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PubMed2005

Anatomical evidence for glutamatergic transmission in primary sensory neurons and onto postganglionic neurons controlling penile erection in rats: an ultrastructural study with neuronal tracing and immunocytochemistry.

In male rats, the dorsal penile nerve (DPN) conveys sensory information from the genitals to the lumbosacral spinal segments of the spinal cord. DPN is the afferent limb of a reflex loop that supports reflexive erections, and that includes a network of spinal interneurons and autonomic and somatic motoneurons to the penis and perineal striated muscles. Autonomic efferent pathways to the penis relay in the major pelvic ganglion (MPG). Glutamate (Glu) is a likely candidate as a neurotransmitter of reflexive erections. Both AMPA and NMDA glutamatergic receptor subunits are present in the lumbosacral spinal cord, and AMPA and NMDA receptor antagonists block reflexive erections. In the present study, we used tract-tracing experiments combined with immunohistochemical and immunocytochemical techniques to ascertain the presence of Glu at two different levels of the network controlling reflexive erections. DPN afferents were localized in the dorsal horn of the lumbosacral cord and displayed the characteristics of either C-fibers or Adelta fibers. DPN terminals (some of them glutamatergic) were mainly distributed in the medial edge of the dorsal horn in the L6 spinal segment. GluR1 subunits were present in some DPN afferents, suggesting that they could be autoreceptors. DPN fibers were also present in the MPG, as were Glu terminals and GluR4 subunits. The results reveal the presence of Glu in DPN fibers and terminals and suggest that both the spinal cord and the MPG use glutamatergic transmission to control reflexive erections.

Animals↗
PubMed1988

Decrementing expiratory neurons of the Bötzinger complex. II. Direct inhibitory synaptic linkage with ventral respiratory group neurons.

In Nembutal-anesthetized, immobilized and artificially ventilated cats, decrementing expiratory (E-DEC) neurons which were excited by lung inflation were isolated in the vicinity of the Bötzinger complex. Then intracellular recordings were made from the respiratory neurons in the contralateral ventral respiratory group (VRG). The intracellular membrane potentials were averaged using extracellular spikes of the E-DEC neurons as triggers (spike-triggered averaging method). Hyperpolarizing potentials locked to the triggering spikes were obtained and they were shown to be unitary IPSPs since their polarity was reversed when averaged during passage of hyperpolarizing current. The latencies of antidromic activation of the E-DEC neurons from the area of intracellular recordings were shorter by about 0.2 ms than those of unitary IPSPs. This showed that the connections were monosynaptic. A total of 47 pairs were analyzed and unitary IPSPs were found in 12 pairs. The E-DEC neurons inhibited both inspiratory and expiratory neurons, including bulbospinal inspiratory neurons, propriobulbar inspiratory neurons, and vagal motoneurons with expiratory activity. These inhibitory E-DEC neurons, receiving excitatory inputs from the stretch receptors of the lungs, presumably intervene in reflex loops such as the Hering-Breuer reflex and may make some contribution to normal breathing.

Action Potentials↗
PubMed1987

Neural mechanisms generating the leech swimming rhythm: swim-initiator neurons excite the network of swim oscillator neurons.

This paper describes newly identified excitatory connections linking the segmentally iterated swim-initiator interneurons with the network of oscillator neurons that generates the leech swimming rhythm. Apparently monosynaptic excitatory chemical connections are made from one class of swim-initiator neurons (cells 204/205) to several members of the swim oscillator network, including cells 28, 115 and, as described by Weeks (1982c), cell 208. A second class of swim-initiator neurons, cells 21 and 61, also excites this subset of the oscillator neurons. The unpaired swim oscillator neuron, cell 208, also chemically excites cells 28 and 115, apparently directly. Thus, in addition to its role as a member of the swim oscillator, the excitatory output from cell 208 to the swim oscillator adds to that provided by the swim-initiator neurons. The results of this paper enlarge the subset of identified swim oscillator neurons synaptically excited by the swim-initiator neurons. These newly described targets of the swim-initiators strengthen the hypotheses that: 1) the swim-initiator neurons supply much of the tonic excitatory drive responsible for activation and maintenance of the swim central motor program, and 2) the two classes of swim-initiators, cells 204/205 and cells 21/61, act synergistically to initiate and maintain swimming.

Animals↗
PubMed1986

A study of the connection between the interneuron initiating pacemaker activity in a bursting neuron and the bursting neuron of the snail Helix pomatia.

The connection between an interneuron initiating pacemaker activity in the bursting RPa1 neuron and the bursting neuron itself (Pin and Gola, 1983) has been analyzed in the snail Helix pomatia. Prolonged depolarization of the interneuronal membrane produced in it a series of action potentials as well as a parallel initiation or enhancement of bursting activity in the RPa1 neuron. If the discharge in the interneuron was evoked by short current pulses of threshold amplitude, no bursting activity was seen in the RPa1 neuron. However, short stimuli delivered on the background of subthreshold depolarization of the interneuronal membrane produced bursting activity in the RPa1 neuron. Under voltage-clamp conditions a slow inward current could be recorded in the RPa1 neuronal membrane after stimulation of the interneuron with a latency of about 2 sec. Short shifts of the holding potential in the hyperpolarizing direction at the maximum of this current produced a transient outward current. Replacement of extracellular Ca2+ by Mg2+ ions, as well as addition of 1 mM CdCl2 to the external solution, prevented the response to the interneuronal stimulation in the RPa1 neuron. Electron microscopic investigation of the interneuron has shown the abundance of Golgi complexes in its cytoplasm with electron-dense granules in their vicinity. It is concluded that the connection between the interneuron and the bursting neuron is of chemical origin, based on secretion by the former of some substances which activate at least two types of ionic channels in the membrane of the RPa1 neuron.

Action Potentials↗
PubMed1987

Brain neurons develop in a serum and glial free environment: effects of transferrin, insulin, insulin-like growth factor-I and thyroid hormone on neuronal survival, growth and differentiation.

We have developed a pure cortical neuronal culture free of glial cells, grown in a serum-free environment. The cultured cells immunostained positively with neurofilament antibody while they displayed virtually no glial cell characteristics, such as glial fibrillary acidic protein, glycerol phosphate dehydrogenase or glutamine synthetase. Insulin and transferrin were necessary and sufficient for neuronal survival, neurite extension and glutamic acid decarboxylase (GAD) expression. Insulin-like growth factor-I was able to replace insulin and was active close to its physiological concentration, suggesting it might be the in vivo factor influencing neuronal growth in the brain. The dynamics of the developmental process were striking. The neurons moved on the poly-D-lysine covered plastic dish, and rearrangements in contacts between cells were observed. At first the neurons underwent a general cellular growth manifested by a large increase in the culture total protein content and by the initiation of neurites. A more specific differentiation, as indicated by the sharp increase in GAD levels which was concurrent with an increase in interneuronal contacts, lagged behind the initial growth. Thyroid hormone (TH) affected the differentiation process, causing a future increase in GAD levels during the same time of increase in neurite growth, in interneuronal contacts, in thyroid hormone receptors and thyroid gland maturation. Removal of each of the hormones after a few days of cell growth revealed that transferrin was still required for neuronal survival while insulin became essential for general cellular growth but not specific neuronal differentiation, since it caused an increase in both the total protein and GAD levels but not in GAD specific activity. TH, on the other hand, affected the differentiation process as evident by its ability to increase GAD specific activity. This action of TH, however, required the presence of insulin, without which no increase in GAD level by TH was observed. This neuronal culture, glial and serum-free, provides a new system for investigating neuronal development and function in the complex mammalian central nervous system.

Animals↗
PubMed1996

Survival and regeneration of neurons of the supraoptic nucleus following surgical transection of neurohypophysial axons depend on the existence of collateral projections of these neurons to the dorsolateral hypothalamus.

The aim of the present study was to compare the postlesional responses of vasopressin-producing (VP) and oxytocin-producing (OT) neurons of the supraoptic nucleus (SON) to transection of neurohypophysial axons. At different times after sectioning the median eminence of adult rats, immunocytochemical staining of both types of neuronal cell bodies and axons indicated that: (1) the number of OT neurons detected within the SON was only slightly decreased as compared with controls (-20%), whereas the number of VP neurons was severely decreased (-60%); and (2) the large majority of axonal sprouts that regenerated into the external layer of the median eminence were OT neurohypophysial axons. The injection of a retrograde tracer into various areas surrounding the SON further showed that numerous SON neurons could be retrogradely labeled when the injection was centered in the lateral hypothalamus dorsal to the SON. The immunocytochemical identification of these retrogradely labeled neurons demonstrated that most of them were OT neurons. When animals were subjected to median eminence transection and to a unilateral surgical cut placed in the lateral hypothalamus above the SON, the survival of both OT and VP neurons was dramatically reduced in the SON ipsilateral to the hypothalamic lesion, as compared to the contralateral SON. Taken together, these data indicate that OT (and to a lesser extent VP) neurons of the SON display collateral projections towards the lateral hypothalamus that protect them from retrograde degeneration following the lesion of their neurohypophysial projections.

Animals↗
PubMed1995

Degeneration of rat cholinergic basal forebrain neurons and reactive changes in nerve growth factor expression after chronic neurotoxic injury--I. Degeneration and plastic response of basal forebrain neurons.

The process of degeneration and dendritic reorganization of cholinergic neurons was investigated in the rat basal forebrain under the conditions of chronic neurotoxic injury induced by long-term consumption of ethanol. After 28 weeks of ethanol treatment (20% v/v), both the number of choline acetyltransferase-immunoreactive basal forebrain neurons and levels of biochemical measures of cholinergic neurons, such as the activity of choline acetyltransferase and the synthesis and content of acetylcholine, were decreased by about 60-80%. The number of cholinergic neurons showing a positive hybridization signal to choline acetyltransferase messenger RNA was decreased to a similar extent. On the contrary, the reduction in the number of neurons immunoreactive for nerve growth factor receptor p75, which in control brains is highly co-localized with the expression of choline acetyltransferase, was much less pronounced and reached only 20-30%. The loss of choline acetyltransferase expression was associated with a cellular hypertrophy. Neurons which had survived the neurotoxic damage, furthermore, showed a remodelling of the dendritic organization which was quantitatively investigated after Golgi impregnation. This process of dendritic reorganization was mainly characterized by an increase in number and length of terminal dendritic segments. The results indicate that under the conditions of the present paradigm of chronic neurodegeneration, a certain number of cholinergic neurons persists in a form where they lost their ability to express detectable amounts of choline acetyltransferase messenger RNA and the enzyme protein. Persisting neurons, however, show both expression of nerve growth factor receptor p75 and signs of perikaryal and dendritic growth. It might, therefore, be hypothesized that chronic degeneration of cholinergic basal forebrain neurons triggers reactive attempts of repair which involve the action of trophic factors such as nerve growth factor.

Alcohol Drinking↗
PubMed1987

The role of neuron death in the development of the gender difference in the number of neurons in the rat superior cervical ganglion.

Adult male rats have more neurons in their superior cervical ganglia than do adult females. This difference arises over the first two postnatal weeks, and is apparently related to perinatal levels of circulating testosterone. Exposure of neonatal rats to testosterone or estradiol during the first postnatal weeks results in an increase in the number of neurons in the superior cervical ganglion seen at 15, 30 or 60 days postnatally. The present studies were undertaken to determine whether this observed increase in neurons is due to an increase in neuronal proliferation or to a decrease in neuronal death. Results of autoradiographic studies show no evidence of enhanced neuronal proliferation following postnatal exposure to estradiol, but do show an increased survival of a prenatally labeled population of cells. Counts of degenerating cells in the superior cervical ganglion show that during the peak period of normal neuronal degeneration, on postnatal day 5, 17-beta-estradiol or testosterone propionate treated animals have significantly fewer degenerating superior cervical ganglion cells than do vehicle-injected littermate controls. In addition, vehicle-injected females have more degenerating cells on day 5 than do vehicle-injected males. Taken together these results provide strong evidence that the increase in superior cervical ganglion neurons seen after neonatal exposure to estradiol results from a reduction in developmental neuron death.

Animals↗
PubMed2006

Novel gut afferents: Intrinsic afferent neurons and intestinofugal neurons.

Information about the conditions of all tissues in the body is conveyed to the central nervous system through afferent neurons. Uniquely amongst peripheral organs, the intestine has numerous additional afferent neurons, intrinsic primary afferent neurons that have their cell bodies and processes in the enteric plexuses and do not project to the central nervous system. They detect conditions within the gut and convey that information to intrinsic reflex pathways that are also entirely contained inside the gut wall. Intrinsic primary afferent neurons respond both to the presence of material in the gut lumen and to distension of the gut wall and initiate reflex changes in contractile activity, fluid transport across the mucosa and local blood flow. They also function as nociceptors that initiate tissue-protective propulsive and secretory reflexes to rid the gut of pathogens. The regulation of excitability of intrinsic primary afferent neurons is through multiple ion channels and ion channel regulators, and their excitability is critical to setting the strength of enteric reflexes. The intestine also provides afferent signals to sympathetic pre-vertebral ganglia. The signals are conveyed from the gut by intestinofugal neurons that have their cell bodies within enteric ganglia and form synapses in the sympathetic ganglia. Intestinofugal neurons form parts of the afferent limbs of entero-enteric inhibitory reflexes. Because the unusual afferent neurons of the small intestine and colon make their synaptic connections outside the central nervous system, the neurons and the reflex centres that they affect are potential targets for non-central penetrant therapeutic compounds.

Animals↗
PubMed2002

Deficiency of neuronal nitric oxide synthase (nNOS) worsens alcohol-induced microencephaly and neuronal loss in developing mice.

Previous work conducted in vitro suggests that nitric oxide (NO) protects developing neurons against the toxic effects of alcohol. We tested the hypothesis that neonatal mice carrying a null mutation for neuronal nitric oxide synthase (nNOS), the enzyme which synthesizes NO in neurons, have increased vulnerability to alcohol-induced microencephaly and neuronal loss. Wild-type mice and mutant (nNOS(-/-)) mice received a single intraperitoneal injection of ethanol (0.0, 2.2, 3.3, or 4.4 g/kg) daily over postnatal days (PD) 4-9 and were sacrificed on PD 10. Peak blood alcohol concentrations were approximately 170, 280, and 385 mg/dl for the 2.2, 3.3 and 4.4 g/kg/day treatment groups, respectively, and did not differ significantly between wild-type and nNOS(-/-) strains. Exposure to alcohol induced dose-dependent reductions in total brain weight, forebrain weight and cerebellum weight in both strains of mice. However, the reductions in brain weight were significantly more severe in the nNOS(-/-) mice than in wild type. Quantification of cerebellar neurons revealed that alcohol-induced losses of Purkinje cells and granule cells were both significantly greater in the nNOS(-/-) mice than in wild type. The increased vulnerability of nNOS-deficient neurons to alcohol-induced cell death was confirmed in vitro. Cerebellar granule cell cultures derived from nNOS(-/-) and wild-type mice were exposed for 24 h to 0, 100, 200 or 400 mg/dl ethanol. At each alcohol concentration, the nNOS(-/-) neurons had a significantly greater cell loss than did the wild-type neurons. The results demonstrate that deficiency of nNOS decreases the ability of developing neurons to survive the toxic effects of alcohol. Because NO upregulates intracellular cGMP, which can activate cGMP-dependent protein kinase (PKG), we hypothesize that the NO-cGMP-PKG pathway has a neuroprotective role against alcohol toxicity within the developing brain.

Animals↗
PubMed2000

Basal forebrain nitric oxide synthase (NOS)-containing neurons project to microvessels and NOS neurons in the rat neocortex: cellular basis for cortical blood flow regulation.

Stimulation of basal forebrain neurons results in local increases in cortical cerebral blood flow that are dependent upon cholinergic and nitrergic mechanisms. In the present study, we investigated the possibility that basal forebrain nitric oxide synthase (NOS)-containing neurons project to microvessels and NOS interneurons in the rat cerebral cortex. We performed quisqualic (QUIS) acid lesions of the basal forebrain and evaluated their effects on cortical NOS immunostained nerve terminals, with emphasis on those associated with microvessels and NOS interneurons, both at the light and/or electron microscopic levels. The results show that basal forebrain NOS neurons provide about one third of the overall cortical NOS innervation. Further, the data indicate that basalocortical NOS fibres establish privileged associations with microvessels and NOS neurons, as respective denervations of 60 and 45% were observed following lesion. At the electron microscopic level, most perivascular NOS neuronal elements corresponded to nerve terminals and a majority ( approximately 25%) of these were located in the immediate vicinity of the blood vessels, similar to the perivascular distribution reported previously for classic neurotransmitters/neuromediators. NOS terminals abutting on cortical NOS neurons were primarily nonjunctional. Altogether, these results raise the possibility that not only cholinergic but also nitrergic basal forebrain neurons are involved in the flow response observed following stimulation of the basal forebrain. Further, they suggest interactions between basalocortical and intracortical NOS neurons. We conclude that these interactions are involved in the spatial and temporal regulation of cortical perfusion following basal forebrain activation, and that they may become dysfunctional in pathologies such as Alzheimer's disease which affects both the basal forebrain and the cortical NOS neurons.

Acetylcholine↗
PubMedDate not supplied

Neuron-specific monoclonal antibodies raised against the low molecular weight fraction of a brain homogenate of the pond snail Lymnaea stagnalis immunoreact with neurons in the central nervous system of the cockroach, the guppy, the wall lizard, the rat and man.

Monoclonal antibodies were raised against the small molecular weight fraction (less than 30 kilodaltons) of an extract from 200 central nervous systems (CNS) of the freshwater snail Lymnaea stagnalis. In a first screening step the supernatants of the 297 emerging hybridomas were immunocytochemically tested on sections of the CNS of L. stagnalis. Sixty-six appeared to produce neuron-specific antibodies, five reacted with non-neuronal elements. In a second step the 66 neuron-specific antibodies were tested on sections of the CNS of the guppy. Three reacted positively. In the third step the three antibodies were tested on the CNS of the rat. One antibody (Mab4H5) appeared to give positive results. In the snail brain Mab4H5 stains two identified giant neurons, one in the visceral ganglion (VD1), and one in the right parietal ganglion (RPD2)--these neurons form part of the network controlling the respiratory system--and a small number of cells in the cerebral ganglia (in the anterior and ventral lobes). Ultrastructural observations using immunogold labelling in VD1 showed the antigen to be localized to the secretory vesicles. In the guppy Mab4H5 stains fibres in the tectum and cell bodies in the reticular formation. In rat CNS staining was observed in Purkinje neurons of the cerebellum, in cortical pyramidal neurons and in neurons and fibres in other brain areas. Subsequent Mab4H5 staining of the CNS of the lizard, the cockroach and parts of the human CNS showed that these tissues also contain Mab4H5-positive neurons. In the human cortex and cerebellum the staining pattern appeared to be similar to that of the rat. On the basis of the results it is hypothesized that the antibody reacts with phylogenetically ancient amino acid sequences.

Animals↗
PubMed1994

gamma-Aminobutyric acid receptor-mediated regulation of periventricular-hypophysial dopaminergic neurons: possible role in mediating stress- and 5-hydroxytryptamine-induced decreases in neuronal activity.

The present study examined the effects of gamma-aminobutyric acid (GABA) agonists and antagonists on basal periventricular-hypophysial dopaminergic (PHDA) neuronal activity with a focus on the role of endogenous GABA in mediating 5-hydroxytryptamine- and stress-induced decreases in PHDA neuronal activity. PHDA neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in terminals of these neurons in the intermediate lobe of the pituitary. Plasma concentrations of alpha-melanocyte-stimulating hormone (alpha MSH) also were determined to provide a further index of PHDA neuronal activity. Administration of the GABAB agonist baclofen, but not the GABAA agonist isoguvacine, produced dose- and time-related decreases in intermediate lobe DOPAC concentrations and corresponding increases in plasma alpha MSH concentrations. Administration of either the GABAA antagonist SR-95,531 [2-(3-carboxypropyl)-3-amino-6-(4-methoxyphenyl)-pyridazinium bromide] or GABAB antagonists 2-hydroxysaclofen and CGP-35,348 [P-(3-aminopropyl)-P-diethoxymethyl-phosphinic acid; SR-95-531 did not alter basal intermediate lobe DOPAC concentrations or plasma alpha MSH concentrations per se, indicating that endogenous GABA does not tonically inhibit PHDA neuronal activity or alpha MSH secretion. 2-Hydroxysaclofen and CGP-35,348 did, however, reverse the baclofen-induced decrease in intermediate lobe DOPAC concentrations and increase in plasma alpha MSH concentrations. In a similar fashion, 2-hydroxysaclofen blocked the inhibitory effects of stress and the 5-hydroxytryptamine2/1c receptor agonist DOI [1-(2,5-dimethoxy-4-iodophenyl-2-aminopropane] on PHDA neuronal activity. These results indicate that GABAB and not GABAA receptor activation inhibits basal PHDA neuronal activity, and that GABAB receptor activation mediates the inhibitory effects of 5-hydroxytryptamine and stress on PHDA neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Expression of the gene for the neuronal intermediate filament protein alpha-internexin coincides with the onset of neuronal differentiation in the developing rat nervous system.

While neurofilaments have long been considered early markers of neuronal differentiation, they cannot be detected in most newly postmitotic neurons of the developing central nervous system (CNS). Here we show that these neurons already express the neuronal intermediate filament protein alpha-internexin at high levels. alpha-internexin is expressed by most, if not all, neurons as they begin differentiation and shows no overlap with vimentin, whose expression in the CNS is restricted to mitotic neuronal precursors. In the adult, alpha-internexin is the only intermediate filament gene expressed by the cerebellar granule cells, the source of the thin-caliber parallel fibers; conversely, neurofilament proteins are highly expressed in large neurons, which express alpha-internexin at low levels. These data suggest that neuronal intermediate filaments may regulate axonal stability and/or diameter through changes not only in their number, but also in their subunit composition.

Animals↗
PubMed1991

The ontogeny of luteinizing hormone-releasing hormone (LHRH) producing neurons in the chick embryo: possible evidence for migrating LHRH neurons from the olfactory epithelium expressing a highly polysialylated neural cell adhesion molecule.

The development of neurons expressing luteinizing hormone-releasing hormone (LHRH) has been studied immunohistochemically in the chick embryo from the 3.5 embryonic day (ED) to the day of hatching. At ED-3.5, LHRH-immunoreactive neurons were first detected in the medial epithelium of the olfactory pit, but their appearance in the brain was delayed to ED-4.5. On EDs-6-7, cords of the LHRH-immunoreactive cells extended across the nasal septum towards the ventromedial forebrain with the olfactory nerve. By double staining for LHRH and, a highly polysialylated form of neural cell adhesion molecule (NCAM-H), the LHRH-positive neurons in the olfactory-forebrain system were found strongly NCAM-H-positive. At ED-8, a marked decrease in the number of LHRH-positive cells in the olfactory epithelium and a concomitant increase in the LHRH-positive cells in the forebrain area were noted. From ED-11 to the day of hatching, the majority of LHRH-positive neurons tended to move into their usual adult position, whereas the LHRH-positive cells had almost disappeared in the olfactory epithelium. No LHRH-immunoreactive neurons were found strongly positive to NCAM-H. These results suggest that LHRH neurons originate from the olfactory placode, then as they develop they migrate across the nasal septum and enter the forebrain with the olfactory nerve. The close association of NCAM-H with the developing LHRH neurons raises the possibility that NCAM-H plays some role in guiding the migrating LHRH neurons from the olfactory epithelium to the forebrain.

Animals↗