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PubMed2000

Odour recognition and segmentation by a model olfactory bulb and cortex.

We present a model of an olfactory system that performs odour segmentation. Based on the anatomy and physiology of natural olfactory systems, it consists of a pair of coupled modules, bulb and cortex. The bulb encodes the odour inputs as oscillating patterns. The cortex functions as an associative memory: when the input from the bulb matches a pattern stored in the connections between its units, the cortical units resonate in an oscillatory pattern characteristic of that odour. Further circuitry transforms this oscillatory signal to a slowly varying feedback to the bulb. This feedback implements olfactory segmentation by suppressing the bulbar response to the pre-existing odour, thereby allowing subsequent odours to be singled out for recognition.

Afferent Pathways↗
PubMed2001

Expression of Fos in the piriform cortex after acquisition of olfactory learning: an immunohistochemical study in the rat.

The piriform cortex (PCx), the main area of the primary olfactory cortex, is assumed to play a role in olfactory memory. Involvement of this paleocortex in mnesic processes was investigated by using Fos immunocytochemistry after acquisition of a two-odor discrimination task. Trained rats had to associate one odor of a pair with water reward while pseudo-trained rats were randomly rewarded. We further used non-trained rats and home cage control animals to determine the effect of manipulation and basal Fos level respectively. Except in control rats, Fos immunoreactivity was mainly distributed in brain areas involved in olfactory processing, learning and arousal. The trained, pseudo-trained, and non-trained rats showed a high Fos labeling in the entire PCx. However, quantitative analysis demonstrated a statistically higher Fos immunoreactivity in the anterior PCx in comparison with the posterior PCx for these rats. Furthermore, behavioral data allowed us to distinguish two groups of trained rats according to the number of days required to acquire the task. Rats with slow acquisition showed a higher Fos immunoreactivity in the whole PCx in comparison with the rats exhibiting a fast acquisition. Our findings support the assumption of a PCx rostro-caudal heterogeneity which could sustain differential information processing.

Animals↗
PubMed2007

Cholinergic suppression of excitatory synaptic responses in layer II of the medial entorhinal cortex.

Theta-frequency (4-12 Hz) electroencephalographic activity is thought to play a role in mechanisms mediating sensory and mnemonic processing in the entorhinal cortex and hippocampus, but the effects of acetylcholine on excitatory synaptic inputs to the entorhinal cortex are not well understood. Field excitatory postsynaptic potentials (fEPSPs) evoked by stimulation of the piriform (olfactory) cortex were recorded in the medial entorhinal cortex during behaviors associated with theta activity (active mobility) and were compared with those recorded during nontheta behaviors (awake immobility and slow wave sleep). Synaptic responses were smaller during behavioral activity than during awake immobility and sleep, and responses recorded during movement were largest during the negative phase of the theta rhythm. Systemic administration of cholinergic agonists reduced the amplitude of fEPSPs, and the muscarinic receptor blocker scopolamine strongly enhanced fEPSPs, suggesting that the theta-related suppression of fEPSPs is mediated in part by cholinergic inputs. The reduction in fEPSPs was investigated using in vitro intracellular recordings of EPSPs in Layer II neurons evoked by stimulation of Layer I afferents. Constant bath application of the muscarinic agonist carbachol depolarized membrane potential and suppressed EPSP amplitude in Layer II neurons. The suppression of EPSPs was not associated with a substantial change in input resistance, and could not be accounted for by a depolarization-induced reduction in driving force on the EPSP. The GABA(A) receptor-blocker bicuculline (50 microM) did not prevent the cholinergic suppression of EPSPs, suggesting that the suppression is not dependent on inhibitory mechanisms. Paired-pulse facilitation of field and intracellular EPSPs were enhanced by carbachol, indicating that the suppression is likely due to inhibition of presynaptic glutamate release. These results indicate that, in addition to well known effects on postsynaptic conductances that increase cellular excitability, cholinergic activation in the entorhinal cortex results in a strong reduction in strength of excitatory synaptic inputs from the piriform cortex.

Animals↗
PubMed1976

Temperature influence on the development of electrical activities in mammalian brain slice during incubation.

Thin slices, 500 mum in thickness, prepared from the guinea pig olfactory cortex and maintained in vitro, generate presynaptic and postsynaptic potentials following electrical stimulation of the lateral olfactory tract. These responses, however, cannot be elicited immediately after slice preparation; they start to develop gradually as the incubation continues. It was found that there was a remarkable time lag for the development between the pre- and the postsynaptic potentials. The presynaptic potential appeared early and developed its maximum height within 10 to 20 min from the onset of incubation. This time course was only slightly influenced by low temperature. Development of the postsynaptic potential in incubation was delayed and the time required to obtain the maximum height was about 30 min at 37 degrees C and 70 min at 22 degrees C. Upon step-like warming from 24 degrees C to 37 degrees C, there was a rapid increase in the amplitude of the response. In the glucose-deficient solution the presynaptic potential maintained its amplitude longer than the postsynaptic potential. Frequency potentiation of the postsynaptic potential was studied by applying a train of six stimuli. The maximum augmented ratio among six responses was the highest in early incubation and reached a steady at 50 min. The ratio of the post-tetanic potentiation of olfactory neurons was the highest at 5 min incubation and reached a steady at 20 min.

Action Potentials↗
PubMed1993

[The sense of smell: analysis of odors and olfactory memory].

Olfactory transduction is mediated by neuroepithelial cells localized on turbinal crests in naris. Odorant molecules are uptaked by the mucosa which flows on epithelial surface and some of the molecules enter in contact with olfactory cells tentacles. Odorant molecules interact with molecular receptors bound to cell membrane and induced successive reactions leading to ion channels opening and then to receptor potential appearance. The receptor cells degenerate when molecular receptors are saturated and, further regenerate, according a genetic program and olfactory learning action potentials which appear at the basal pole of the receptor cell are propagated along the small olfactory nerves to the olfactory bulb glomerulus. Several hundred axons enter in one glomerulus among others and make synaptic contacts with one dendritic tree of a mitral cell. The selection of the numerous signals which converge in the glomerulus, the codage in intensity, duration and contrast are made at this level. One odorant molecule activates some glomeruli (rarely one); a complex odor activates a great number of glomeruli according a complex spatial distribution. Following odor stimulation, the electrical signals are analysed in the olfactory bulb which delivers to the olfactory cortex various informations about the odor components that are to be selected and compared to anterior olfactory learning. Animal experimentation and clinical data show that memory storage is made using short, medium and long term memorization. This memory is integrated in the limbic system at the interface of neural structures which regulate the main behaviors and physiological functions. This explains the modulatory role of smell in some behaviors but complicate our understanding of access to olfactory memory.

Epithelial Cells↗
PubMed1984

Quantitative autoradiography of nicotinic [3H]acetylcholine binding sites in rat brain.

Quantitative autoradiography was used to localize nicotinic [3H]acetylcholine (ACh) binding sites in rat brain. High concentrations of nicotinic [3H]ACh binding sites were observed in the anterior and medial nuclei of the thalamus, the medial habenula and the superficial layer of the superior colliculus. Moderate levels of binding sites were observed in a variety of brain regions such as the frontoparietal cortex and the hippocampus. Low levels of nicotinic ACh sites occurred throughout the hypothalamus and the primary olfactory cortex.

Acetylcholine↗
PubMedDate not supplied

Immunolocalization of the proton-coupled oligopeptide transporter PEPT2 in developing rat brain.

This study examined the tissue distribution, cellular localization, and developmental expression of the PEPT2 protein in rat brain. Immunoblot and immunocytochemistry analyses were performed with specific rat PEPT1 and PEPT2 antisera developed in our laboratory. Rats were examined from fetus (gestation for 17 days) to adult (day 75). On immunoblot analysis, the PEPT2 protein was detected in cerebral cortex, olfactory bulb, basal ganglia, cerebellum, and hindbrain sections of adult brain, with the strongest signals in cerebral cortex. No PEPT1 protein was found in brain. Expression levels of the PEPT2 protein in cerebral cortex were maximal in the fetus and declined rapidly with advancing age. Adult protein levels were approximately 14% of that observed in fetus. In immunofluorescence experiments, the strongest PEPT2 signals were observed in epithelial cells of the choroid plexus for both adult and neonate brains. The PEPT2 protein was exclusively expressed on the apical membrane (CSF-facing) of choroid plexus epithelia. In double labeling experiments, PEPT2 immunoreactivity in adult brain colocalized with NeuN, a neuronal marker, but not with GFAP, an astrocyte marker. In contrast, in neonatal brain, PEPT2 immunoreactivity colocalized with both GFAP and NeuN. These findings demonstrate that the PEPT2 protein is found throughout the brain. The apical expression of PEPT2 in choroid plexus suggests that it is involved in the export of neuropeptides, peptide fragments, and peptide-like drugs from cerebrospinal fluid. PEPT2 may also play a role in the regulation of neuropeptide concentrations in extracellular fluid, especially during early development.

Aging↗
PubMed1973

On the mechanism of halothane anaesthesia.

1. The effects of halothane on the evoked potentials of in vitro preparations of guinea-pig olfactory cortex were studied.2. The evoked potentials recorded from the cortical surface comprised an initial diphasic wave - the lateral olfactory tract (l.o.t.) compound action potential - followed by a negative wave of 1-3 mV amplitude and about 10 msec duration. Superimposed on the negative wave was a number of positive peaks. The negative wave has been identified as an extracellularly recorded, monosynaptic, excitatory post-synaptic potential (e.p.s.p.) and the positive peaks have been shown to reflect the discharge of the cortical cell population in response to the evoked e.p.s.p. and are therefore termed ;population spikes'.3. When halothane (0.4-1.5%) was added to the gas stream that superfused the surface of the preparation the evoked e.p.s.p.s became smaller in amplitude and the size of the population spikes diminished. The l.o.t. compound action potential was unaffected by these levels of halothane. Higher levels of halothane (above 2%) further reduced the amplitude of the evoked e.p.s.p.s, abolished the population spikes, decreased the amplitude of the l.o.t. compound action potential and slowed its time course. The effects of halothane on the evoked potentials were dose-related and were independent (after the first 10 min of treatment) of the duration of the exposure to halothane.4. The decrease in the size of the population spike caused by the exposure to halothane implied that transmission through the cortical relay had been impaired. This was also shown by the decrease in the evoked activity of units in the prepiriform cortex. Of eleven units, eight were depressed by halothane (0.5-1.5%) two were unaffected and one showed a transient increase in the number of spikes generated in response to a l.o.t. volley.5. Halothane (up to 1.5%) had no effect on the threshold of the l.o.t. fibres to electrical stimulation or on that of the post-synaptic cells to synaptic excitation.6. Post-tetanic potentiation and frequency potentiation of the evoked e.p.s.p.s were enhanced in the presence of 1% halothane.7. It is concluded that halothane reduces excitatory synaptic transmission not by an increase in the electrical threshold of the post-synaptic cells to synaptic excitation but by interference with the process of chemical transmission either by reducing the output of transmitter from the pre-synaptic nerve terminal or by reducing the sensitivity of the post-synaptic membrane to the released transmitter substance.

Action Potentials↗
PubMed1986

Effect of bilateral transection of the lateral olfactory tract on the male-induced implantation failure (the Bruce effect) in mice.

Bilateral transection of the lateral olfactory tract (LOT) at the rostral level induced anosmia in female mice; by contrast, sectioning of the LOT at more caudal levels failed to induce anosmia in females. Transection of the LOT at all the levels inhibited the alien male-induced implantation failure in newly inseminated mice (the Bruce effect). Sham-operated as well as intact females exhibited a high rate of implantation failure following alien male exposure. The results suggest that the inhibition of the Bruce effect in LOT-transected females is not due to anosmia induced by the operation procedure, but due to interruption of the primary olfactory bulb projections to the posterior parts of the olfactory cortex. Our results rule out the involvement of the nervus terminalis in the Bruce effect. The present report lends support to the involvement of the accessory olfactory system in the transmission of the pheromonal stimulus involved in the male-induced implantation failure.

Animals↗
PubMed1991

Toward a pharmacology of odor receptors and the processing of odor images.

Odor molecules may be considered as molecular ligands which bind to receptors in the olfactory sensory neurons to give rise to the sensory response. Binding studies in whole sensory epithelia suggest that the receptors also bind muscarinic cholinergic antagonists. Preliminary electrophysiological evidence indicates that muscarinic and beta adrenergic antagonists block odor-elicited membrane currents in single isolated salamander sensory neurons. These results support the idea that models developed for analyzing ligand binding by members of the 7 transmembrane domain family of membrane receptors may apply rather closely to olfactory transduction. We suggest that sensory neurons express single receptor types with differing degrees of affinity for different ligands. We further suggest that glomeruli in the olfactory bulb function as labeled lines for particular sets of odor ligand determinants, and that interglomerular circuits bind together similar glomeruli and enhance contrast between dissimilar glomeruli. The odor image laid down in the sensory neuron population is thus subjected to abstracting and enhancement at the glomerular stage, prior to being transmitted for further processing in the deeper layers of the olfactory bulb and in the olfactory cortex.

Animals↗
PubMed1993

Long distance transplant-to-host axon elongation without target deafferentation.

To confirm the entire course of the long distance transplant-to-host axon elongation, the Thy-1 mouse allelic system was used for marking the olfactory bulb (OB) transplant. Axons from OB transplanted into the lateral ventricle and adjacent areas extended for a long distance, through three routes, to the frontal cortical surface, to the olfactory tubercle, the primary olfactory cortex and OB. Because of the OB graft insertion from the dorsal aspect through the neocortex, the host olfactory system remained unaffected. These results demonstrated that the transplanted OB could express its intrinsic ability of the long distance axon elongation without target deafferentation and even if the OB is inserted in the rather mature host.

Animals↗
PubMed1997

Electroconvulsive seizures increase levels of PS4, the TRH-enhancing peptide [prepro-TRH(160-169)], in rat brain.

We report the development of a radioimmunoassay for prepro-TRH(160-169) (PS4), a thyrotropin-releasing hormone (TRH) enhancing peptide, and its use in characterizing the effect of electroconvulsive seizures on the levels of this peptide in various brain regions of male Wistar rats. We found that electroconvulsive seizures significantly elevated the PS4 levels in hippocampus, amygdala, pyriform (olfactory) cortex, and anterior cortex but not in striatum, motor cortex, locus ceruleus, or ventral lateral medulla. The levels of PS4 were highly correlated with the corresponding TRH (p-Glu-His-Pro-NH2) and TRH-Gly (p-Glu-His-Pro-Gly) levels in hippocampus, amygdala, and pyriform cortex, consistent with the prepro-TRH source of all of these peptides. The PS4 levels in hippocampus and amygdala were significantly correlated with the immobility time in the Porsolt forced swim test, an established animal model for antidepressant effects. The PS4 levels in peripheral blood, hypothalamus, anterior cortex, amygdala, and eyes increased severalfold at 20 min following intracisternal injection of 228 microg of this peptide, suggesting that it readily crosses the blood-brain barrier. The pituitary levels of PS4 and TRH-Gly, on the other hand, were decreased within 20 min by intracisternal PS4, suggesting PS4 stimulated the release of prepro-TRH peptides from the pituitary. Fresh rat and human serum rapidly degraded PS4, indicating that it may act primarily as a paracrine modulator of TRH effects in pituitary, brain, and reproductive system.

Amino Acid Sequence↗
PubMed1994

Expression of mouse brain soluble guanylyl cyclase and NO synthase during ontogeny.

The spatial and temporal distribution of soluble guanylyl cyclase and nitric oxide synthase mRNA was determined during embryonic and postnatal development of the mouse brain. This was achieved by in situ hybridization of specific probes for soluble beta 1 guanylyl cyclase subunit and nitric oxide synthase mRNA on mouse brain sections at late fetal development (19-day embryo) and different stages of postnatal development (3, 7, 15 days, and adult). In the embryo, soluble guanylyl cyclase transcripts are weakly expressed in the central nervous system. Following birth their expression increases in the striatum and neocortex, and they are widely distributed in the adult brain (layer II and V-VI of the cortex, olfactory bulb, striatum, Purkinje cell layer of the cerebellum). In contrast, nitric oxide synthase mRNA was expressed in several embryonic structures of the brain (different layers of the cortical neuroepithelium, colliculi neuroepithelium, pons), and markedly reduced at early postnatal stage, except in the accessory olfactory bulb and pediculopontine nuclei. Nitric oxide synthase transcripts progressively appear, within two weeks following birth, in the striatum and the cerebral cortex but they were specifically confined to isolated cells. During this period, this mRNA also increased in hippocampus, in discrete nuclei (hypothalamus, pontine) and in the molecular layer of the cerebellum. The situation in the adult was similar to the one observed at 15 days. These results show a general lack of regional colocalization of soluble guanylyl cyclase and NOS mRNA during ontogeny, thus suggesting an independent regulation of the related genes.

Amino Acid Oxidoreductases↗
PubMed2005

Brain mechanisms for extracting spatial information from smell.

Forty years ago, von Békésy demonstrated that the spatial source of an odorant is determined by comparing input across nostrils, but it is unknown how this comparison is effected in the brain. To address this, we delivered odorants to the left or right of the nose, and contrasted olfactory left versus right localization with olfactory identification during brain imaging. We found nostril-specific responses in primary olfactory cortex that were predictive of the accuracy of left versus right localization, thus providing a neural substrate for the behavior described by von Békésy. Additionally, left versus right localization preferentially engaged a portion of the superior temporal gyrus previously implicated in visual and auditory localization, suggesting that localization information extracted from smell was then processed in a convergent brain system for spatial representation of multisensory inputs.

Adult↗
PubMed1993

Functional organization of the main olfactory bulb.

Complete understanding of the role of the mammalian main olfactory bulb in sensory processing has remained elusive despite many detailed studies on its anatomy and physiology. Several lines of recent evidence viewed in the context of earlier knowledge have provided new insights into the bulbar mechanisms of olfactory coding. The output cells of the olfactory bulb receive a localized olfactory nerve input and interneuronal input via dendrodendritic synapses on distinct sets of dendrites. The spatial arrangement of granule cell contacts on output cell basal dendrites suggests that lateral inhibitory interactions may occur between neighboring output cells. The input from olfactory receptor cell axons to the bulb also has spatial order, but does not represent a precise map of the receptor surface. Recent studies with antibodies and lectins suggest that different groups of axons from chemically similar receptor cells collect into certain glomeruli, even if the axons originate from cells that are not contiguous in the mucosa. Electrophysiological studies have begun to explore the participation of spatially organized circuits in olfactory processing. The degree to which neighboring output cells respond similarly to odor stimulation, for example, depends on the distance between the cells, with those further apart showing complementary responses. Also, a single output cell can show 2 or more different temporal response patterns when different odors are presented. Intracellular recordings indicate that these responses are shaped by IPSPs. Electrical stimulation during such recordings shows that some mitral cells are excited by nerve inputs close to their glomerular tufts, while they are inhibited by nerve inputs to other parts of the bulb. Finally, recordings from granule and periglomerular cells indicate their potential in mediating components of output cell odor responses. These considerations suggest that the olfactory bulb performs a spatially based analysis on the information coming from the receptor cells. While the spatial organization of the olfactory bulb is probably not faithfully represented in the projections to the olfactory cortex, bulbocortical projections are not random. The fact that spatial factors exist at each of these levels in the olfactory system must be considered in developing models of central olfactory processing.

Animals↗
PubMed1978

Depression of evoked potentials in brain slices by adenosine compounds.

1 A study has been made of the action of adenosine on surface slices of guinea-pig olfactory cortex in vitro. 2 With extracellular recordings from the pial surface and stimulation of the presynaptic input, the lateral olfactory tract (LOT) generated a monosynaptic negative wave representing dendritic excitatory potentials. This negative wave was depressed by bath application of 1 micron adenosine with increasing effect up to 1 mM. Adenosine 5'--triphosphate (ATP), adenosine 5'-monophosphate (AMP) and cyclic adenosine 3',5'-monophosphate (cyclic AMP) had similar depressant actions. Adenine and guanosine were very weak depressants. 3 Theophylline concentrations in the range 10 micron to 3 mM progressively antagonized the action of adenosine. 4 Dibuyryl cyclic AMP (100 micron) and agents which increase intracellular cyclic AMP were not depressants, suggesting that the action of adenosine was not cyclic AMP-mediated. 5 Intracellular recordings confirmed the depressant effect of adenosine on excitatory potentials generated by LOT stimulation and also showed that postsynatpic action potentials and the membrane of the soma were unaffected by adenosine. 6 Since presynaptic action potentials were also unaffected by adenosine, these experiments suggest that adenosine reduces excitatory transmission at LOT synapses and fortifies the idea that adenosine has a 'neurohumoral' action.

Adenine Nucleotides↗
PubMedDate not supplied

45Ca exchange in rat cortex slices in conditions of long-term potentiation.

Existing data on the role of Ca2+ ions in the development of long-term potentiation were used as a basis for studying changes in different Ca2+ compartments in cells in living rat olfactory cortex slices during potentiation. The kinetics of 45Ca2+ exchange were studied at 5, 15, and 30 min of potentiation. During the induction phase (1-5 min) of long-term potentiation, the fraction of tightly-bound intracellular Ca2+ decreased. There were no changes in the content of Ca2+ ions in other fractions at this stage. During maintenance of potentiation, which lasted 15-25 min, Ca2+ levels in the extracellular and intracellular compartments did not differ from controls. At 30 min, during extinction of long-term potentiation, there was a significant redistribution of Ca2+ in cells: the levels of free and loosely-bound Ca increased, as did extracellular Ca2+.

Animals↗
PubMed1989

Mercury accumulation in tissues from dental staff and controls in relation to exposure.

Samples, mainly from occipital cortex and pituitary gland, but also from rental cortex, olfactory bulbs, thyroid gland and liver were collected from autopsies of 8 dental staff cases and 27 controls. These samples were analysed for total mercury content using radiochemical neutron activation analyses. The results revealed high mercury concentrations (median 815, range 135-4,040 micrograms Hg/kg wet weight) in pituitaries from the dental staff cases compared to controls (N = 23, median 23 range 6-1, 170 micrograms Hg/kg). In occipital cortex, the cases had a median of 17, range of 4-300 micrograms Hg/kg and the controls (N = 20) had a median of 10, range 2-29 micrograms Hg/kg. A few samples from olfactory bulbs show low mercury concentrations for both cases and controls. Renal cortex was analysed from three cases and contained clearly higher concentrations (945, 1,545, 2,110 micrograms Hg/kg) compared to controls (N = 12, median 180, range 21-810 micrograms Hg/kg). There is no control material for the other analysed samples, but one thyroid sample had an extremely high concentration of 28,000 micrograms Hg/kg.

Adolescent↗