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PubMed2002

GABAergic mechanisms of heroin-induced brain activation assessed with functional MRI.

Heroin has been hypothesized to activate opiate receptors and inhibit gamma-aminobutyric acid (GABA) release from inhibitory GABAergic interneurons which, in turn, activates dopamine projection cells. Since the distal sites and consequences of this disinhibition are not well understood on a systems level, heroin-induced brain activity was measured using functional MRI (fMRI) in rats. A significant blood oxygen level-dependent (BOLD) signal increase was seen in cortical regions, including prefrontal cortex, cingulate, and olfactory cortex following acute heroin administration. In contrast, a significant signal decrease was seen in several subcortical areas, including the caudate and putamen, nucleus accumbens, thalamus, and hypothalamus. Pretreatment of gamma-vinyl GABA (GVG), an irreversible GABA transaminase inhibitor, significantly attenuated the heroin-induced BOLD signal changes. Pretreatment of naloxone, an opiate mu receptor antagonist, eliminated the heroin-induced BOLD signal changes and posttreatment of naloxone reversed the heroin-induced BOLD signal changes. It is suggested that the heroin-induced negative and positive BOLD changes are due to direct inhibitory and indirect disinhibitory mechanisms of GABAergic activities. Administration of GVG altered these mechanisms and further suggested that involvement of the opiate's pharmacological actions can, at least in part, be mediated by inhibiting brain GABA release.

Analgesics, Opioid↗
PubMed2004

Opiate tolerance by heroin self-administration: an fMRI study in rat.

Functional MRI (fMRI) was employed to determine whether repeated heroin self-administration (SA) produces tolerance or sensitization in the brain of heroin-SA rats. Twelve rats were evenly divided into saline and heroin (0.06 mg/kg, 4 hr/day) SA groups. There was a progressive increase in drug-SA behavior and daily heroin intake during the 8-9 days of heroin-SA training. Within 24 hr after the last session of daily SA, acute heroin (0.1 mg/kg) administration induced regional blood oxygen level-dependent (BOLD) signals in both groups of rats. The positive BOLD signals appeared mainly in the cortical regions, including the prefrontal cortex, cingulate, and olfactory cortex, while the negative BOLD signals were predominantly located in subcortical regions such as caudate and putamen, nucleus accumbens, thalamus, and hypothalamus. However, the number of activated voxels or BOLD-signal intensity was significantly less in heroin-SA rat in regions of prefrontal cortex, nucleus accumbens, and thalamus, etc., compared to the changes in the saline control rats. Application of gamma-vinyl GABA (100 mg/kg), an irreversible GABA-transaminase inhibitor, failed to block opiate actions in the heroin-SA rats. Together, these data suggest that repeated heroin-SA produces tolerance or desensitization of opiate actions in the rat brain, which may in turn potentiate drug SA behavior and drug intake.

Animals↗
PubMed1984

Relationship between drug-induced increases of GABA levels in discrete brain areas and different pharmacological effects in rats.

Following the administration of two gamma-aminobutyric acid-(GABA) elevating drugs, namely aminooxyacetic acid (AOAA) and valproic acid (VPA), in rats, the relationship between the magnitude and the time course of increases in GABA levels of 11 brain regions and a number of pharmacological effects was studied. AOAA (30 mg/kg i.p.) caused significant GABA increases in all brain areas but the degree and time course of these increases showed considerable variation from region to region. The most marked effects were seen in the olfactory bulb, frontal cortex and hippocampus, in which maximum GABA elevations of 100-200% were reached 4-6 hr after AOAA injection. In all the other regions studied (corpus striatum, thalamus, hypothalamus, superior and inferior colliculus, substantia nigra, pons, medulla, cerebellum), increases in GABA were less marked and, at least in part, maximum increases (30-60% over control) were already reached by 1-2 hr. In contrast to AOAA, VPA (200 mg/kg i.p.) produced significant increases in GABA levels only in the cortex, olfactory bulb, corpus striatum, hypothalamus and cerebellum, maximum effects (15-35%) being already reached 5-30 min after VPA administration. As regards pharmacological effects, AOAA caused marked hypothermia, which was maximal by 1 hr and could be reversed by increasing ambient temperature, whereas effects of VPA on body temperature were only moderate. On the other hand, both drugs exerted an almost equal, pronounced antinociceptive effect in the hot plate test. Anticonvulsant efficacy was evaluated in three seizure models, namely the maximal (tonic extension) electroconvulsive threshold, and seizures induced by pentylenetetrazol and 3-mercaptopropionic acid. Anticonvulsant effects of AOAA against electroshock and pentylenetetrazol could only be determined 1 hr after injection, at which time AOAA was inactive against 3-mercaptopropionic acid-induced seizures. VPA proved to be clearly superior to AOAA in both anticonvulsant potency and duration of action. The marked differences in functional effects between VPA and AOAA could not be related to their differential effects on GABA levels in discrete brain regions. The data thus suggest that measurement of total GABA in brain regions without consideration of the compartmentalization of the neurotransmitter is only of limited value to use in an attempt to correlate elevation of GABA levels and pharmacological effects.

Aminooxyacetic Acid↗
PubMed1977

The effects of neonatal androgenization on the in vivo transport of alpha-aminoisobutyric acid into specific regions of the rat brain.

The purpose of the present study was to determine if the administration of testosterone propionate (TP) to neonatal rats is followed in vivo by alterations in the transport of the non-metabolizable amino acid, alpha-aminoisobutyric acid (AIB), into specific regions of the brain. Forty-eigh hours after birth, male and female rats were injected s.c. with either 1,25 mg TP or an equivalent volume of vehicle. Five, 10 and 17 days after birth, control and TP-treated rats were decapitated at intervals of 2, 5, 60 and 300 min after the i.p. injection of 0.25 muCi [1-14C]alpha-aminoisobutyric acid/g body weight. Twelve brain regions, i.e., amygdala, cerebellum, corpora quadrigemina, frontal cortex, hypothalamus, medulla, occipital cortex, olfactory bulbs, olfactory tubercles, parietal cortex, pons, pyriform cortex and samples of serum were analyzed in terms of disint./min/mg tissue and as tissue/serum (T/S) ratios. At the end of 300 min there was a significant increase in the active transport of AIB in all brain regions of the 5-days-old TP-treated rats. Similarly, by 300 min, the active transport of AIB was significantly increased in all brain regions sxcept cerebellum and pons of the 10-day-old TP-treated rats. The administration of TP to neonatal rats did not alter the accumulation and/or active transport of AIB in brain regions of the 17-day-old rat at any of the tested intervals. These data indicate that (1) neonatally administered TP enhanced (either directly or indirectly) the transport and/or accumuation of AIB in specific brain regions of 5- and 10-day-old rats and (2) the effectiveness of the steroid decreased with the age of the rat.

Aminoisobutyric Acids↗
PubMed1995

Distribution of mRNA encoding the inwardly rectifying K+ channel, BIR1 in rat tissues.

The distribution of mRNA encoding the inwardly rectifying K+ channel, BIR1 [1] was investigated in rat tissues, and a comparison made with the expression of related genes rcKATP and GIRK1 using the reverse transcription-polymerase chain reaction (RT-PCR). This showed BIR1 to be expressed in all areas of the brain examined, in the eye but not in any other peripheral tissue. This pattern was distinct from rcKATP and GIRK1. Additional in situ hybridisation studies of the central expression of BIR1 demonstrated high levels of BIR1 mRNA in the hippocampus, dentate gyrus, taenia tecta and cerebellum and at lower levels in the cortex, habenular nucleus, olfactory bulb, primary olfactory cortex, thalamus, pontine nucleus and amygdaloid nucleus.

Animals↗
PubMed1990

Induction of ornithine decarboxylase by subseizure stimulation in the hippocampus in vivo.

Electrical stimulation of the Schaffer-collateral axonal system under conditions which do not elicit detectable seizure activity causes an increase in the activity of ornithine decarboxylase (ODC), the rate limiting enzyme of polyamine synthesis, in the hippocampus, olfactory cortex, neocortex and olfactory bulb. The degree of ODC activation is dependent upon the stimulus parameters. The results support the hypothesis that neuronal activity regulates hippocampal polyamine concentrations.

Animals↗
PubMedDate not supplied

Distribution of prostaglandins E and F in different regions of the rat brain.

The regional distribution of prostaglandins E and F in 24 different areas of the rat brain was studied. For bioassay the rat uterine horn preparation was used. Prior to bioassay the samples were purified with organic solvents and in some cases by chromatography on silica as well. For measurement of PGF2 alpha content in certain areas a radioimmunoassay was used. Each region was found to contain prostaglandins but in uneven concentrations. Highest concentration, related to the protein content, was present in the median eminence, 57.6 ng PGE and 34.4 ng PGF per mg protein. Parietal cortex, olfactory tubercle, cerebellar cortex, caudate nucleus, substantia nigra, and paraventricular nucleus are also rich in prostaglandins. Low values were found in frontal cortex, thalamus, and septum. The distribution of prostaglandins throughout the areas examined do not show any direct correlation with that of transmitter substances. The uneven distribution can be attributed to differences in the endogenous biosynthetic capacity of each region.

Animals↗
PubMed1998

Correlation between potentiation of AP1 DNA binding and expression of c-Fos in association with phosphorylation of CREB at serine133 in thalamus of gerbils with ischemia.

Protein biosynthesis is mainly under the control at the level of gene transcription in eukaryotes. Transcription factors are nuclear proteins with abilities to modulate the activity of RNA polymerase II which is responsible for the formation of messenger RNA from double stranded DNA in the cell nuclei. Binding of a radiolabeled oligonucleotide probe for the transcription factor activator protein-1 (AP1) was transiently potentiated 1 to 6 h after the recirculation of blood supply in the thalamus and striatum, but not in the entorhinal cortex, olfactory bulb, frontal cortex, cerebellar cortex and medulla-pons, in gerbils with transient global forebrain ischemia for 5 min, in addition to the hippocampal subregions. The ischemic insult not only increased the immunoreactivity with an antibody against cyclic AMP response element binding protein (CREB) phosphorylated at serine133, but also induced the expression of both c-Jun and c-Fos family proteins 3 h after the recirculation in the thalamus. Limited proteolysis by Staphylococcus aureus (S. aureus) V8 protease revealed the expression of different partner proteins of AP1 in response to ischemic signals in the thalamus. Moreover, ischemia for 2 min led to more prolonged elevation of AP1 binding in the thalamus at least up to 12 h after the reperfusion than that seen with ischemia for 5 min. These results suggest that potentiation of AP1 DNA binding may at least in part involve mechanisms associated with the expression of c-Fos protein through phosphorylation of CREB at serine133 in the thalamus of gerbils with ischemia.

Amino Acid Sequence↗
PubMed1999

The short-acting anesthetic propofol produces biphasic effects-depression and withdrawal rebound overshoot-on some (but not all) limbic evoked potentials in the behaving rat.

Propofol, the relatively new, short-acting general anesthetic, markedly enhances the action of GABA at the GABAA receptor. To evaluate its effects on field potentials evoked in the dentate gyrus (DG) during the anesthetic and recovery periods, propofol was administered intraperitoneally to behaving rats bearing stimulating electrodes in the dorsal perforant path (DPP), where medial perforant path fibers predominate, and in the anterior piriform cortex (PC; i.e., olfactory cortex), and recording electrodes in the DG. Input from the PC reaches the DG via the lateral perforant path. Population slow waves (SWs) were evoked by paired-pulse stimulation of the PC at a 32 ms interstimulus interval (ISI) to produce paired-pulse facilitation in the awake animal. We had previously demonstrated that amplitude of SW2 (produced by the second stimulus) was greatly decreased by GABAergic drugs and increased by antiGABAergic convulsant agents. After administration of propofol, mean amplitude of SW2 decreased immediately and remained low for 30-60 min during propofol-induced sleep (as expected), then unexpectedly increased to about 1.5- to 2-fold above pretreatment levels at 2-4 h before gradually returning to pretreatment levels. In addition, the DPP was stimulated to produce either paired-pulse inhibition (20 ms ISI) or facilitation (32 ms ISI) of DG population spikes (PSs) in the awake animal. PS2 was much more inhibited during propofol-induced sleep, than during the pretreatment period, consistent with an expected marked increase in recurrent inhibition. An overshoot in PS2 amplitude was observed only occasionally during recovery, suggesting that withdrawal overshoot in amplitudes is more characteristic of PC-evoked DG SW2 potentials. The overshoot in SW2 amplitude during recovery may have been related to propofol's 'rapid on-rapid off' actions on the GABAA receptor, perhaps resulting in a phenomenon like the 'GABA withdrawal syndrome'. Such an effect, if true, may help explain the rare occurrence of seizures, especially during recovery, associated with its use clinically.

Anesthetics, Intravenous↗
PubMed1999

Effect of depth electrode implantation with or without subsequent kindling on GABA turnover in various rat brain regions.

Kindling is a chronic model of epilepsy characterized by a progressive increase in response to the same regularly applied electrical stimulus. The biological basis of the kindling phenomenon requires to be determined, but several studies indicate that impairment of GABAergic inhibition may be involved. In the present experiments, GABA turnover was determined in vivo by the GABA aminotransferase (GABA-T) inhibition method in 13 brain regions in three groups of rats: (1) a group which was kindled via electrical stimulation of intra-amygdala electrodes and was sacrificed 36 days after the last fully kindled seizure for neurochemical determinations; (2) a group of implanted but non-stimulated rats (sham control group) in which neurochemical measurements were done at the same time after electrode implantation as in the kindled group; and (3) a group of non-implanted, naive control rats. Regional GABA levels were determined after vehicle injection as well as 30 and 90 min after administration of aminooxyacetic acid (AOAA) at a dose which completely inhibits GABA-T. Compared to naive controls, prolonged electrode implantation in the amygdala induced a significant reduction of AOAA-induced GABA accumulation in amygdala, hippocampus, piriform cortex, olfactory bulb, frontal cortex, striatum, hypothalamus, tectum, and cerebellar cortex. In view of the GABA hypothesis of kindling, reduced GABA turnover in response to electrode implantation would suggest that the implantation per se exerts a pro-kindling effect, which was recently demonstrated in rats with intraamygdala electrodes. However, amygdala kindling itself appeared to antagonize the effect of electrode implantation in most regions. Thus, although, compared to naive controls, the predominant change in kindled rats was a decrease in GABA turnover, this decrease was less marked than in sham controls. In thalamus and brainstem kindling markedly increased GABA turnover above the levels determined in both naive and sham controls, possibly in response to impaired postsynaptic GABAergic function. The data indicate that both electrode implantation and kindling significantly alter regional GABA turnover, which might contribute to the pathophysiology of the kindling phenomenon. Furthermore, the data substantiate that the choice of adequate controls is critical in neurochemical and functional studies on the kindling phenomenon.

4-Aminobutyrate Transaminase↗
PubMed2003

Detection of pathologic prion protein in the olfactory epithelium in sporadic Creutzfeldt-Jakob disease.

BACKGROUND: Olfactory cortexes and the olfactory tracts are involved in sporadic Creutzfeldt-Jakob disease. We examined peripheral regions of the olfactory sensory pathway, including the olfactory mucosa, to assess whether pathologic infectious prion protein (PrPSc) is deposited in the epithelium lining the nasal cavity. METHODS: We studied nine patients with neuropathologically confirmed sporadic Creutzfeldt-Jakob disease. We obtained the brain, the cribriform plate with the attached olfactory mucosa, and the surrounding respiratory epithelium at autopsy. Control samples of nasal mucosa were obtained post mortem or at biopsy from age-matched control subjects and from control patients with other neurodegenerative diseases. The olfactory and respiratory mucosa and the intracranial olfactory system were analyzed by light microscopy, immunohistochemistry, and Western blotting for pathological changes and for deposition of PrPSc. RESULTS: In all nine patients with sporadic Creutzfeldt-Jakob disease, PrPSc was found in the olfactory cilia and central olfactory pathway but not in the respiratory mucosa. No PrPSc was detected in any of the tissue samples from the 11 controls. CONCLUSIONS: Our pathological and biochemical studies show that PrPSc is deposited in the neuroepithelium of the olfactory mucosa in patients with sporadic Creutzfeldt-Jakob disease, indicating that olfactory biopsy may provide diagnostic information in living patients. The olfactory pathway may represent a route of infection and a means of spreading prions.

Antibodies, Monoclonal↗
PubMed1998

Computation of molecular information in mammalian olfactory systems.

The olfactory system is unique in that the sensory input is in the form of molecular information carried in odour molecules and that a huge variety of compounds can function as odour molecules. The mammalian olfactory system has neuronal networks that can process and integrate the molecular information for discrimination of odour molecules and for perception of olfactory images of objects. Recent rapid advances have begun to provide new insights into the functional logic employed by the main olfactory system for odour discrimination, for odour classification and for olfactory perception of objects. This review discusses how the odour molecule information is encoded, transmitted, processed and decoded at distinct anatomical structures (sensory epithelium, olfactory bulb and olfactory cortex) of the olfactory nervous system. We also discuss the functional network in the accessory olfactory system with regard to the processing of pheromonal information.

Animals↗
PubMed1998

Localization of 5-HT2A receptor in rat cerebral cortex and olfactory system revealed by immunohistochemistry using two antibodies raised in rabbit and chicken.

Serotonin 2A receptor (5-HT2A receptor) is widely distributed in the central nervous system, and has been suggested to be involved in a variety of behavioral conditions and neuropsychiatric disorders. Two polyclonal antibodies were raised against the N-terminus peptide of rat 5-HT2A receptor in chickens (5-HT2A-N) and a glutathione S-transferase fusion protein that contained the C-terminus of the mouse 5-HT2A receptor in rabbits (5-HT2A-C). Affinity-purified 5-HT2A-N and -C antibodies reacted strongly with a single band of 77-78 kDa in postsynaptic density proteins prepared from the rat cortex. The distribution pattern of immunoreactive structures in the rat brain was virtually the same for the two antibodies. The highest levels of immunoreactivity were observed in the olfactory bulb, neocortex, claustrum, piriform cortex, mamillary bodies, pontine nuclei, red nucleus and cranial motor nuclei. In the olfactory bulb, mitral cells were intensely labeled. In the neocortex, many immunoreactive neurons were found in layers II-VI. In layer IV of the neocortex, strong neuropil labeling was observed. In a double-labeling study using chicken 5-HT2A-N and rabbit anti-glial fibrillary acidic protein (GFAP) antibody, a considerable number of GFAP positive cells also showed 5-HT2A immunoreactivity. By using an immunoelectron microscopic technique, 5-HT2A receptor immunoreaction was shown to be localized just beneath the postsynaptic membrane thickening of asymmetric synapses.

Amino Acid Sequence↗
PubMed1984

Selective retrograde transport of tritiated D-aspartate from the olfactory bulb to the anterior olfactory nucleus, pyriform cortex and nucleus of the lateral olfactory tract in the rat.

After an injection of [3H]D-aspartate into the olfactory bulb of the rat, retrogradely labeled cells were detected bilaterally in the anterior olfactory nucleus (AON), and ipsilaterally in the pyriform cortex (PC) and nucleus of the lateral olfactory tract (NLOT). These results suggest a certain selective retrograde transport of this amino acid, and are discussed in relation to transmitter candidates in the olfactory bulb.

Animals↗
PubMed1996

The role of the piriform cortex in kindling.

In epilepsy research, there is growing interest in the role of the piriform cortex (PC) in the development and maintenance of limbic kindling and other types of limbic epileptogenesis leading to complex partial seizures, i.e. the most common type of seizures in human epilepsy. The PC ("primary olfactory cortex") is the largest area of the mammalian olfactory cortex and receives direct projections from the olfactory bulb via the lateral olfactory tract (LOT). Beside the obvious involvement in olfactory perception and discrimination, the PC, because of its unique intrinsic associative fiber system and its various connections to and from other limbic nuclei, has been implicated in the study of memory processing, spread of excitatory waves, and in the study of brain disorders such as epilepsy with particular emphasis on the kindling model of temporal lobe epilepsy with complex partial seizures. The interest in the kindling model is based primarily on the following observations. (1) The PC contains the most susceptible neural circuits of all forebrain regions for electrical (or chemical) induction of limbic seizures. (2) During electrical stimulation of other limbic brain regions, broad and large afterdischarges can be observed in the ipsilateral PC, indicating that the PC is activated early during the kindling process. (3) The interictal discharge, which many consider to be the hallmark of epilepsy, originates in the PC, independent of which structure serves as the kindled focus. (4) Autoradiographic studies of cerebral metabolism in rat amygdala kindling show that, during focal seizures, the area which exhibits the most consistent increase in glucose utilization is the ipsilateral paleocortex, particularly the PC. (5) During the commonly short initial afterdischarges induced by stimulation of the amygdala at the early stages of kindling, the PC is the first region that exhibits induction of immediate-early genes, such as c-fos. (6) The PC is the most sensitive brain structure to brain damage by continuous or frequent stimulation of the amygdala or hippocampus. (7) Amygdala kindling leads to a circumscribed loss of GABAergic neurons in the ipsilateral PC, which is likely to explain the increase in excitability of PC pyramidal neurons during kindling. (8) Kindling of the amygdala or hippocampus induces astrogliosis in the PC, indicating neuronal death in this brain region. Furthermore, activation of microglia is seen in the PC after amygdala kindling. (9) Complete bilateral lesions of the PC block the generalization of seizures upon kindling from the hippocampus or olfactory bulb. Incomplete or unilateral lesions are less effective in this regard, but large unilateral lesions of the PC and adjacent endopiriform nucleus markedly increase the threshold for induction of focal seizures from stimulation of the basolateral amygdala (BLA) prior to and after kindling, indicating that the PC critically contributes to regulation of excitability in the amygdala. (10) Potentiation of GABAergic neurotransmission in the PC markedly increases the threshold for induction of kindled seizures via stimulation of the BLA, again indicating a critical role of the PC in regulation of seizure susceptibility of the amygdala. Microinjections of NMDA antagonists or sodium channel blockers into the PC block seizure generalization during kindling development. (11) Neurophysiological studies on the amygdala-PC slice preparation from kindled rats showed that kindling of the amygdala induces long-lasting changes in synaptic efficacy in the ipsilateral PC, including spontaneous discharges and enhanced susceptibility to evoked burst responses. The epileptiform potentials in PC slice preparations from kindled rats seem to originate in neuron at the deep boundary of PC. Spontaneous firing and enhanced excitability of PC neurons in response to kindling from other sites is also seen in vivo, substantiating the fact that kindling induces long-lasting changes in the PC c

Animals↗
PubMed1994

Recovery of olfactory behavior. II. Neonatal olfactory bulb transplants enhance the rate of behavioral recovery.

Previous experiments in this laboratory have shown that transplants of a fetal olfactory bulb into a neonatal rat are viable and that they establish connections with the olfactory peduncle and olfactory cortex. The focus of this experiment was to investigate the anatomical correlates of any behavioral recovery seen in rats that had one olfactory bulb removed along with an immediate transplant of a fetal olfactory bulb. Anatomical details, such as transplant organization and olfactory nerve repenetration patterns were analyzed using a variety of histological and immunohistochemical techniques. The rats in this experiment showed behavioral recovery of olfactory ability. The recovery rates observed in these animals were compared to two other groups of rats that this laboratory has shown to be behaviorally competent: normal rats and rats with neonatal ablations of the olfactory bulb but no transplant. Although the animals with transplants did not recover to completely normal levels of olfactory ability, they did start behavioral testing in a more behaviorally competent condition than rats with simple neonatal lesions. Anatomical analysis revealed that the transplanted olfactory bulb was heavily penetrated by incoming olfactory nerve fibers but olfactory nerve penetration was not limited to the transplanted olfactory bulb. The extra-bulbar host regions that were penetrated included the orbital frontal cortex and three olfaction-related areas; olfactory cortex, olfactory peduncle and the subependymal cell layer. The olfactory nerve penetration patterns observed beyond the transplant were essentially the same as those observed in rats with only neonatal lesions of the olfactory bulb. Thus, multiple pathways may have contributed to the recovery observed in the rats with olfactory bulb transplants.

Animals↗
PubMed2005

Functional magnetic resonance imaging study of human olfaction and normal aging.

BACKGROUND: The function of human olfaction declines with advancing age. An important question centers on whether functional alterations to olfactory brain structures accompany age-related behavioral changes. In the present study, we tested the hypothesis that aged adults have intact though reduced activity in the central olfactory system using functional magnetic resonance imaging (fMRI). METHODS: University of Pennsylvania Smell Identification Test (UPSIT) was used to test the smell function of 11 young (23.9 +/- 1.6 years) and 8 aged (66.4 +/- 4.4 years) healthy participants. Then, the participants received fMRI at 3.0 T with lavender and spearmint as stimulants. After fMRI, the participants provided ratings for the odorants' intensity and pleasantness. RESULTS: The average UPSIT score of the aged adults was 34.1 +/- 1.5, which was significantly lower than that of the young adults (37.3 +/- 1.1) (p =.0004). Both age groups showed significant activation in major olfactory brain structures, including the primary olfactory cortex, entorhinal cortex, hippocampus and parahippocampal cortex, thalamus, hypothalamus, orbitofrontal cortex, and insular cortex and its extension into the inferior lateral frontal region. The aged adults showed less brain activity in olfactory structures (p =.022), consistent with lower ratings of odor intensity and UPSIT scores. Activation intensity in bilateral primary olfactory cortex areas and right insular cortex was also comparatively weaker (p <.019). CONCLUSION: Results demonstrate that significant activation in aged adults can be observed in all the olfactory brain structures that are activated in young adults, but with lower activation volume and intensity. This finding provides a necessary baseline for further investigations in olfaction and aging.

Adult↗