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PubMed1998

Neurexins: three genes and 1001 products.

The human brain has approximately 10(12) neurons, three orders of magnitude more than there are basepairs in the human genome. Each neuron is connected to other neurons by thousands of synapses, creating a dense network of communicating neurons. Cell-recognition events between neurons at, and outside of synapses, are likely to guide the development and maintenance of the complex network formed by neurons. However, little is known about which proteins are important for neuronal cell recognition. Neurexins, a family of polymorphic cell-surface proteins, might mediate some of these cell recognition events. Thousands of neurexin isoforms are generated from three genes by usage of alternative promoters and alternative splicing. These isoforms are displayed on the neuronal cell surface, with different classes of neurons expressing distinct combinations of isoforms. Neurexins probably have a multitude of ligands, some of which interact only with subsets of neurexin isoforms. This review describes the properties of the neurexin protein family and their potential roles in neuronal cell adhesion and intercellular signaling.

Alternative Splicing↗
PubMed2002

Short-term effects of pilocarpine on rat hippocampal neurons in culture.

PURPOSE: Status epilepticus (SE) has been considered an epileptogenic factor in humans. In the pilocarpine (PILO) model, after a brief period marked by SE, the rats exhibit recurrent spontaneous seizures, mimicking the clinical features of temporal lobe epilepsy. The aim of our study was to identify the molecular actions of PILO that could account for its ability to induce SE. METHODS: Whole-cell mode of the patch-clamp technique was applied to cultured hippocampal neurons (2-3 weeks old) in the absence and in the presence of PILO (1-10 microM), to study the spontaneous activity, the evoked, and the miniature postsynaptic currents. The postsynaptic currents were isolated pharmacologically. RESULTS: PILO (1 and 10 microM) caused an initial increase followed by a decrease in the frequency of spontaneous activity. The increase in the frequency of excitatory postsynaptic currents (EPSCs) and inhibitory PSCs (IPSCs) was blocked by atropine (1 microM), indicating that this effect is mediated through muscarinic receptors. PILO also promoted a brief increase of the amplitude of IPSCs indirectly evoked by stimulation of a neuron synaptically connected to the neuron under study. Conversely, PILO promoted a sustained increase on the amplitude of electrically evoked EPSCs. In presence of tetrodotoxin (TTX; 300 nM), PILO (1 microM) increased the frequency of miniature EPSCs and IPSCs without changing their amplitude during the first 3 min of application. CONCLUSIONS: These results indicate that PILO acting through muscarinic receptor causes an imbalance between excitatory and inhibitory transmission that can result in the generation of SE observed in animals acutely treated with PILO.

Animals↗
PubMed2004

Presence and connections of auditory neurons in the rostrodorsal and rostrolateral parts of the thalamic reticular nucleus.

OBJECTIVE: Auditory neurons have been identified in the caudoventral part of the thalamic reticular nucleus (TRN). We examined the acoustic input to single cells in the rostrodorsal part of the TRN. MATERIAL AND METHODS: In alpha-chloralose-anesthetized cats, we extracellularly recorded the responses of single neurons in the rostral TRN to acoustic and light stimuli. Next, to examine efferent projections of auditory neurons in the rostral TRN, we injected wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) into other thalamic nuclei where auditory neurons were detected, including the lateral posterior nucleus (LP), the lateral medial and suprageniculate nuclei and the centromedian nucleus. Finally, intracortical microstimulation of the LP was performed to demonstrate antidromic activation of the auditory neurons in the rostral TRN. RESULTS: In the rostral TRN, 2 types of response to auditory stimuli were observed: brief, short-latency bursts (13-20 ms; mean 16.5 ms) and longer bursts with a long latency (38.8-50 ms; mean 44.8 ms). Injection of WGA-HRP into the medial LP labeled cells only in the rostrodorsal TRN, while extending the injection to the other nuclei labeled cells in the rostrodorsal and rostrolateral parts of the nucleus. Auditory neurons in the rostral TRN were activated antidromically by microstimulation of auditory neurons in the LP, with a latency of 1.2 ms. CONCLUSIONS: These results strongly suggest that auditory neurons in the rostrodorsal TRN project to auditory neurons in the LP. The rostral auditory TRN may be involved in transmission of auditory information via the non-specific association system of the thalamus.

Acoustic Stimulation↗
PubMed1998

Using neural networks as an aid in the determination of disease status: comparison of clinical diagnosis to neural-network predictions in a pedigree with autosomal dominant limb-girdle muscular dystrophy.

Studies of the genetics of certain inherited diseases require expertise in the determination of disease status even for single-locus traits. For example, in the diagnosis of autosomal dominant limb-girdle muscular dystrophy (LGMD1A), it is not always possible to make a clear-cut determination of disease, because of variability in the diagnostic criteria, age at onset, and differential presentation of disease. Mapping such diseases is greatly simplified if the data present a homogeneous genetic trait and if disease status can be reliably determined. Here, we present an approach to determination of disease status, using methods of artificial neural-network analysis. The method entails "training" an artificial neural network, with input facts (based on diagnostic criteria) and related results (based on disease diagnosis). The network contains weight factors connecting input "neurons" to output "neurons," and these connections are adjusted until the network can reliably produce the appropriate outputs for the given input facts. The trained network can be "tested" with a second set of facts, in which the outcomes are known but not provided to the network, to see how well the training has worked. The method was applied to members of a pedigree with LGMD1A, now mapped to chromosome 5q. We used diagnostic criteria and disease status to train a neural network to classify individuals as "affected" or "not affected." The trained network reproduced the disease diagnosis of all individuals of known phenotype, with 98% reliability. This approach defined an appropriate choice of clinical factors for determination of disease status. Additionally, it provided insight into disease classification of those considered to have an "unknown" phenotype on the basis of standard clinical diagnostic methods.

Adolescent↗
PubMed2006

BDNF promotes connections of corticospinal neurons onto spared descending interneurons in spinal cord injured rats.

Although regeneration of injured axons is inhibited within the adult CNS, moderate recovery can be found in patients and animals with incomplete spinal cord injury (SCI). This can be partly attributed to sprouting of spared and injured axons, rostral and caudal to the lesion, respectively. Recently, it has been reported that following a thoracic SCI such sprouting can result in indirect reconnections of the lesioned axons to caudal targets via propriospinal interneurons (PrI). Here, we attempted to further promote this spontaneous repair mechanism by applying the neurotrophic factor BDNF (brain-derived neurotrophic factor), in the vicinity of the cell bodies of lesioned corticospinal neurons or NT-3, intrathecally to the cervical spinal cord. We performed a dorsal over-hemisection at the thoracic spinal cord sparing only the left ventrolateral quadrant. This type of lesion did not promote sprouting of injured corticospinal axons or re-routing via commissural PrI. Also, in rats that received NT-3 at the cervical enlargement, no increase in sprouting was found. However, animals receiving BDNF at the cell bodies of lesioned corticospinal neurons showed a significant increase in collateral sprouting and in the number of contacts with PrI. This was not observed when BDNF was administered to unlesioned animals. Although no statistical difference in the horizontal ladder walking was found between the groups, the increase in collateral sprouting and in the number of contacts correlated with the functional recovery. Hence, cell body treatment can promote plasticity of the injured CNS and may be a valuable treatment approach in conjunction with local regeneration promoting strategies.

Animals↗
PubMed1996

Synaptic connections between spiny neurons of the direct and indirect pathways in the neostriatum of the rat: evidence from dopamine receptor and neuropeptide immunostaining.

UNLABELLED: The flow of cortical information through the basal ganglia occurs through the so-called 'direct pathway' and 'indirect pathways'. The object of the present work was to attempt to determine whether spiny neurons in the neostriatum that give rise to the direct pathway (i.e. the striatonigral/entopeduncular pathway) and those giving rise to the indirect pathways (i.e. striatopallidal pathway) are synaptically interconnected. The approach was to carry out double immunocytochemistry at the electron microscopic level using antibodies against peptides or dopamine receptor subtypes that are selectively associated with the neurons that give rise to the direct (substance P or D1 receptors) and indirect pathways (enkephalin or D2 receptors). Sections of perfuse-fixed rat neostriatum were immunostained to reveal both substance P immunoreactivity and D2 receptor immunoreactivity or enkephalin and D1 receptor immunoreactivity, respectively. Double peroxidase methods were employed using different chromogens that were distinguishable at both the light and electron microscopic levels. In the electron microscope substance P-immunoreactive terminals were seen in synaptic contact with dendritic structures that displayed immunoreactivity for D2 receptor. Similarly, enkephalin-immunoreactive terminals were seen in synaptic contact with D1-immunoreactive dendritic structures. Thus, axon collaterals of neurons giving rise to the direct pathway form synaptic contacts with neurons that give rise to the indirect pathway and axon collaterals of neurons giving rise to the indirect pathway form synaptic contact with neurons that give rise to the direct pathway. These results indicate that the two pathways of information flow through the basal ganglia are synaptically linked at the level of the neostriatum. KEYWORDS: spiny neurons, direct pathway,indirect pathways, rat neostriatum

Animals↗
PubMed2004

Characterization of subpopulations of neurons producing melanin-concentrating hormone in the rat ventral diencephalon.

Neurons producing melanin-concentrating hormone (MCH) are involved in a large array of functions. Some of these functions may be mediated by specific subpopulations. One such subpopulation was characterized by the expression of the neurokinin 3 receptor and the 'cocaine- and amphetamine-regulated transcript' (CART) peptide, while another expresses neither one of these two molecules. MCH+/CART+ axons were traced throughout the brain and showed a strikingly different pattern of distribution than that of MCH+/CART- axons. Particularly, many MCH+/CART+ axons are observed in the telencephalon, while MCH+/CART- projections are mostly directed toward the brainstem. Calbindin, a protein involved in calcium homeostasis, has been largely used in many structures of the brain for the identification of neuronal phenotypes. However, few MCH neurons were labeled for this protein. On the other hand, neurons producing the peptides hypocretins (Hcrt), and codistributed with the MCH neurons, were all labeled for calbindin. Thus, at least two subpopulations of MCH neurons can be distinguished on the basis of neuronal phenotypes and connections. These neurons may be involved in distinct circuitry and in distinct functions.

Animals↗
PubMed2005

Hypothalamic hamartoma: a paradigm/model for studying the onset of puberty.

This article discusses the potential mechanisms by which hypothalamic hamartomas (HHs) are formed and cause precocious puberty. The hypothesis is presented suggesting that HHs accelerate sexual development by producing bioactive substances that mimic - in an accelerated time-course - the cascade of events underlying the normal initiation of puberty. It is also proposed that because HHs contain key transcriptional and signaling networks required to initiate and sustain a pubertal mode of gonadotropin-releasing hormone (GnRH) release, they are able to trigger the pubertal process at an earlier age. The cellular components of this activating complex may include: (a) neurons able to produce GnRH within the HH: (b) controlling neurons synaptically connected to GnRH neurons in the HH itself and/or to neuronal networks (including GnRH neurons) in the patient's hypothalamus, and (c) signaling-competent astrocytic and ependymoglial cells. It is also possible that the developmental abnormalities leading to the formation of HHs result from sporadic defects affecting the same genes and hence the same morphogenic pathways involved in the embryonic development of the ventral hypothalamus and the floor of the third ventricle.

Child↗
PubMed1995

Programmed cell death enhances uniformity in rat cerebral hemispheres.

Programmed cell death (apoptosis) in rat cerebral hemispheres (CH) reportedly occurs around postnatal day 7 and kills 15-75% of all cells whose continuing presence would be of disadvantage for the organism: neurons erroneously connected, or supranumerary neurons that do not find targets and are not protected by neurotrophins. In the present paper we report that apoptosis (or a concomitant phenomenon) reduces also variability (coefficient of variation, CV) of CH parameters: weight, DNA content and protein content (presented here as a percent of the mean of each of these parameters). Postapoptotic brains have significantly lower CV of these parameters than the preapoptotic brains. Presumably, this trend toward uniformity offers selective advantages (for rat) and established itself during evolution. The mechanisms and the control of this phenomenon are at present largely unknown.

Animals↗
PubMed1988

Subfornical organ connections with septal neurons projecting to the median eminence.

We have examined the effect of electrical stimulation in the subfornical organ (SFO) on the activity of neurons in the medial septum and diagonal band of Broca (MS-DBB) which project to the median eminence in the rat. Previous studies have suggested that septal neurons with such projections are luteinizing hormone releasing hormone neurons. Extracellular single-unit recordings were obtained from 69 neurons in the MS-DBB which were antidromically identified as projecting to the median eminence. Electrical stimulation (100-400 microA) in the SFO resulted in a relatively short-latency (22.8 +/- 0.8 ms), short-duration (9.2 +/- 0.8 ms) activation of 85% of 41 antidromically identified MS-DBB neurons tested. One neuron was inhibited by SFO stimulation, while the remaining 12% were unaffected. Stimulation in nearby regions, including the hippocampal commissure and paraventricular nucleus of the thalamus, failed to elicit a similar excitatory response from 19 identified MS-DBB neurons. These results identify a neuronal pathway between the SFO and septal neurons which project to the median eminence, supporting a possible role for the SFO in the control of luteinizing hormone releasing hormone release and hence gonadotropin secretion.

Action Potentials↗
PubMed1999

The organophosphate sarin, at low concentrations, inhibits the evoked release of GABA in rat hippocampal slices.

In the present study, the whole-cell mode of the patch-clamp technique was applied to neurons of the CA1 pyramidal layer of rat hippocampal slices to investigate the effects of the organophosphate (OP) sarin on field stimulation-evoked and on tetrodotoxin (TTX)-insensitive postsynaptic currents (PSCs) mediated by activation of type A gamma-aminobutyric acid (GABA) receptors or AMPA-type glutamate receptors. At 0.3-1 nM, sarin reduced the amplitude of GABA-mediated PSCs and had no effect on the amplitude of glutamatergic PSCs evoked by field stimulation of neurons synaptically connected to the neuron under study. The effect of sarin on evoked GABAergic PSCs was unrelated to cholinesterase inhibition, was partially reversed upon washing of the neurons with sarin-free external solution, and was mediated by a direct interaction of the OP with muscarinic acetylcholine receptors present on presynaptic GABAergic neurons. Sarin had no effect on the amplitude or kinetics of GABA- or glutamate-mediated miniature postsynaptic currents (MPSCs) recorded in the presence of the Na+-channel blocker TTX (300 nM), indicating that the OP does not interact with GABA(A) or glutamate receptors. Further, sarin did not alter the frequency of GABAergic or glutamatergic MPSCs, a finding that led to the conclusion that this OP does not affect the TTX-insensitive release of neurotransmitters. A selective reduction by sarin of the action potential-dependent release of GABA in the hippocampus can account for the occurrence of seizures in intoxicated subjects.

Animals↗
PubMedDate not supplied

[The effect of acetylcholine and atropine on the temporal connection in the neuronal populations of the motor cortex].

On alert non-immobilized rabbits the activity of neurones in the sensorimotor cortex was studied at pair combination of brain structures stimulations. During omission of the reinforcing stimulus at the place of its expected presentation a complicated complex develops of neurones impulses reconstructions, consisting in reproduction of responses and activity changes which by their configuration differ from them and usually appear in later terms. Direct acetylcholine application on the cortex promotes manifestation of both types of neurones activity reconstructions. But atropine application depresses mainly the second type of reconstructions. Besides, acetylcholine increases the general duration of the given conditioned effects, but atropine decreases it.

Acetylcholine↗