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PubMed1977

Regional distribution of choline acetyltransferase and acetylcholinesterase within the amygdaloid complex and stria terminalis system.

The distribution of "marker" enzymes for cholinergic neurons has been studied in 10 subdivisions of the amygdaloid complex of the rat brain. Choline acetyltransferase activity was measured using a radiochemical method in samples dissected from fresh serial sections. Acetylcholinesterase was studied using a histochemical procedure. Both enzymes had similar patterns of distribution within the amygdaloid complex and were most concentrated in the posterior lateral and basolateral nuclei and in the nucleus of the lateral olfactory tract. These enzymes were much less concentrated in the cortical, medial, central, and basomedial nuclei. Large differences in acetylcholinesterase staining were found within the lateral posterior and the basolateral nuclei and within the pyriform cortex. Biochemical studies showed a parallel distribution of choline acetyltransferase within these nuclei. The results indicate that cholinergic neural elements in the amygdala are concentrated primarily in the basolateral complex and suggest that this region may be innervated by cholinergic fibers traveling in the ventral amygdalo-fugal pathway.

Acetylcholinesterase↗
PubMed1975

Electrically-induced epileptogenesis in rabbit olfactory bulb: electrophysiological plasticity in a simple cortical system.

Sustained seizure activity can be induced in rabbit olfactory bulb by application of brief low-level current via chronically implanted micro-electrodes. Sensitivity to such stimulation is markedly augmented by prior surgical isolation of the ipsilateral or contralateral bulb. The isolated rabbit olfactory bulb apparently possesses an intrinsic system sufficient to acquire and retain altered neuronal excitability of an epileptiform kind. The preparation described here offers promise as a model for further studies of electrophysiological plasticity in a simple cortical system.

Amygdala↗
PubMed1995

Synaptic and non-synaptic cholinergic innervation of the various types of neurons in the main olfactory bulb of adult rat: immunocytochemistry of choline acetyltransferase.

The cholinergic neuronal structures and their synaptic connections in the main olfactory bulb of adult rats were analysed by using choline acetyltransferase immunocytochemistry. Within the glomeruli, cholinergic nerve fibers were restricted to strands which subdivided the neuropil into small compartments, the interior of which contained sensory axons but was devoid of cholinergic axons. Small numbers of choline acetyltransferase neurons were detected in all layers. Ultrastructural analysis revealed selective triadic synaptic relationships with different neuron classes in the intraglomerular area and in the external plexiform layer. These triads were made up of (i) a cholinergic axon, (ii) one or several periglomerular or granule cell dendrites, and (iii) usually one relay cell dendrite. In these triads, asymmetric cholinergic synapses were selectively focused on dendrites (gemmules and spines) of periglomerular or granule cells. Within the glomerulus, mitral and tufted cell dendrites were closely apposed to some cholinergic axon varicosities, most abundantly near arborizations of the apical dendrites. However, cholinergic synapses were never seen on any relay cell dendrite. In the external plexiform layer, cholinergic synapses were present on all parts of the superficial short-axon cells. In the internal plexiform layer and the granule cell layer, cholinergic axon varicosities exhibited close apposition or asymmetric synapses with granule cell gemmules. The data suggest that cholinergic projections from the basal forebrain to the main olfactory bulb focus synaptic innervation on interneurons. On relay cells, direct acetylcholine effects may occur, but these must be based on non-synaptic acetylcholine release at the surface of their dendrites.

Animals↗
PubMed1992

Peripheral origin of olfactory nerve fibers by-passing the olfactory bulb in Xenopus laevis.

After DiI injections into the diencephalon of Xenopus, two types of retrogradely labelled cells were found in the nasal area: (i) receptor cells in the olfactory epithelium and (ii) a small cell group located between the main olfactory epithelium and the vomeronasal system. These results reveal an extensive extrabulbar olfactory projection of olfactory receptor cells. Fibers of these cells do not terminate in the olfactory bulb but innervate targets in the diencephalon directly. The other type of retrogradely labelled cells, apparently, are not part of any epithelium. They resemble similar cell groups which have previously been regarded as part of the nervus terminalis system in other vertebrates.

Animals↗
PubMed2002

Development of the facial midline.

"Intellectual excellence lies in having faith in the observation of apparently nontranscendental and unimportant facts. To observe an anatomic element calmly, with an open, analytical spirit, and with spiritual freedom, can lead to an explosive vortex of new knowledge."-Miguel Orticochea, M.D.(1) Traditional descriptive embryology based upon the interaction of frontonasal, lateral nasal, and medial nasal prominences is incapable of explaining the three-dimensional development of the facial midline. The internal structure of the nose and that of the oronasal midline can best be explained by the presence of paired A fields originating from the prechordal mesendoderm, associated with the nasal and optic placodes, supplied by the internal carotid artery, and sharing a common genetic coding with the prosomeres of the forebrain. Mesial drift of these fields leads to fusion of their medial walls; this in turn provides bilateral functional matrics within which form the orbits ethmoids, lacrimals, turbinates, premaxillae, vomerine bones, and the cartilages of the nose. This two-part paper reports six lines of evidence supporting the field theory model of facial development: (1) An apparent watershed exists in the midline of the base between the territories of the internal and external carotid systems. Isolation of the ICA in injected fetal specimens confirmed that the demarcation was distinct and restricted to the embryonic nasal capsule. (2) Field theory explains the developmental anatomy of the contents of the nasal capsule. (3) The neuromeric model of CNS development provides a genetic basis for the anatomy and behavior of fields. (4) Mutants for the Dlx5 gene demonstrate A field deletion patterns. These experiments relate the nasal placode to the structures of the A fields. (5) Separate regions of the original nasal placodes give rise to neurons, which are dedicated to separate sensory and endocrine systems. The A fields constitute the pathways by which these neurons reach the brain. (6) Non-cleft lip-related cleft palate, holoprosencephaly, and the Kallmann syndrome are clinical models that demonstrate the effects of anatomic disturbances within the A fields.

Animals↗
PubMed1983

Early recovery of function after olfactory tract section correlated with reinnervation of olfactory tubercle.

Behavioral recovery and cortical reinnervation after early olfactory tract section were assessed in the infant golden hamster (Mesocricetus auratus). Hamster pups show strong thermotaxis at birth which declines abruptly after postnatal day (P) 8 in normal pups. Unilateral olfactory bulbectomy on P5 causes persistent thermotaxis through the second postnatal week. In this study, the bulb's output pathway, the lateral olfactory tract, was unilaterally severed on P5 and pup thermotaxis was tested through P15. Complete tract section, like bulbectomy, prolonged thermal responding beyond P8. In contrast to bulbectomy, however, some tract-sectioned pups showed recovery before P15 while others continued to show persistent thermotaxis throughout testing. The olfactory bulb projection was examined 10 days after tract section in order to determine whether recovery and persistent thermotaxis were associated with different patterns of cortical innervation. Eleven pups with complete transections showed recovery during the second week. In 10 of these pups, olfactory bulb fibers had penetrated the damaged region after surgery to reinnervate the olfactory tubercle. Three of these pups also exhibited some reinnervation of piriform cortex. The lesions of pups showing persistent thermotaxis were more severe, extending bilaterally or into deep cortical layers, and olfactory fibers had failed to reinnervate caudal terminal fields. All pups with olfactory tract sections showed extensive sprouting rostral to the cut, regardless of their behavioral profile. In no case had postlesion growth innervated the entorhinal or amygdaloid areas. Inhibition of thermotaxis was associated with reinnervation of the olfactory tubercle rather than more rostral, lateral or caudal olfactory cortex. We conclude that regrowth of olfactory tract fibers caudal to early transection is rapid and has functional consequences for early behavioral development.

Animals↗
PubMed1991

Ruffed cells in the olfactory bulb of freshwater teleosts. II. A Golgi/EM study of the ruff.

The morphological characteristics of the synaptic contacts in the ruff of the cichlid fish Hemichromis bimaculatus were studies using the combined Golgi-electron microscope technique. Ruffed cells were located in the glomerular and plexiform layers and exhibited a pyriform or round cell body and numerous thin dendritic branches that were highly ramified. Four different segments could be distinguished on the initial portion of the axon (IP) according to the number and density of protrusions. These protrusions or lateral appendages are highly interdigitated, forming a characteristic synaptic field: the ruff. The ruff displayed a very high number of synapses with terminals showing a varied morphology. Protrusions of the ruff were both presynaptic and postsynaptic, taking also part in reciprocal pairs of synapses. Synapses from the ruff to the adjacent prolongation are asymmetrical, the prolongation to protrusion synapses being symmetrical. The axonal shaft participates in fewer synaptic contacts. Boutons contacting with one protrusion can synapt with other one, and can also receive an asymmetric synapse from another terminal, forming a serial synapse. This constitutes the most complex synaptic system observed in the glomerular layer of the olfactory bulb in any vertebrate. The synaptology of the ruffed cell IP is compared with previous reports on other species, with the teleostean mitral cells and with the IP of higher vertebrates neurons, the ruffed cells showing a completely different synaptic pattern.

Animals↗
PubMed1996

Induction of differentiation of human olfactory neuroblastoma cells into odorant-responsive cells.

Olfactory neuroblastoma is a rare malignancy of the olfactory mucosa that may be derived from the olfactory epithelium. To characterize this tumor, we cultured olfactory neuroblastoma cells in the presence or absence of growth factors (transforming growth factor alpha and basic fibroblast growth factor) known to affect olfactory tissue and assessed their responsiveness to known odorants by measuring changes in intracellular calcium. Untreated cells did not respond to odorants. Basic fibroblast growth factor treatment had cytotoxic effects, and treated cells did not respond to odorants. Transforming growth factor alpha treatment resulted in the induction of odor responsiveness in these cells. Cells responded to odorants at 100 nM to 100 microM concentrations and responded with both increases and decreases in intracellular calcium. Increases in intracellular calcium were mediated by a calcium influx and were reversibly blocked by compounds known to inhibit second messenger pathways in olfactory receptor neurons. The calcium responses of the olfactory neuroblastoma cells were thus specific to the odorants and similar to those found in olfactory receptor neurons. The results support the notion that olfactory neuroblastoma cells may be of olfactory origin and thus they can be used as a model cell line to study human olfaction.

Calcium↗
PubMed1995

Evidence that a Gq-protein mediates excitatory odor transduction in lobster olfactory receptor neurons.

Non-hydrolysable analogs of GTP and GDP alter odor-evoked inward and outward currents in voltage-clamped cultured lobster olfactory receptor neurons. Currents of both polarities are pertussis and cholera toxin-insensitive. Antibodies directed against the alpha subunits of G(olf), G(o), G11, an internal Gq sequence, the common carboxyl terminal sequence of Gq and G11 (anti-Gq/11), and the transducin beta subunit, fail to perturb the outward current, but anti-G(o) and anti-Gq/11 selectively block the inward current. Anti-Gq/11 immunolabels a band of approximately 45 kDa by Western blot analysis, but the anti-G(o) immunolabeling is non-specific. These results suggest that the excitatory olfactory signalling pathway that leads to an odor-evoked inward current may be coupled via a member of the Gq family, while the odor-evoked outward current is transduced by a different G protein.

Amino Acid Sequence↗
PubMed1996

Deletion of glycoprotein gE reduces the propagation of pseudorabies virus in the nervous system of mice after intranasal inoculation.

A pseudorabies virus (PrV) mutant, deficient in the nonessential glycoprotein E (gE) and expressing the LacZ gene (gE- beta gal+ PrV), and its rescued virus were inoculated intranasally in mice. The median lethal dose of gE- beta gal+ PrV was similar to that of the parental Kaplan strain, but mice survived longer and did not develop symptoms of pseudorabies. In the nasal mucosa, gE- beta gal+ PrV replicated less efficiently than rescued virus. gE- beta gal+ PrV could infect first-order trigeminal and sympathetic neurons innervating the nasal mucosa. However, transneuronal transfer to second-order cells groups did not occur in trigeminal pathways and was severely reduced in sympathetic pathways. The mutant was also unable to propagate in the parasympathetic system. In contrast, gE-rescued virus was transferred transneuronally in trigeminal, sympathetic, and parasympathetic pathways, like wild-type PrV. These findings provide further evidence that deletion of gE specifically affects transneuronal transfer of PrV more than penetration and multiplication of the virus in first-order neurons.

Administration, Intranasal↗
PubMedDate not supplied

[Kallmann De Morsier syndrome: FGF-signaling insufficiency?].

Kallmann syndrome (KAL) associates hypogonadotropic hypogonadism and anosmia, i.e. a deficiency of the sense of smell. Anosmia is related to the absence or the hypoplasia of the olfactory bulbs. Hypogonadism is due to GnRH deficiency, and is likely to result from the failed embryonic migration of GnRH-synthesizing neurons. These cells normally migrate from the olfactory epithelium to the forebrain along the olfactory nerve pathway. Kallmann syndrome is genetically heterogeneous. The gene responsible for the X-chromosome linked form of the disease, KAL-1, has been identified in 1991. KAL1 encodes a ~95 kDa glycoprotein of unknown function, which is present locally in various extracellular matrices during the period of organogenesis. The recent finding that FGFR1 mutations are involved in an autosomal dominant form of Kallmann syndrome (KAL-2), combined to the analysis of mutant mouse embryos that no longer express Fgfr1 in the telencephalon, suggests that the disease results from a deficiency in FGF-signaling at the earliest stage of olfactory bulb morphogenesis. We propose that the role of the KAL1 gene product, the extracellular matrix protein anosmin-1, is to enhance FGF-signaling, and suggest that the gender difference in anosmin-1 dosage (because KAL1 partially escapes X-inactivation) explains the higher prevalence of the disease in males.

Biomedical Research↗
PubMed2004

Kallmann syndrome: fibroblast growth factor signaling insufficiency?

Kallmann syndrome (KAL) is a developmental disease that combines hypogonadotropic hypogonadism and anosmia. Anosmia is related to the absence or hypoplasia of the olfactory bulbs. Hypogonadism is due to GnRH deficiency and is likely to result from the failed embryonic migration of GnRH-synthesizing neurons. These cells normally migrate from the olfactory epithelium to the forebrain along the olfactory nerve pathway. KAL is phenotypically and genetically heterogeneous. The gene responsible for the X-chromosome linked form of the disease (KAL1) has been identified in 1991. KAL1 encodes anosmin-1, an approximately 95-kDa glycoprotein of unknown function which is present locally in various extracellular matrices during the period of organogenesis. The recent finding that FGFR1 mutations are involved in an autosomal dominant form of Kallmann syndrome (KAL2), combined with the analysis of mutant mouse embryos that no longer express Fgfr1 in the telencephalon, suggests that the disease results from a deficiency in FGF signaling at the earliest stage of olfactory bulb morphogenesis. We propose that the role of anosmin-1 is to enhance FGF signaling and suggest that the gender difference in anosmin-1 dose (because KAL1 partially escapes X-inactivation) explains the higher prevalence of the disease in males.

Extracellular Matrix Proteins↗
PubMed2001

Vomeronasal organ: electrical stimulation activates Fos in mating pathways and in GnRH neurons.

Electrical stimulation of the vomeronasal organ in male hamsters activated Fos expression in neurons of the chemosensory pathways, as in experiments where animals were stimulated with female chemical stimuli. Fos was also activated in gonadotropin hormone releasing hormone (GnRH, or LHRH) neurons in the rostral medial preoptic region of the brain, a possible substrate for GnRH influence on chemosensory-dependent reproductive behavior.

Animals↗
PubMed1985

The zona incerta: another source of centrifugal fibers to the main olfactory bulb.

Neurons in the ipsilateral anteropolar division of the zona incerta were retrogradely labeled following injections of horseradish peroxidase in the main olfactory bulb. In addition, labeled cell bodies were found in the dorsal hypothalamus. Fewer and less densely labeled neuron cell bodies were seen in the contralateral zona incerta and dorsal hypothalamus. Most of the cells had a characteristic fusiform shaped soma, but a small number of the hypothalamic cells had spherical or conical shaped cell bodies.

Animals↗
PubMed2000

Effects of excitotoxic lesions in the ventral striatopallidal--thalamocortical pathway on odor reversal learning: inability to extinguish an incorrect response.

The role of the ventral striatopallidal pathway and related cortical areas in stimulus-reward association reversal behavior was studied by inducing bilateral lesions with the excitotoxin, N-methyl-D-aspartate (NMDA) at restricted sites in the system. The areas lesioned were the ventral pallidum (VP), the ventral striatum (VS), the medial prefrontal cortex (mPFC) [i.e., the prelimbic (PL) and infralimbic (IL) cortexes], and the orbital cortex [i.e., the dorsolateral orbital (DLO), ventral lateral orbital (VLO), and lateral orbital (LO) cortexes]. Rats with lesions of the dorsal caudate nucleus and putamen (CPu) served as a positive control in this study. Water-deprived rats were trained on a go, no-go two-odor olfactory discrimination task to respond to one odor (S+) with water as a reward and to suppress responding to the other odor (S-). The rats were then tested for their ability to reverse the associated stimuli. The number of errors made before successfully learning the stimulus-reward association were measured in relation to a sham lesion control group which did not receive injections of NMDA. In experimental rats, the lesions did not affect their ability to learn stimulus-reward associations for novel odors, but did result in an increase in the number of false alarms after the significance of the associated stimuli were reversed. That is, the lesioned animals persisted in responding to the formerly rewarded but now unrewarded stimulus. Rats with damage to the CPu did not show a significant effect when compared with the controls during reversal problems. The results support the hypothesis that the ventral striatopallidal system, together with related thalamic and frontal cortical structures, functions in reversal learning by suppressing inappropriate responses to stimuli that are no longer rewarded.

Animals↗
PubMed1994

Nonlinear relationship between impulse flow, dopamine release and dopamine elimination in the rat brain in vivo.

Central dopaminergic neurons exhibit two kinds of discharge activity: single spikes and bursts of two to six action potentials. Since these neurons can switch from one discharge pattern to the other whereas the mean discharge rate remains little affected, bursts may be more potent in triggering the release of their neurotransmitter, dopamine. Electrical stimulations mimicking the bursting pattern were actually twice as potent as regularly spaced stimulations to enhance the dopamine extracellular concentration. This suggested that dopamine release might be facilitated by increasing the impulse flow frequency. The high extracellular overflow evoked by a burst might also be due to accumulation of the released dopamine whereas, at lower frequencies, dopamine might be readily eliminated between every action potential. In the present study the dopamine overflow evoked by electrical stimulation of the dopaminergic pathway was measured in vivo by carbon fibre electrodes combined with continuous amperometry. We observed a small facilitation of the release per pulse during stimulations mimicking a burst but only in mesolimbic areas. The high extra-cellular dopamine level evoked by a burst was mainly due to accumulation of the released dopamine.

Action Potentials↗
PubMed2002

Oscillatory current responses of olfactory receptor neurons to odorants and computer simulation based on a cyclic AMP transduction model.

Neural oscillatory activities triggered by odorant stimulation have been often reported at various levels of olfactory nervous systems in vertebrates. To elucidate the origin of neural oscillations, we studied first the oscillatory properties of current responses of isolated olfactory receptor neurons (ORNs) of the rainbow trout to amino acid odorants, using a whole-cell voltage-clamp technique and found that the damped current oscillations were intrinsic in both ciliated and microvillous ORNs and occurred when ORNs were stimulated by odorants at high intensities. Continuous wavelet analysis using the Gabor function revealed that the dominant frequency of oscillations was 1.89 +/- 0.50 Hz (mean +/- SD, n = 92). There was no significant difference in oscillation frequency between the two types of ORNs and between different perfusion conditions with standard and Na(+)-free (choline) Ringer's solutions, but there was a slight difference in oscillation frequency between different holding potential conditions of negative and positive potentials. We then performed a computer simulation of the current responses with a cAMP olfactory transduction model. The model was based on the assumption that the current responses of ORNs were linearly related to the sum of concentrations of active cyclic-nucleotide-gated channels and Ca(2+)-activated Cl(-) channels, and was expressed by 12 differential equations with 44 different parameters. The simulation revealed that the oscillations of current responses of ORNs were mainly due to the oscillatory properties of intracellular cAMP and Ca(2+) concentrations. The necessary reaction component for the oscillations in the transduction model was direct inhibition of adenylate cyclase activity by Ca(2+). High Ca(2+) efflux by the Na(+)-Ca(2+) exchanger and cAMP-phosphodiesterase activity were most influential on the oscillations. The simulation completely represented the characteristics of current responses of ORNs: odorant-intensity-dependent response, intensity-dependent latency and adaptation. Thus, the simulation is generally applicable to current and voltage responses of ORNs equipped with cAMP olfactory transduction pathway in other vertebrate species. The simulation programs for Macintosh (cAMP 9.2.7 and 9.2.8 for MacOS 8.1 or later) and cAMP JAVA applet versions based on cAMP 9.2.8 have been published on the world wide web (http://bio2.sci.hokudai.ac.jp/bio/chinou1/noriyo_home.html).

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1982

Somatostatin connections between the hypothalamus and the limbic system of the rat brain.

Somatostatin (SRIF) content of several brain structures was evaluated by radioimmunoassay in rats bearing various types of hypothalamic transections, as well as lesions of the amygdala. Analysis of the regional changes in SRIF concentrations after surgery suggest the following conclusions: (1) hypothalamic somatostatinergic neurons project to the limbic system, with the exception of the amygdaloid nuclei; (2) the olfactory tubercle, the lateral septal nucleus, the habenula and probably the hippocampus receive somatostatin projections from periventricular SRIF-containing cells; (3) somatostatin-containing fibers take a lateral course after leaving periventricular cells and join the medial forebrain bundle; (4) somatostatin innervation of the amygdala seems to be intrinsic.

Amygdala↗