Olfactory bulb: Difference between revisions

Olfactory bulb
Olfactory bulb
	Vesalius' Fabrica, 1543. Olfactory Bulbs and Olfactory tracts outlined in red
	Coronal image of mouse main olfactory bulb cell nuclei. Blue - Glomerular layer; Red - External Plexiform and Mitral cell layer; Green - Internal Plexiform and Granule cell layer. Top of image is dorsal aspect, right of image is lateral aspect. Scale, ventral to dorsal, is approximately 2mm.
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System	Olfactory
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Latin	bulbus olfactorius
MeSH	D009830
NeuroNames	279
NeuroLex ID	birnlex_1137
TA98	A14.1.09.429
TA2	5538
FMA	77624
	Anatomical terms of neuroanatomy [edit on Wikidata]

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The olfactory bulb is a structure of the vertebrate forebrain involved in olfaction, the perception of odors.^[1]

Anatomy

In most vertebrates, the olfactory bulb is the most rostral (forward) part of the brain. In humans, however, the olfactory bulb is on the inferior (bottom) side of the brain. The olfactory bulb is supported and protected by the cribriform plate of the ethmoid bone, which in mammals separates it from the olfactory epithelium, and which is perforated by olfactory nerve axons. The bulb is divided into two distinct structures: the main olfactory bulb and the accessory olfactory bulb.

Main olfactory bulb

The main olfactory bulb has a multi-layered cellular architecture. In order from surface to the center the layers are

Glomerular layer
External plexiform layer
Mitral cell layer
Internal plexiform layer
Granule cell layer

The olfactory bulb transmits smell information from the nose to the brain, and is thus necessary for a proper sense of smell. As a neural circuit, the glomerular layer receives direct input from olfactory nerves, made up of the axons from approximately ten million olfactory receptor neurons in the olfactory mucosa, a region of the nasal cavity. The ends of the axons cluster in spherical structures known as glomeruli such that each glomerulus receives input primarily from olfactory receptor neurons that express the same olfactory receptor.The glomeruli layer of the olfactory bulb is the first level of synaptic processing.^[2] The glomeruli layer represents a spatial odor map organized by chemical structure of odorants like functional group and carbon chain length. This spatial map is divided into zones and clusters, which represent similar glomeruli and therefore similar odors. One cluster in particular is associated with rank, spoiled smells which are represented by certain chemical characteristics. This classification may be evolutionary to help identify food that is no longer good to eat. The spatial map of the glomeruli layer may be used for perception of odor in the olfactory cortex. ^[3] The next level of synaptic processing in the olfactory bulb occurs in the external plexiform layer, between the glomerular layer and the mitral cell layer. The external plexiform layer contains astrocytes, interneurons and some mitral cells. It does not contain many cell bodies, rather mostly dendrites of mitral cells and GABAergic granule cells.^[4] are also permeated by dendrites from neurons called mitral cells, which in turn output to the olfactory cortex. Numerous interneuron types exist in the olfactory bulb including periglomerular cells which synapse within and between glomeruli, and granule cells which synapse with mitral cells. The granule cell layer is the deepest layer in the olfactory bulb. It is made up of dendrodendritic granule cells that synapse to the mitral cell layer.^[5]

Function

As a neural circuit, the olfactory bulb has one source of sensory input (axons from olfactory receptor neurons of the olfactory epithelium), and one output (mitral cell axons). As a result, it is generally assumed that it functions as a filter, as opposed to an associative circuit that has many inputs and many outputs. However, the olfactory bulb also receives "top-down" information from such brain areas as the amygdala, neocortex, hippocampus, locus coeruleus, and substantia nigra. With this in mind, its potential functions can be placed into four non-exclusive categories:

discriminating among odors
enhancing sensitivity of odor detection
filtering out many background odors to enhance the transmission of a few select odors
permitting higher brain areas involved in arousal and attention to modify the detection or the discrimination of odors

While all of these functions could theoretically arise from the olfactory bulb's circuit layout, it is unclear which, if any, of these functions are performed exclusively by the olfactory bulb. By analogy to similar parts of the brain such as the retina, many researchers have focused on how the olfactory bulb filters incoming information from receptor neurons in space, or how it filters incoming information in time. At the core of these proposed filters are the two classes of interneurons; the periglomerular cells, and the granule cells. Processing occurs at each level of the main olfactory bulb, beginning with the spatial maps that categorize odors in the glomeruli layer.^[3]

Interneurons in the external plexiform layer are responsive to pre-synaptic action potentials and exhibit both excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Neural firing varies temporally, there are periods of fast, spontaneous firing and slow modulation of firing. These patterns may be related to sniffing or change in intensity and concentration of odorant.^[4] Temporal patterns may have effect in later processing of spatial awareness of odorant. The interneurons in the external plexiform layer perform feedback inhibition on the mitral cells to control back propagation. They also participate in lateral inhibition of the mitral cells. This inhibition is an important part of olfaction as it aids in odor discrimination by decreasing firing in response to background odors and differentiating the responses of olfactory nerve inputs in the mitral cell layer.^[2] Inhibition of the mitral cell layer by the other layers contributes to odor discrimination and higher level processing by modulating the output from the olfactory bulb. These hyperpolarizations during odor stimulation shape the responses of the mitral cells to make them more specific to an odor.^[5]

Currently there is a lack of information regarding the function of the internal plexiform layer which lies between the mitral cell layer and the granule cell layer.

The basal dendrites of mitral cells are connected to interneurons known as granule cells, which by some theories produce lateral inhibition between mitral cells. The synapse between mitral and granule cells is of a rare class of synapses that are "dendro-dendritic" which means that both sides of the synapse are dendrites that release neurotransmitter. In this specific case, mitral cells release the excitatory neurotransmitter glutamate, and granule cells release the inhibitory neurotransmitter Gamma-aminobutyric acid (GABA). As a result of its bi-directionality, the dendro-dendritic synapse can cause mitral cells to inhibit themselves (auto-inhibition), as well as neighboring mitral cells (lateral inhibition). More specifically, the granule cell layer receives excitatory glutamate signals from the basal dendrites of the mitral and tufted cells. The granule cell in turn releases GABA to cause an inhibitory effect on the mitral cell. More neurotransmitter is released from the activated mitral cell to the connected dendrite of the granule cell, making the inhibitory effect from the granule cell to the activated mitral cell stronger than the surrounding mitral cells.^[5] It is not clear what the functional role of lateral inhibition would be, though it may be involved in boosting the signal-to-noise ratio of odor signals by silencing the basal firing rate of surrounding non-activated neurons. This in turn aids in odor discrimination.^[2] Other research suggest that the lateral inhibition contributes to differentiated odor responses, which aids in the processing and perception of distinct odors.^[5] There is also evidence of cholinergic effects on granule cells that enhance depolarization of granule cells making them more excitable which in turn increases inhibition of mitral cells. This may contribute to a more specific output from the olfactory bulb that would closer resemble the glomerular odor map.^[6]

Olfaction is distinct from the other sensory systems where peripheral sensory receptors have a relay in the diencephalon. Therefore the olfactory bulb plays this role for the olfactory system.

Accessory olfactory bulb

The accessory olfactory bulb, which resides on the dorsal-posterior region of the main olfactory bulb, forms a parallel pathway independent from the main olfactory bulb. The vomernasal organ sends projections to the accessory olfactory bulb ^[7] making it the second processing stage of the accessory olfactory system. As in the main olfactory bulb, axonal input to the accessory olfactory bulb forms synapses with mitral cells within glomeruli. The accessory olfactory bulb receives axonal input from the vomeronasal organ, a distinct sensory epithelium from the main olfactory epithelium that detects pheromones, among other chemical stimuli. In order for the vomernasal pump to turn on the main olfactory epithelium must first detect the appropriate odor.^[8] The vomernasal organ then send axonal projections to the accessory olfactory bulb. The accessory olfactory bulb provides direct excitatory inputs to the principle neurons called mitral cells ^[9] which are transmitted to the amygdala and hypothalamus,which are directly involved in sex hormone activity and may influence aggressive and mating behavior.^[10] Axons of the vomeronasal sensory neurons express a given receptor type which diverge between 6 and 30 glomeruli in the accessory olfactory bulb. Mitral cell dendritic endings go through a dramatic period of targeting and clustering just after presynaptic unification of the sensory neuron axons. The vomernasal sensory neurons to mi- tral cell connectivity is precise, with mitral cell dendrites targeting glomeruli.^[9] The olfactory bulb also helps humans sense when danger is near by. There is evidence against the presence of a functional accessory olfactory bulb in humans and other higher primates.^[11]

The areas of the brain related to olfactory processing is much larger in rodents than in humans. This means that animal olfactory systems for example rodents are much stronger than those of humans. The accessory olfactory bulb is good at detecting single pheromones or pheromonal blends within a complex chemical background such as body odor because the vomernasal receptor neurons are narrowly tuned. This system is extremely important for animals because the detection of pheromones helps in the mating process as well as the recognition of individuality. Although the accessory olfactory bulb participates in individual descrimination its' chemosignal detection is unknown.^[12]

Further Olfactory Processing

The olfactory bulb sends olfactory information to be further processed in the amygdala, the olfactory cortex (OFC) and the hippocampus where it plays a role in emotion, memory and learning. The main olfactory bulb connects to the amygdala via the piriform cortex of the primary olfactory cortex and directly projects from the main olfactory bulb to specific amygdala areas.^[13] The amygdala passes olfactory information on to the hippocampus. The olfactory cortex, amygdala, hippocampus, thalamus, and olfactory bulb have many interconnections directly and indirectly through the cortices of the primary olfactory cortex. These connections are indicative of the association between the olfactory bulb and higher areas of processing, specifically those related to emotion and memory.^[13]

Amygdala

Associative learning takes place in the amygdala takes place between odors and behavioral responses. The odors serve as the reinforcers or the punishers during the associative learning process; odors that occur with positive states reinforce the behavior that resulted in the positive state while odors that occur with negative states do the opposite. Odor cues are coded by neurons in the amygdala with the behavioral effect or emotion that they produce. In this way odors reflect certain emotions or physiological states.^[14] Odors become associated with pleasant and unpleasant responses, and eventually the odor becomes a cue and can cause an emotional response. These odor associations contribute to emotional states such as fear. Brain imaging shows amygdala activation correlated with pleasant and unpleasant odors, reflecting the association between odors and emotions.^[14]

Hippocampus

The hippocampus aids in olfactory memory and learning as well. Several olfaction-memory processes occur in the hippocampus. Similar to the process in the amygdala, an odor is associated with a particular reward, i.e. the smell of food with receiving sustenance.^[15] Odor in the hippocampus also contributes to the formation of episodic memory; the memories of events at a specific place or time. The time at which certain neurons fire in the hippocampus is associated by neurons with a stimulus such as an odor. Presentation of the odor at a different time may cause recall of the memory, therefore odor aids in recall of episodic memories.^[15]

Olfactory Bulb and Depression Models

Further evidence of the link between the olfactory bulb and emotion and memory is shown through animal depression models. Olfactory bulb removal in rats effectively causes structural changes in the amygdala and hippocampus and behavioral changes similar to that of a person with depression. Researchers use rats with olfactory bulbectomies to research antidepressants.^[16] Research has shown that removal of the olfactory bulb in rats leads to dendrite reorganization, disrupted cell growth in the hippocampus, and decreased neuroplasticity in the hippocampus. These hippocampal changes due to olfactory bulb removal are associated with behavioral changes characteristic of depression, demonstrating the correlation between the olfactory bulb and emotion.^[17] The hippocampus and amygdala effect odor perception. During certain physiological states such as hunger a food odor may seem more pleasant and rewarding due to the associations in the amygdala and hippocampus of the food odor stimulus with the reward of eating.^[14]

The Olfactory Cortex

The OFC contributes to this odor-reward association as well as it evaluates the value of a reward, i.e. the nutritional value of a food. The OFC also associates odors with other stimuli, such as taste.^[14] Odor perception and discrimination also involve the olfactory cortex. The spatial odor map in the glomeruli layer of the olfactory bulb may contribute to these functions. The odor map begins processing of olfactory information by spatially organizing the glomeruli. This organizing aids the olfactory cortex in it's functions of perceiving and discriminating odors.^[3]

Adult Neurogenesis

The olfactory bulb is one of only two structures in the adult brain that undergoes neuronal replacement. In most mammals, new neurons are born from neural stem cells in the sub-ventricular zone and migrate rostrally towards the core of the olfactory bulb^[18] . Within the olfactory bulb these immature neuroblasts develop into fully functional granule cell interneurons and periglomerular cell interneurons that reside in the granule cell layer and glomerular layers, respectively. In addition, the olfactory sensory neuron axons that form synapses in olfactory bulb glomeruli are also capable of regeneration following regrowth of an olfactory sensory neuron residing in the olfactory epithelium. Despite dynamic turnover of sensory axons and interneurons, the projection neurons (mitral and tufted neurons) that form synapses with these axons are not structurally plastic.

The function of adult neurogenesis in this region remains a matter or study. The survival of immature neurons as they enter the circuit is highly snesitive to olfactory activity and in particular associative learning tasks. This has led to the hypothesis that new neurons participate in learning processes^[19]. However, no definitive behavioral effect has been observed in loss-of-function experiments suggesting that the function of this process, if at all related to olfactory processing, may be subtile.

Olfactory Dysfunctions

Olfactory problems can be divided into different types based on their malfunction. The olfactory dysfunction can be total called anosmia, incomplete like partial anosmia, hyposmia, or microsmia, distorted such as dysosmias, and spontaneous sensations like phantosmias. The inability to recognize odors can occur independently of a normally function olfactory system called olfactory agnosia. The rare condition of abnormally acute smell function is called hyperosmia. Like vision and hearing, the olfactory problems can be bilateral or unilateral meaning if a person has anosmia on the right side of the nose but not the left, it is a unilateral right anosmia. On the other hand, if it is on both sides of the nose it is called bilateral anosmia or total anosmia.^[20]

Causes of Olfactory Dysfunction

There are 5 more common causes of olfactory dysfunction: Age, Viral Infections, Exposure to Toxic Chemicals, Head Truama, and Neurodegenerative diseases.^[20]

Age

Age is the strongest reason for olfactory decline in healthy adults having more impact than cigarette smoking. Age-related changes in smell function often go unnoticed and small ability is rarely tested clinically unlike hearing and vision. 2% of people under 65 years of age have chronic smelling problems. This increases greatly between people of ages 65 and 80 with about half experiencing significant problems smelling. Then for adults over 80, the numbers rise to almost 75%.^[21] The basis for age-related changes in smell function include closure of the cribriform plate,^[20] and cumulative damage to the olfactory receptors from repeated viral and other insults throughout life.

Viral Infections

The most common cause of permanent hyposmia and anosmia is upper respiratory infections. Such dysfunctions, show no change over time and can sometimes reflect damage not only in the olfactory epithelium but also to the central olfactory structures as a resutl of viral invasions into the brain. Among these virus-related disorder are the common cold, hepatitis, flu-lie infections, and herpes. Most viral infections are unrecognizable because they are so mild or entirely asymptomatic.^[20]

Exposure to Toxic Chemicals

Chronic exposure to some airborne toxins such as heribicides, pesticides, solents, and heavy metals (cadmium, chromium, nickel, and manganese), can alter the ability to smell.^[22] These agents not only damage the olfactory epithelium but they are likely to enter the brain via the olfactory mucosa.^[23]

Head Trauma

Trauma-related olfactory dysfunction depends on the severity of the trauma and whether strong acceleration/deceleration of the head occurred. Occipital and side impact causes more damage to the olfactory system than frontal impact.^[24]

Neurodegenerative Diseases

Neurologists have observed that olfactory dysfunction is a cardinal feature of several neurodegenerative diseases such as Alzheimer's Disease and Parkinson's Disease. Most f these patients are unaware of an olfactory deficit until after testing where 85% to 90% of early-stage patients showed decrease activity in central odor processing structures.^[25]

Other neurodegenerative diseases that affect olfactory dysfunction include Huntington's disease, multiinfract dementia, amyotrophic lateral sclerosis, and schizophrenia. These diseases more moderately affect the smelling system than Alzheimer's disease and Parkinson's disease.^[26] Furthermore, progressive supranculear palsy and parkinsonism are associated with only minor olfactory problems. These findings have led to the suggestion that olfactory testing may help in the diagnosis of several different neurodegenerative diseases.^[27]

Neurodegenerative diseases with well-established genetic determinants are also associated with olfactory dysfunction. Such dysfunction, for example, is found in patients with familial Parkinson's disease and those with Down syndrome.^[28] But further studies have concludedd that olfactory loss may be associated with retardation, rather than Alzheimer's disease like pathology.^[29]

Huntington's disease is also associated with problems in odor identification, detection, discrimination, and memory. The problem is prevalent once the phenotypic elements of the disorder appear, although it is unknown how far in advance the olfactory loss precedes the phenotypic expression.^[20]

Evolution

Comparing the structure of the olfactory bulb among vertebrate species, such as the leopard frog and the lab mouse, reveals that they all share the same fundamental layout (five layers containing the nuclei of three major cell types; see "Anatomy" for details), despite being dissimilar in shape and size. Of note, a similar structure is shared by the analogous olfactory center in the fruit fly Drosophila melanogaster, the antennal lobe. One possibility is that vertebrate olfactory bulb and insect antennal lobe structure may be similar because they contain an optimal solution to a computational problem experienced by all olfactory systems and thus may have evolved independently in different phyla - a phenomenon generally known as convergent evolution.

"The increase of brain size relative to body size—encephalization—is intimately linked with human evolution. However, two genetically different evolutionary lineages, Neanderthals and modern humans, have produced similarly large-brained human species. Thus, understanding human brain evolution should include research into specific cerebral reorganization, possibly reflected by brain shape changes. Here we exploit developmental integration between the brain and its underlying skeletal base to test hypotheses about brain evolution in Homo. Three-dimensional geometric morphometric analyses of endobasicranial shape reveal previously undocumented details of evolutionary changes in Homo sapiens. Larger olfactory bulbs, relatively wider orbitofrontal cortex, relatively increased and forward projecting temporal lobe poles appear unique to modern humans. Such brain reorganization, beside physical consequences for overall skull shape, might have contributed to the evolution of H. sapiens' learning and social capacities, in which higher olfactory functions and its cognitive, neurological behavioral implications could have been hitherto underestimated factors."^[30]

References

^ "olfactory bulb". Retrieved 2009-11-20.
^ ^a ^b ^c Hamilton, K.A. ;Heinbockel, T.; Ennis, M.; Szabó, G.; Erdélyi, F.; Hayar, A. Properties of external plexiform layer interneurons in mouse olfactory bulb slices. Neuroscience, 2005 January, 133.3, pp 819–829. doi=10.1016/j.neuroscience.2005.03.008
^ ^a ^b ^c Mori, K; Takahashi, YK; Igarashi, KM; Yamaguchi, M. Maps of odorant molecular features in the Mammalian olfactory bulb.Physiological reviews, 2006 Apr, 86.2, pp 409-433. pmid=16601265
^ ^a ^b Spors, H.; Albeanu, D. F.; Murthy, V. N.; Rinberg, D.; Uchida, N.; Wachowiak, M.; Friedrich, R. W. Illuminating Vertebrate Olfactory Processing. Journal of Neuroscience, 10 October 2012, 32.41, pp 14102–14108a. doi=10.1523/JNEUROSCI.3328-12.2012
^ ^a ^b ^c ^d Scott, JW; Wellis, DP; Riggott, MJ; Buonviso, N. Functional organization of the main olfactory bulb. Microscopy research and technique, 1993 Feb 1, 24.2, pp 142-56.pmid=8457726
^ Pressler, R. T. (10 October 2007). "Muscarinic Receptor Activation Modulates Granule Cell Excitability and Potentiates Inhibition onto Mitral Cells in the Rat Olfactory Bulb". Journal of Neuroscience. 27 (41): 10969–10981. doi:10.1523/JNEUROSCI.2961-07.2007. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); zero width space character in |doi= at position 9 (help)
^ Taniguchi, K (2011 Feb). "Phylogenic outline of the olfactory system in vertebrates". The Journal of veterinary medical science / the Japanese Society of Veterinary Science. 73 (2): 139–47. PMID 20877153. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ Slotnick, Burton (2010). "Accessory olfactory bulb function is modulated by input from the main olfactory epithelium". European Journal of Neuroscience. 31 (6): 1108–1116. doi:10.1111/j.1460-9568.2010.07141.x. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
^ ^a ^b Hovis, Kenneth R. (6). "Activity Regulates Functional Connectivity from the Vomeronasal Organ to the Accessory Olfactory Bulb" (PDF). The Journal of Neuroscience. 32 (23): 7907–7916. Retrieved 10 November 2013. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
^ Trotier, D (2011). "Vomeronasal organ and human pheromones". European Annals of Otorhinolaryngology, Head and Neck Diseases. 128 (4): 184–190. Retrieved 10 November 2013. {{cite journal}}: Unknown parameter |month= ignored (help)
^ "Pheromonal communication in vertebrates". Nature. 444: 308–315. 2006. doi:10.1038/nature05404. PMID 17108955. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ Restrpo, Diego (September). "Emerging views on the distinct but related roles of the main and accessory olfactory systems in responsiveness to chemosensory signals in mice". Hormones and Behavior. 46 (3): 247–256. Retrieved 10 November 2013. {{cite journal}}: Check date values in: |year= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: year (link)
^ ^a ^b Royet, Jean-Pierre, Jane Plailly. Lateralization of Olfactory Processes Chemical Senses, 2004, 29.8, pp 731-745. http://chemse.oxfordjournals.org/content/29/8/731.full.pdf+html
^ ^a ^b ^c ^d Kadohisa, M. Effects of odor on emotion, with implications. Frontiers in systems neuroscience, 2013 Oct, 7, pp 66 pmid=24124415
^ ^a ^b Rolls, Edmund. A computational theory of episodic memory formation in the hippocampus. Behavioral Brain Research, 2010 December, 215.2, pp 180-196 url=http://www.sciencedirect.com/science/article/pii/S0166432810002135
^ Song, Cai (2005). "The olfactory bulbectomised rat as a model of depression". Neuroscience & Biobehavioral Reviews. 29 (4–5): 627–647. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ Morales-Medina, J.C (16). "Impaired structural hippocampal plasticity is associated with emotional and memory deficits in the olfactory bulbectomized rat". Neuroscience. 236: 233–243. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
^ Lazarini, Francoise (2011). "Is adult neurogenesis essential for olfaction?". Trends Neurosci. 34 (1): 20. PMID 20980064. {{cite journal}}: More than one of |pages= and |page= specified (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
^ Lepousez, Gabriel (2013). "The impact of adult neurogenesis on olfactory bulb circuits and computations". Annual Reviews of Physiology. 75: 339. PMID 23190074. {{cite journal}}: More than one of |pages= and |page= specified (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ ^a ^b ^c ^d ^e Doty, Richard (12 February 2009). "The Olfactory System and Its Disorders". Seminars in Neurology. 29 (01): 074–081. doi:10.1055/s-0028-1124025.
^ Doty, Richard L. (1984). "Development of the university of pennsylvania smell identification test: A standardized microencapsulated test of olfactory function". Physiology & Behavior. 32 (3): 489–502. doi:10.1016/0031-9384(84)90269-5. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
^ Doty, RL (2001). "Neurotoxic exposure and olfactory impairment". Clin Occupat Environ Med. 1: 547–575. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ Tjalve, H (1996; 79(6): 347-356). "Uptake of manganese and cadmium from the nasal mucosa into the central nervous system via olfactory pathways in rats". Pharmacol Toxicol. 79 (6): 347–356. {{cite journal}}: Check date values in: |year= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: year (link)
^ Doty, RL (1997). "Olfactory dysfunction in patients with head trauma". Arch Neurol. 54 (9): 1131–1140. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ Quinn, N P (1 January 1987). "Olfactory threshold in Parkinson's disease". Journal of Neurology, Neurosurgery & Psychiatry. 50 (1): 88–89. doi:10.1136/jnnp.50.1.88. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ Doty, Richard L. (1995). "Olfactory Testing as an Aid in the Diagnosis of Parkinson's Disease: Development of Optimal Discrimination Criteria". Neurodegeneration. 4 (1): 93–97. doi:10.1006/neur.1995.0011. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
^ Doty, R. L. (1 May 1993). "Olfactory testing differentiates between progressive supranuclear palsy and idiopathic Parkinson's disease". Neurology. 43 (5): 962–962. doi:10.1212/WNL.43.5.962. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ CHEN, M (2006). "Nasal health in Down syndrome: A cross-sectional study". Otolaryngology - Head and Neck Surgery. 134 (5): 741–745. doi:10.1016/j.otohns.2005.12.035. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
^ McKeown, D A (1 October 1996). "Olfactory function in young adolescents with Down's syndrome". Journal of Neurology, Neurosurgery & Psychiatry. 61 (4): 412–414. doi:10.1136/jnnp.61.4.412. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
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Shepherd, G. The Synaptic Organization of the Brain, Oxford University Press, 5th edition (November, 2003). ISBN 0-19-515956-X
Halpern, M; Martínez-Marcos, A (2003). "Structure and function of the vomeronasal system: An update". Progress in neurobiology. 70 (3): 245–318. doi:10.1016/S0301-0082(03)00103-5. PMID 12951145.
Ache, BW; Young, JM (2005). "Olfaction: Diverse species, conserved principles". Neuron. 48 (3): 417–30. doi:10.1016/j.neuron.2005.10.022. PMID 16269360.

Additional images

Base of brain.
Plan of olfactory neurons.
The pterygopalatine ganglion and its branches.
Human brainstem anterior view
Olfactory nerve
Nose diagram
Schema of the Early Olfactory System
Progression of spatial representations for odorant molecular length and carbon number]]
Olfactory bulb
Cerebrum. Optic and olfactory nerves.Inferior view. Deep dissection.
Cerebrum.Inferior view. Deep dissection.
Cerebrum. Inferior view.Deep dissection

External links

[urlolfactory_bulb-1] "olfactory bulb". Retrieved 2009-11-20.

[Hamilton2005-2] Hamilton, K.A. ;Heinbockel, T.; Ennis, M.; Szabó, G.; Erdélyi, F.; Hayar, A. Properties of external plexiform layer interneurons in mouse olfactory bulb slices. Neuroscience, 2005 January, 133.3, pp 819–829. doi=10.1016/j.neuroscience.2005.03.008

[Mori2006-3] Mori, K; Takahashi, YK; Igarashi, KM; Yamaguchi, M. Maps of odorant molecular features in the Mammalian olfactory bulb.Physiological reviews, 2006 Apr, 86.2, pp 409-433. pmid=16601265

[Spors2012-4] Spors, H.; Albeanu, D. F.; Murthy, V. N.; Rinberg, D.; Uchida, N.; Wachowiak, M.; Friedrich, R. W. Illuminating Vertebrate Olfactory Processing. Journal of Neuroscience, 10 October 2012, 32.41, pp 14102–14108a. doi=10.1523/JNEUROSCI.3328-12.2012

[Scott1993-5] Scott, JW; Wellis, DP; Riggott, MJ; Buonviso, N. Functional organization of the main olfactory bulb. Microscopy research and technique, 1993 Feb 1, 24.2, pp 142-56.pmid=8457726

[6] Pressler, R. T. (10 October 2007). "Muscarinic Receptor Activation Modulates Granule Cell Excitability and Potentiates Inhibition onto Mitral Cells in the Rat Olfactory Bulb". Journal of Neuroscience. 27 (41): 10969–10981. doi:10.1523/JNEUROSCI.2961-07.2007. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); zero width space character in |doi= at position 9 (help)

[7] Taniguchi, K (2011 Feb). "Phylogenic outline of the olfactory system in vertebrates". The Journal of veterinary medical science / the Japanese Society of Veterinary Science. 73 (2): 139–47. PMID 20877153. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)

[8] Slotnick, Burton (2010). "Accessory olfactory bulb function is modulated by input from the main olfactory epithelium". European Journal of Neuroscience. 31 (6): 1108–1116. doi:10.1111/j.1460-9568.2010.07141.x. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

[Hovis2012-9] Hovis, Kenneth R. (6). "Activity Regulates Functional Connectivity from the Vomeronasal Organ to the Accessory Olfactory Bulb" (PDF). The Journal of Neuroscience. 32 (23): 7907–7916. Retrieved 10 November 2013. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

[10] Trotier, D (2011). "Vomeronasal organ and human pheromones". European Annals of Otorhinolaryngology, Head and Neck Diseases. 128 (4): 184–190. Retrieved 10 November 2013. {{cite journal}}: Unknown parameter |month= ignored (help)

[Pheromonal_communication_in_vertebrates-11] "Pheromonal communication in vertebrates". Nature. 444: 308–315. 2006. doi:10.1038/nature05404. PMID 17108955. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)

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 ==Adult Neurogenesis==
-The olfactory bulb is one of only two structures in the adult brain that undergoes neuronal replacement.  In most mammals, new neurons are born from neural stem cells in the sub-ventricular zone and migrate rostrally towards the core of the olfactory bulb.  Within the olfactory bulb these immature neuroblasts develop into fully functional granule cell interneurons and periglomerular cell interneurons.  In addition, the olfactory sensory neuron axons that form synapses in olfactory bulb glomeruli are also capable of regeneration, as are the olfactory sensory neurons that reside in the olfactory epithelium.  Despite dynamic turnover of sensory axons and interneurons, the projection neurons (mitral and tufted neurons) of the olfactory bulb are structurally non-plastic.
+The olfactory bulb is one of only two structures in the adult brain that undergoes neuronal replacement.  In most mammals, new neurons are born from neural stem cells in the sub-ventricular zone and migrate rostrally towards the core of the olfactory bulb<ref>{{cite journal|last=Lazarini|first=Francoise|coauthors=1|title=Is adult neurogenesis essential for olfaction?|journal=Trends Neurosci.|year=2011|month=January|volume=34|issue=1|page=20|pages=30|pmid=20980064}}</ref> .  Within the olfactory bulb these immature neuroblasts develop into fully functional granule cell interneurons and periglomerular cell interneurons that reside in the granule cell layer and glomerular layers, respectively.  In addition, the olfactory sensory neuron axons that form synapses in olfactory bulb glomeruli are also capable of regeneration following regrowth of an olfactory sensory neuron residing in the olfactory epithelium.  Despite dynamic turnover of sensory axons and interneurons, the projection neurons (mitral and tufted neurons) that form synapses with these axons are not structurally plastic.
+The function of adult neurogenesis in this region remains a matter or study.  The survival of immature neurons as they enter the circuit is highly snesitive to olfactory activity and in particular associative learning tasks.  This has led to the hypothesis that new neurons participate in learning processes<ref>{{cite journal|last=Lepousez|first=Gabriel|coauthors=2|title=The impact of adult neurogenesis on olfactory bulb circuits and computations.|journal=Annual Reviews of Physiology|year=2013|volume=75|page=339|pages=363|pmid=23190074}}</ref>.  However, no definitive behavioral effect has been observed in loss-of-function experiments suggesting that the function of this process, if at all related to olfactory processing, may be subtile.
 ==Olfactory Dysfunctions==