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PubMed1997

Deafferentation causes apoptosis in cortical sensory neurons in the adult rat.

The present study provides an experimental model of the apoptotic death of pyramidal neurons in rat olfactory cortex after total bulbectomy. Terminal transferase (TdT)-mediated deoxyuridine triphosphate (d-UTP)-biotin nick end labeling (TUNEL), DNA electrophoresis, and neuronal ultrastructure were used to provide evidence of apoptosis; neurons in olfactory cortex were counted by stereology. Maximal TUNEL staining occurred in the piriform cortex between 18 and 26 hr postbulbectomy. Within the survival times used in the present study (up to 48 hr postlesion), cell death was observed exclusively in the piriform cortex; there was no evidence of cell death in any other areas connected with the olfactory bulb. Neurons undergoing apoptosis were pyramidal cells receiving inputs from, but not projecting to, the olfactory bulb. The apical dendrites of these neurons were contacted by large numbers of degenerating axonal terminals. Gel electrophoresis of DNA purified from lesioned olfactory cortex showed a ladder pattern of fragmentation. Inflammatory cells or phagocytes were absent in the environment of degenerating neurons in the early stages of the apoptotic process. The present model suggests that deafferentation injury in sensory systems can cause apoptosis. In addition, olfactory bulbectomy can be used for investigating molecular mechanisms that underlie apoptosis in mature mammalian cortical neurons and for evaluating strategies to prevent the degeneration of cortical neurons.

Afferent Pathways↗
PubMed2001

Functional magnetic resonance imaging of human olfaction.

Olfaction is our basic sense phylogenetically and embryologically. Little is known, however, about how the human brain encodes the quality of odors, odor-associated memories, and emotions. Olfactory information is projected from the olfactory bulb to the primary olfactory cortex, which is composed of the anterior olfactory nucleus, the olfactory tubercle, the piriform cortex, the amygdala, the periamygdaloid region, and the entorhinal cortex. From there, the primary olfactory cortex projects to secondary olfactory regions including the hippocampus, ventral striatum and pallidum, hypothalamus, thalamus, orbitofrontal cortex, agranular insular cortex, and cingulate gyrus. Functional MR studies using olfactory stimuli as paradigms show activation of many of these areas and can advance our understanding of odor perception in humans.

Adult↗
PubMed2005

Stereological analysis of forebrain regions in kainate-treated epileptic rats.

Patients and models of temporal lobe epilepsy display neuron loss in the hippocampal formation, but neuropathological changes also occur in other forebrain regions. We sought to evaluate the specificity and extent of volume loss of the major forebrain regions in epileptic rats months after kainate-induced status epilepticus. In systematic series of Nissl-stained sections, the areas of major forebrain regions were measured, and volumes were estimated using the Cavalieri principle. In some regions, the optical fractionator method was used to estimate neuron numbers. Most kainate-treated rats showed significant volume loss in the amygdala, olfactory cortex, and septal region, but others displayed different patterns, with significant loss only in the hippocampus or thalamus, for example. Average volume loss was most severe in the amygdala and olfactory cortex (82-83% of controls), especially the caudal parts of both regions. In the piriform cortex (including the endopiriform nucleus) of epileptic rats, an average of approximately one-third of Nissl-stained neurons and one-third of the GABAergic interneurons labeled by in situ hybridization for GAD67 mRNA were lost, and the extent of neuron loss was correlated with the extent of volume loss. Volumetric analysis of major forebrain regions was insensitive to specific neuron loss in subregions such as layer III of the entorhinal cortex and the hilus of the dentate gyrus. These findings provide quantitative evidence that kainate-treated rats tend to display extensive neuron and volume loss in the amygdala and olfactory cortex, although the patterns and extent of loss in forebrain regions vary considerably among individuals. In this status epilepticus-based model, extrahippocampal damage appears to be more extensive and hippocampal damage appears to be less extensive than that reported for patients with temporal lobe epilepsy.

Analysis of Variance↗
PubMed2002

Conditioned opioid withdrawal decreases nociceptin/orphanin FQ levels in the frontal cortex and olfactory tubercle.

Clinical evidence suggests that individuals experiencing drug withdrawal can become conditioned to environmental situations, whereby previously neutral stimuli can produce symptoms of withdrawal. It is believed that this "conditioned withdrawal" can have motivational significance, but the neurobiological basis for conditioned withdrawal is unknown. The goal of this study was to determine adaptations in endogenous opioid systems that may be responsible for expression of conditioned withdrawal. Opioid-dependent rats trained to lever press for food were exposed to tone and scent cues in the presence of naloxone or saline. Naloxone but not saline predictably suppressed responding for food. One month later and in a post-dependent state, all rats again were exposed to the cues but not naloxone. The conditioned cues alone suppressed responding for food in the rats previously paired with naloxone, but no suppression was seen in rats previously paired with saline. Radioimmunoassay (RIA) analysis for nociceptin/orphanin FQ (nociceptin), met-enkephalin-Arg-Phe (MEAP), and dynorphin A (dyn A) was performed from dissections of various brain regions of the rats undergoing conditioned withdrawal. Significant reductions in nociceptin peptide levels were seen in the frontal cortex and olfactory tubercle of these rats. Unconditioned opioid withdrawal and unconditioned footshock stress produced different patterns of opioid peptide regulation in separate groups of rats. These results shed light on adaptations of endogenous opioid systems to conditioned cues, stress, and withdrawal, all factors that play a role in motivating drug intake.

Animals↗
PubMed2002

Hebbian imprinting and retrieval in oscillatory neural networks.

We introduce a model of generalized Hebbian learning and retrieval in oscillatory neural networks modeling cortical areas such as hippocampus and olfactory cortex. Recent experiments have shown that synaptic plasticity depends on spike timing, especially on synapses from excitatory pyramidal cells, in hippocampus, and in sensory and cerebellar cortex. Here we study how such plasticity can be used to form memories and input representations when the neural dynamics are oscillatory, as is common in the brain (particularly in the hippocampus and olfactory cortex). Learning is assumed to occur in a phase of neural plasticity, in which the network is clamped to external teaching signals. By suitable manipulation of the nonlinearity of the neurons or the oscillation frequencies during learning, the model can be made, in a retrieval phase, either to categorize new inputs or to map them, in a continuous fashion, onto the space spanned by the imprinted patterns. We identify the first of these possibilities with the function of olfactory cortex and the second with the observed response characteristics of place cells in hippocampus. We investigate both kinds of networks analytically and by computer simulations, and we link the models with experimental findings, exploring, in particular, how the spike timing dependence of the synaptic plasticity constrains the computational function of the network and vice versa.

Hippocampus↗
PubMed1989

Cholinergic and peptidergic projections from the medial septum and the nucleus of the diagonal band of Broca to dorsal hippocampus, cingulate cortex and olfactory bulb: a combined wheatgerm agglutinin-apohorseradish peroxidase-gold immunohistochemical study.

We have examined the distribution pattern and the density of various neuropeptide, neurotransmitter and enzyme containing neurons in the rat medial septum and the nucleus of the diagonal band of Broca to assess their possible involvement in the septohippocampal, septocortical and septobulbar pathways. Immunohistochemical methods were combined with the retrograde transport of a protein-gold complex injected in the hippocampus, the cingulate cortex or the olfactory bulb. Cholinergic neurons were the most numerous. Galanin-positive neurons were about two or three times less numerous than cholinergic cells. Both these cell types had a similar location though the choline acetyl transferase-like immunoreactive cells extended more caudally in the horizontal limb of the nucleus of the diagonal band of Broca. Immunoreactive cells for other neuroactive substances were few (calcitonin gene-related peptide, luteinizing hormone releasing hormone. [Met]enkephalin-arg-gly-leu) or occasional (dynorphin B, vasoactive intestinal polypeptide, somatostatin, neurotensin, cholecystokinin, neuropeptide Y and substance P). No immunoreactive cells for bombesin, alpha atrial natriuretic factor, corticotropin releasing factor, 5-hydroxytryptamine, melanocyte stimulating hormone, oxytocin, prolactin, tyrosine hydroxylase or arg-vasopressin were present. Choline acetyltransferase- and galanin-like immunoreactive cells densely participate to septal efferents. Cholinergic neurons constituted the bulk of septal efferent neurons. Galanin-positive cells were 22% of septohippocampal, 8% of septocortical, and 9% of septobulbar neurons. Galanin containing septohippocampal neurons were found in the medial septum and the nucleus of the diagonal band of Broca; galanin-positive septobulbar and septocortical cells were limited to the nucleus of the diagonal band of Broca. Occasional double-labellings were noticed with some peptides other than galanin. Luteinizing hormone-releasing hormone, calcitonin gene-related peptide and enkephalin were the most often observed; some other projecting cells stained for vasoactive intestinal polypeptide or dynorphin B. Luteinizing hormone-releasing hormone, calcitonin gene-related peptide and enkephalin were observed in septohippocampal neurons; luteinizing hormone-releasing hormone and vasoactive intestinal peptide were observed in septocortical neurons and calcitonin gene-related peptide, luteinizing hormone-releasing hormone and dynorphin B were observed in septo-bulbar cells. These results show that, in addition to acetylcholine, galanin is a major cellular neuroactive substance in septal projections to the hippocampus, the cingulate cortex and the olfactory bulb. The presence of septal projecting neurons immunoreactive for other peptides shows that a variety of distinct peptides may also participate, but in a smaller number, to septal efferent pathways.

Animals↗
PubMed2004

Involvement of right piriform cortex in olfactory familiarity judgments.

Previous studies have shown activation of right orbitofrontal cortex during judgments of odor familiarity. In the present study, we sought to extend our knowledge about the neural circuits involved in such a task by exploring the involvement of the right prefrontal areas and limbic/primary olfactory structures. Fourteen right-handed male subjects were tested using fMRI with a single functional run of two olfactory conditions (odor detection and familiarity judgments). Each condition included three epochs. During the familiarity condition, subjects rated whether odors were familiar or unfamiliar. During the detection condition, participants decided if odors were present. When contrasting the familiarity with the detection conditions, activated areas were found mainly in the right piriform cortex (PC) and hippocampus, the left inferior frontal gyrus and amygdala, and bilaterally in the mid-fusiform gyrus. Further analyses demonstrated that the right PC was more strongly activated than the left PC. This result supports the notion that the right PC is preferentially involved in judgments of odor familiarity.

Adolescent↗
PubMed2005

Axonal transport of rubidium and thallium in the olfactory nerve of mice.

Following intranasal administration of radioactive (86)Rb(+) and (201)Tl(+) in mice, we observed this direct transport via the olfactory nerve pathway. The (86)RbCl and (201)TlCl solutions were administered to two groups of mice, the unilateral intranasal and intravenous administration groups. After sacrifice, their heads were divided into the right and left side, which were then subdivided into seven parts; the nasal mucosa and brain regions were separated. Following the unilateral intranasal administration, uptake after 6 h by the olfactory bulb was significantly higher on the ipsilateral side ((86)Rb, 0.7 %dose; (201)Tl, 0.5 %dose) than on the contralateral side ((86)Rb, 0.08 %dose; (201)Tl, 0.15 %dose). Moreover, the (86)Rb and (201)Tl that accumulated in the olfactory bulb were gradually transported to other brain regions of the olfactory tract, the telencephalon and the diencephalon on the side corresponding to the nostril used for administration. Significant differences were observed between the right and left side of the brain regions 6 and 12 h after administration. Further, (201)Tl autoradiography clearly showed striped patterns of dense accumulation, localized in the region around the glomerular layer and granule cell layer of the olfactory bulb and around the olfactory cortex. These results provide clear evidence of axonal transport via the olfactory nerve pathway, from nasal cavity to the olfactory bulb, as well as to the olfactory cortex through the synaptic junctions. The olfactory transport of the (86)Rb(+) and (201)Tl(+) is thought to represent the behavior of K(+) in the olfactory system.

Animals↗
PubMed1998

Contributions of anterior perirhinal cortex to olfactory and contextual fear conditioning.

The present experiments examined the effects of excitotoxic lesions of anterior perirhinal cortex (PRH) on the expression of fear conditioned to an explicit olfactory CS and to the context in which CS-US pairing took place. Animals with anterior PRH lesions exhibited an attenuation of fear conditioned to the explicit CS, but no attenuation of fear conditioned to the training context. These data replicate previous findings in our laboratory examining the effects of aspirative lesions of anterior PRH, and are consistent with the notion that this cortical region comprises a critically important component of the neural system mediating the acquisition and/or expression of associations between olfactory cues and footshock.

Analysis of Variance↗
PubMed2003

Physiologic impairment of olfactory stimulus processing in schizophrenia.

BACKGROUND: Behavioral studies of olfaction have demonstrated impairments in the ability to detect and identify odors in patients with schizophrenia. These deficits appear to be independent of either symptom severity or other cognitive impairment. Only limited efforts have been made to investigate the neurophysiologic substrate of these olfactory abnormalities. This article reports the first examination of olfactory electrophysiologic responses in patients with schizophrenia. METHODS: Olfactory event-related potential responses to three different concentrations of hydrogen sulfide were recorded in a sample of 21 patients and 20 healthy control subjects. Odors were presented via an olfactometer to ensure there was no associated trigeminal nerve stimulation. RESULTS: Patients exhibited abnormalities in the amplitudes of the N1 and P2 components of the olfactory evoked potential, and delayed latency of the P2. The N1 abnormality, which denotes primary olfactory cortex activity, was related to impaired odor detection threshold sensitivity; the P2 abnormality was related to impaired odor identification. CONCLUSIONS: These data indicate the presence of a primary physiologic impairment in the olfactory cortex underlying behavioral olfactory deficits seen in patients with schizophrenia. This is consistent with postmortem and in vitro studies suggesting abnormalities in olfactory receptor neurons. Understanding the nature of these physiologic olfactory impairments could offer clues to the basic neuropathology of this disorder.

Adolescent↗
PubMed1991

Hippocampus and olfactory discrimination learning: effects of entorhinal cortex lesions on olfactory learning and memory in a successive-cue, go-no-go task.

Three experiments assessed the effect of entorhinal cortex lesions on olfactory learning and memory using a successive-cue olfactory discrimination paradigm. In contrast to the results of other studies that used a simultaneous-cue paradigm, lesions of the entorhinal cortex facilitated rats' acquisition of individual odor discrimination problems, with no impairment in memory for the individual odors across both short (24-hr) and long (65-day) retention intervals and despite limited training. When considered together with previous observations of facilitation or impairment in learning after damage to the hippocampal system, the present data suggest that the hippocampus is preferentially involved in encoding relations among multiple stimuli. By this account, facilitation of performance is due to an interaction between hippocampal system dysfunction and task conditions that hinder direct comparisons among cues.

Animals↗
PubMed1978

The afferent connections of the main and the accessory olfactory bulb formations in the rat: an experimental HRP-study.

The afferent connections of the main and accessory olfactory bulbs in the rat were examined by injecting horseradish peroxidase (HRP) into one or the other of these structures either by microelectrophoresis or by hydraulic pressure. Alternate sections were stained with newly developed HRP-procedures using either benzidine dihydrochloride (de Olmos and Heimer, '77) or tetramethyl-benzidine. Eighteen to twenty-four hours after unilateral HRP injections confined to the main olfactory bulb, a large number of HRP-labeled perikaria appeared in the following telencephalic structures on the ipsilateral side: All portions of the anterior olfactory nucleus (AON) except its external part, the lateral transitional field (LT) between AON and the paleocortex, the whole extent of the primary olfactory cortex (POC); the medial forebrain bundle area deep to the olfactory tubercle, the nucleus of the horizontal limb of the diagonal band (NHDB) and the nucleus of the lateral olfactory tract (NLOT). A moderate to small number of labeled cells, furthermore, were seen in the dorsal (DT) and medial (MT) transition fields, the ventral praecommissural hippocampus (tt2), the ventral superficial part of the nucleus of the vertical limb of the diagonal band (NVDB), the sublenticular part of the substantia innominata (SI), the anterior amygdaloid area, the posterolateral cortical amygdaloid nucleus (C2) and the transition region (28 L') between the olfactory cortex and the lateral entorhinal area proper. On the contralateral side a large number of labeled cells were found in all parts of the AON, with especially heavy labeling in its external part. A moderate number of labeled cells could also be detected in the lateral transition field (LT) and the NLOT. In the diencephalon and the brain stem a moderate number of HRP-labeled perikaria were observed in the dorsal, perifornical, and lateral hypothalamus, as well as in locus coeruleus and the dorsal and medial raphae nuclei. Following large HRP injections in the main olfactory bulb a moderate to small number of labeled cells were seen also in the posterior and premammillary hypothalamus and in field CA1 of the retrocommissural hippocampus on the ipsilateral side, as well as in POC on the contralateral side. It is possible, however, that the uptake of label took place in an undetected pool of HRP in the very rostal part of AON rather than in the olfactory bulb. HRP injections in the accessory olfactory bulb resulted in labeled neurons in the posterior ventro-lateral part of the bed nucleus of the stria terminalis, the nucleus of the accessory olfactory tract, the rostrodorsal portions of the medial amygdaloid nucleus, and the whole extent of the posteromedial cortical amygdaloid nucleus (C3) on the ipsilateral side. A few lightly labeled cells were seen also in the contralateral C3.

Amygdala↗
PubMed1989

In situ hybridization mapping of glucocorticoid receptor messenger ribonucleic acid in rat brain.

We have mapped the distribution of glucocorticoid receptor (GR) mRNA in the male adult rat brain using T7 RNA polymerase transcripts of a 1155 base pair rat GR cDNA clone comprising the coding region for amino acids 140-525. Strong expression of GR mRNA was found in the neurons of the CA1 and CA2 fields of the hippocampus and in the paraventricular and periventricular hypothalamic nuclei. Moderate to strong hybridization was found in the dorsal thalamic nuclei, layers II and VI of the cerebral cortex, the anterior olfactory nucleus and primary olfactory cortex, the hypothalamic mammillary nuclei, the subthalamus, and the granule and mitral cells of the olfactory bulb. Weak to moderate hybridization was found in many other regions of the tel- and diencephalon. Mes- and rhomboencephalic neurons displayed very low levels of GR mRNA relative to the levels observed in the tel- and diencephalon. In the cerebellum, moderate to strong levels of mRNA were detected in the granule and Purkinje cell layers with very low levels elsewhere. Nonneuronal brain elements, such as glial cells, the pia mater, and the choroid plexus, were found to express low to moderate amounts of GR mRNA. These results confirm and extend mapping studies of steroid receptors in the brain using radiolabeled steroids or monoclonal antibodies against rat liver GR and demonstrate that the relative distribution of GR protein in different brain nuclei reflects differences in GR mRNA levels. The rat GR cDNA clone is also shown to provide suitable probes for mapping GR gene expression in the mouse brain.

Animals↗
PubMed1998

Elucidating dynamic brain interactions with across-subjects correlational analyses of positron emission tomographic data: the functional connectivity of the amygdala and orbitofrontal cortex during olfactory tasks.

Covariance analyses of positron emission tomography (PET) data are used increasingly to elucidate the functional connectivity between brain regions during different cognitive tasks. Functional connectivity may be estimated by examining the covariance between regions over time or across subjects. In functional brain-mapping studies, across-subjects covariance matrices derived from within-task (nonsubtracted) and between-task (subtracted) data characterize different, complementary aspects of functional interactions. The authors study amygdala-orbitofrontal interactions during three task conditions (aversive olfaction, odor detection, and resting with eyes closed) to illustrate the strengths and limitations of across-subjects covariance analyses based on subtracted and nonsubtracted data. This example underscores the dynamic nature of connectivity between the amygdalae and orbitofrontal cortices and highlights the importance of including data from resting conditions in covariance analyses.

Adult↗
PubMed1982

Insula of the old world monkey. II: Afferent cortical input and comments on the claustrum.

The afferent connections of the insula in the rhesus monkey were studied with axonal transport methods. Injections of horseradish peroxidase (HRP) in the insula revealed labeled neurons in the prefrontal cortex, the lateral orbital region, the frontoparietal operculum, the cingulate gyrus and adjacent medial cortex, the prepiriform olfactory cortex, the temporal pole, the cortex of the superior temporal sulcus, the rhinal cortex, the supratemporal plane, and the posterior parietal lobe. Tritiated amino acid (TAA) injections in some of the cortical regions which contained retrogradely labeled neurons confirmed projections to the insula from prefrontal granular cortex, orbital frontal cortex, prepiriform cortex, temporal pole, rhinal cortex, cingulate gyrus, frontal operculum, and parietal cortex. In these studies, cortical areas that projected to the insula also projected to the claustrum. However, the topographic and quantitative relationships between the projections into the insula and those into the claustrum were inconsistent. Moreover, the claustrum has additional connections which it does not share with the insula. A selected review of the literature suggests that the claustrum and insula differ widely also with respect to ontogenesis and functional specialization.

Afferent Pathways↗
PubMed2003

Distribution of bovine herpesvirus type 5 DNA in the central nervous systems of latently, experimentally infected calves.

Bovine herpesvirus type 5 (BHV-5) is an alphaherpesvirus associated with meningoencephalitis, a disease highly prevalent in South America. In this study, we investigated the distribution of BHV-5 DNA in the brains of latently, experimentally infected calves by using a PCR for the glycoprotein B gene. Twelve calves inoculated intranasally with a Brazilian BHV-5 isolate were divided into two groups: group A calves (n = 4) were euthanized 55 days postinoculation (p.i.) for tissue collection; group B calves (n = 8) were submitted to dexamethasone administration at day 60 p.i. for reactivation of latent infection and were euthanized 50 days later. Latent infection was reactivated in all group B calves, as demonstrated by virus isolation from nasal secretions and/or seroconversion. Three calves developed neurological disease and died or were euthanized in extremis. For group A calves, viral DNA was consistently detected in the trigeminal ganglia (4/4), midbrain (4/4), thalamus (4/4), and olfactory cortex (4/4) and less frequently in the pons (3/4), cerebellum (3/4), anterior cerebral cortex (2/4), and olfactory bulb (2/4). For calves previously submitted to reactivation (group B), viral DNA was detected with roughly the same frequency in the same areas as for the group A calves. In addition, viral DNA was detected in the posterior (5/5) and dorso-lateral cortex (3/5). All DNA-positive tissues were negative for infectivity and viral antigens. These results demonstrated that latent BHV-5 DNA is present in several areas of the brain during latent infection and that virus reactivation may result in the establishment of latent infection in additional sites of the brain.

Acute Disease↗
PubMed2000

Expression of NR1, NR2A-D, and NR3 subunits of the NMDA receptor in the cerebral cortex and olfactory bulb of adult rat.

Quantitative reverse transcriptase - polymerase chain reaction was used to analyze the relative expressions of NR1, NR2A, NR2B, NR2C, NR2D, and NR3 subunits of the NMDA receptor in the piriform, entorhinal, visual, and motor cortices as well as in the olfactory bulb of adult rat. The analysis detected clear differences in the relative proportions of the NMDA receptor subunits between the five forebrain regions examined. These differences were particularly striking when the piriform and motor cortices were compared. In the piriform cortex, NR1 was the predominant transcript. The expression of NR2A was only slightly higher than half of that of NR1. NR2B was expressed even at lower levels ( approximately 30% of NR1). NR2C and NR3 were expressed at levels which were approximately 15% of those of NR1. NR2D had the lowest levels of expression ( approximately 3% of NR1). In contrast, NR2B was the predominant transcript in the motor cortical region, where it was expressed at the levels close to 135% of those of NR1 message. NR2A had the levels of expression of approximately 50% of those of NR1. The NR2C expression was close to 25% that of NR1, and the NR2D and NR3 transcripts were totally absent from this cortical area. These findings suggest a significant regional variability of the NMDA receptors in the adult rat forebrain.

Animals↗
PubMed2006

Neural coding by two classes of principal cells in the mouse piriform cortex.

The piriform (or primary olfactory) cortex is a trilaminar structure that is the first cortical destination of olfactory information, receiving monosynaptic input from the olfactory bulb. Here, we show that the main input layer of the piriform cortex, layer II, is dominated by two classes of principal neurons, superficial pyramidal (SP) and semilunar (SL) cells, with strikingly different properties. Action potentials in SP cells are followed by a Ni2+-sensitive afterdepolarization that promotes burst firing, whereas SL cells fire nonbursting action potentials that are followed by a powerful afterhyperpolarization. Synaptic inputs from the olfactory bulb onto SP cells exhibit prominent paired-pulse facilitation, which is attributable to residual presynaptic Ca2+ and a low probability of neurotransmitter release. In contrast, the same inputs onto SL cells do not facilitate. These distinctive synaptic and firing properties cause SP and SL cells to respond differently to in vivo-like bursts of afferent stimulation: SP cells tend to fire bursts of output action potentials at a higher frequency than the input, whereas SL cells tend to fire at a lower frequency than the input. When connected together in the canonical circuit of the piriform cortex, SP and SL cells transform the pattern of synaptic inputs they receive from the olfactory bulb, dispersing the firing rate and latency of output action potentials to an extent that depends on the strength of the input. Thus, the presence of two types of principal cells in layer II of the piriform cortex may underlie coding strategies used for the representation of odors.

Action Potentials↗