seizure discharges. In hippocampus, concurrent exuberant outgrowth of recurrent excitatory axon collaterals and synapses appear to play a role in the generation of these seizures. As the hippocampus matures, these axons are morphologically remodeled and nearly 50% of branches within arbors are pruned. This pruning of axon branches corresponds in time with the decrease in seizure susceptibility that characterizes adulthood. Developmental remodeling of neuronal connectivity is a common feature of most areas of the central nervous system. Results from an audiogenic seizure model of early onset epilepsy suggest that prevention of axon arbor remodeling by transient sensory deprivation can lead to a permanent overinnervation of target nuclei and chronic seizure susceptibility. Early life seizures may have a similar effect. Recent results in one model have shown that repeated seizures induced by intrahippocampal injections of tetanus toxin during a critical period results in a chronic epilepsy. Future studies should attempt to determine if the synchronized discharging of early-life seizures prevents the remodeling of neuronal connectivity that normally takes place during postnatal development and results in an overinnervated and chronically hyperexcitable hippocampus.

Aging↗
PubMed1988

Correlated electrophysiological and histochemical studies of submucous neurons and their contribution to understanding enteric neural circuits.

Neither submucous ganglia, nor intestinal secretomotor reflexes are mentioned in the majority of the textbooks of physiology; because it has been realized only very recently that the submucous neurons may have important influences on whole body water and electrolyte balance. In the present review, we trace the rapid progress that has been made in determining the physiological properties of submucous neurons with known chemistry and projections in the guinea-pig small intestine, and we analyze how the work relates to studies in vivo of the neuronal control of intestinal trans-epithelial fluid transport. Four types of submucous neurons, which appear to be the full complement in the guinea-pig small intestine, have been identified through electrophysiological and histochemical analysis. (1) Cholinergic secretomotor neurons contain immunoreactivity for choline-acetyltransferase (ChAT), calcitonin gene-related peptide (CGRP), cholecystokinin (CCK), neuropeptide Y (NPY), somatostatin (SOM), and in the majority of cases galanin (GAL); these neurons project to the mucosal epithelium. (2) Non-cholinergic secretomotor neurons contain dynorphin (DYN), GAL and vasoactive intestinal peptide (VIP); these neurons project to the mucosa and provide collaterals to submucous arterioles. (3) Cholinergic interneurons contain ChAT alone; these neurons connect with the secretomotor neurons. (4) Presumed sensory neurons contain ChAT and substance P (SP) and have nerve endings in the mucosa. The two groups of secretomotor neurons receive cholinergic synaptic inputs from both myenteric and submucous ganglia. In addition, the DYN/GAL/VIP neurons receive sympathetic inhibitory inputs as well as inhibitory and non-cholinergic excitatory inputs from myenteric ganglia. The ChAT/SP nerve cells in submucous ganglia receive no or very ineffective inputs. From these data, from experiments on transmission from the neurons to the intestinal epithelium, and from studies of secretomotor reflexes in vivo, a correlated functional and structural circuitry of the submucous ganglia and their connections has been deduced. It is concluded that secretomotor reflexes are stimulated by the contents of the lumen during the digestion and absorption of food and that these reflexes cause a proportion of water and electrolytes that are absorbed with nutrients such as glucose to be returned to the lumen. The balance of absorption and secretion of water and electrolytes is controlled by sympathetic inhibitory inputs to secretomotor neurons, the activity in sympathetic pathways being varied to contribute to whole body water and electrolyte balance.

Action Potentials↗
PubMed1998

Microcutting of living brain slices by a pulsed ultrafine water jet which allows simultaneous electrophysiological recordings (micromingotome).

Up to now microsurgical dissections in living nervous tissue (e.g. in slices or cell cultures) are performed either by micro-scalpels or by laser beams. As an alternative technique, a device for cutting with an ultrafine pulsed water jet was developed to allow precise, visually controled dissections in neuronal circuits even during electrophysiological recordings. Water is ejected by pressure (20-30 bar) from patch pipettes with tip diameters of 10-12 microm. By means of a piezo-element the pipette and the water jet are forced to oscillate vertically with a frequency of 200-400 Hz with an adjustable amplitude. These oscillations facilitate the transsection of neuronal connections even in thick slice preparations. Best results were obtained when the tip of the pipette was about 500 microm above the surface of the submerged slice tissue. This micromingotome offers the following advantages: (i) histological studies show that the water jet cleans the cutting surface, thus avoiding debris and its uncontrolable effects on cells underneath; (ii) the arrangement enables ongoing electrophysiological recordings from hippocampal slices during the cutting procedure and thus facilitates studies of the functions of neuronal connections; (iii) the device allows even disconnection in cultured nervous tissue overgrowing polyamid grids with 50 microm wide meshes.

Animals↗
PubMedDate not supplied

Activation of primary afferent neurons by thermal stimulation. Influence of ruthenium red.

The effect of thermal stimulation on primary afferent neurons and its modulation by Ruthenium Red (RR) has been investigated in the isolated perfused rabbit ear with intact neuronal connection to the animal. Capsaicin, K(+)-depolarization as well as increasing the temperature of the perfusate to 50 degrees C, increased the amount of substance P-like immunoreactivity (SP-IR) in the outflow in a calcium-dependent manner. High performance liquid chromatography (HPLC) revealed that SP-IR which was released by thermal stimulation consisted of two components, one of which co-eluted with synthetic substance P. The same two components of SP-IR were also present in extracts of the auricular nerve and were released by capsaicin. RR attenuated the effect of capsaicin and thermal stimulation but did not reduce potassium-evoked release of SP-IR. To evaluate an inhibitory action of RR on the excitation of primary afferents, the isolated perfused ear with intact neuronal connection to the anaesthetized rabbit was used. Intraarterial injection of capsaicin or bradykinin as well as superfusion of a skin area of approximately 2 cm2 with water at 53 degrees C for 1 min, produced a depressor reflex. RR attenuated the response to thermal stimulation and to capsaicin, but did not block the bradykinin-induced depressor reflex. These results demonstrate that, in the rabbit ear, thermal stimuli excite primary afferent neurons and evoke the calcium-dependent release of neuropeptides from their peripheral terminals by a mechanism which is sensitive to RR.

Animals↗
PubMed1988

Inhibitory action of Purkinje cells in the posterior vermis on fastigio-prepositus circuit of the cat.

Neuronal connections between the posterior vermis including the fastigial nucleus and the prepositus nucleus were studied with electrophysiological and neuropharmacological methods in the cat. Spontaneous discharges of neurons in the prepositus nucleus were depressed by microstimulation of the contralateral vermis, lobule VI. This depressive effect was blocked by the injection of bicuculline into the caudal part of the fastigial nucleus. These prepositus neurons also showed long-lasting poststimulus facilitation following microstimulation of the contralateral fastigial nucleus. These prepositus neurons were reciprocally connected with neurons in the contralateral fastigial nucleus. These findings suggest that Purkinje cells in lobule VI of the vermis depress propositus neuronal activity through the fastigial nucleus and that the reciprocal connectivity between the prepositus and fastigial nuclei generates a significant background facilitation in the two nuclei.

Animals↗
PubMed1979

Computer-controlled double-beam scanning microspectrophotometry for rapid microscopic image reconstructions.

A method for automated collection of various specific data from an entire microscopical preparation and their quantitative evaluation is described. Its application to the study of neuronal connections is discussed in some detail. Brain sections are scanned using a computer-controlled microscope for reflectance, fluorescences or absorbance signals. Two illuminating beams are used, one of them being amplitude modulated. By means of a synchronous detection the two signals are recorded simultaneously: for example, in an autoradiograph, the reflectance (measuring the density of the silver grains in emulsion) and the absorbance (allowing to localize the underlying counterstained cells). The data are stored in a computer. Various off-line processing schemes allow the reconstruction of the data with respect to the corresponding spatial coordinates. Thus pseudo-three-dimensional, analogue or digital, graphic displays may be obtained in which the patterns of neuronal connections can be recognized and interpreted. A method for the detection of weakly labelled nerve fibres based on digital filtering is presented. The whole processing for a frontal section of the mouse brain (7 X 10 mm area) takes less than 1 h. In addition to the evaluation of microscopically labelled material (grains of autoradiographs, horseradish peroxidase, nucleic acids) the technique described has been successfully used for the study of naturally fluorescent intracellular components in living tissue cultures.

Animals↗
PubMed2001

Tau, beta-amyloid and beta-amyloid precursor protein distribution in the entorhinal-hippocampal alvear and perforant pathways in the Alzheimer's brain.

It has been suggested that the pathological lesions of Alzheimer's disease (AD) spread along neuronal connections. This study was designed to examine this hypothesis in the alvear and perforant pathways, two well-defined neuroanatomical pathways that project from the entorhinal cortex to the hippocampus. Paraffin-sections of hippocampal-entorhinal cortex from 25 AD cases were immunolabelled for tau, beta-amyloid (Abeta) and beta-amyloid precursor protein (betaAPP). We used image-analysis to quantify immunolabelling at both ends of the alvear and perforant pathways. At the beginning and the end of the alvear pathway, area of immunolabelling in microm2 per area of field (72000 microm2) were as follows: tau 349 and 821 (P<0.01), Abeta 349 and 61 (P<0.05) and betaAPP 18 and 73 (P<0.01). Corresponding values for the perforant pathway were tau 421 and 387, Abeta 382 and 115 (P<0.05) and betaAPP 55 and 83. Tau was significantly greater at the end than at the beginning of the alvear pathway, but similar at both ends of the perforant pathway. There was significantly more Abeta at the beginning than at the end of the alvear and perforant pathway. These results at least in part reinforce previous work [19] that tau-rich areas may be neuronally connected to Abeta-rich areas.

Aged↗
PubMed1999

Cerebral amyloid induces aberrant axonal sprouting and ectopic terminal formation in amyloid precursor protein transgenic mice.

A characteristic feature of Alzheimer's disease (AD) is the formation of amyloid plaques in the brain. Although this hallmark pathology has been well described, the biological effects of plaques are poorly understood. To study the effect of amyloid plaques on axons and neuronal connectivity, we have examined the axonal projections from the entorhinal cortex in aged amyloid precursor protein (APP) transgenic mice that exhibit cerebral amyloid deposition in plaques and vessels (APP23 mice). Here we report that entorhinal axons form dystrophic boutons around amyloid plaques in the entorhinal termination zone of the hippocampus. More importantly, entorhinal boutons were found associated with amyloid in ectopic locations within the hippocampus, the thalamus, white matter tracts, as well as surrounding vascular amyloid. Many of these ectopic entorhinal boutons were immunopositive for the growth-associated protein GAP-43 and showed light and electron microscopic characteristics of axonal terminals. Our findings suggest that (1) cerebral amyloid deposition has neurotropic effects and is the main cause of aberrant sprouting in AD brain; (2) the magnitude and significance of sprouting in AD have been underestimated; and (3) cerebral amyloid leads to the disruption of neuronal connectivity which, in turn, may significantly contribute to AD dementia.

Amyloid beta-Protein Precursor↗