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PubMed2001

Interference with visual memory in rats following infusion of the functional NMDA receptor antagonist, HA-966, into temporal regions.

Results from lesion studies show that selective damage to the temporal cortex or lateral entorhinal cortex impairs visual memory, whereas damage to the hippocampal region does not affect retention of a visual discrimination task. Major input pathways of the above structures use glutamate as neurotransmitter. The glutamate NMDA receptor appears to play an important role for cognitive functions. The objective of the present study was to examine whether microinjections of the functional NMDA receptor antagonist, 3-amino-1-hydroxy-2-pyrrolidinone ((+)-HA-966), might result in effects mimicking those seen in lesion studies. The results show that infusion of HA-966 into the temporal cortex or lateral entorhinal cortex 1.5-3 h after the learning criterion had been obtained led to an impeded visual memory when tested 13 days later, whereas HA-966 infused into the hippocampal region did not affect memory. A similar retention deficit with HA-966 infusions in the temporal cortex or lateral entorhinal cortex was seen when testing took place 23 days later, whereas a markedly weaker effect was observed when the retention period was reduced to 3 days. It is suggested that the hippocampal region is a temporary storing site for nonspatial memory engrams, and later posttraining memory consolidation involves the temporal and lateral entorhinal cortices. Furthermore, the degree of the effect of HA-966 is related to the length of the retention period.

Analysis of Variance↗
PubMed2004

[Brain volumetric MRI study in healthy elderly persons using statistical parametric mapping].

PURPOSE: To investigate the age-related changes in the brains of healthy elderly subjects, a volumetric MRI was performed using Statistical Parametric Mapping (SPM) and Region of Interest (ROI) methods. We determined the volumes of the whole brain, the gray matter, the prefrontal cortex, the hippocampus and the entorhinal cortex. SUBJECTS AND METHODS: We examined 61 subjects (29 males and 32 females) aged 61 to 91 years (mean +/- SD = 72.4 +/- 7.85) who were residents of Okinawa prefecture, living at home and highly active as demonstrated by sustained participation in senior citizens clubs and/or group activities at senior citizen welfare centers. They had no history of psychiatric disorders, neurological or significant physical illness. They had Mini-Mental State Examination scores of 24 or above (mean +/- SD = 28.3 +/- 1.57), Japanese version of the Geriatric Depression Scale scores of 9 or below, and Tokyo Metropolitan Institute of Gerontology scores of 11 or above. All subjects were dextral. This study received prior approval by the participating medical institution. Informed consent was obtained from the individual subjects. Volumetric MRI was performed using a 1.5 Tesla MRI scanner (Magnetom Vision, Siemens). T1-weighted images were acquired in the coronal plane (perpendicular to anterior commissure-posterior commissure line) using a 3D-FLASH (fast low angle shot) sequence. Imaging parameters were: TR = 35 ms, TE = 5 ms, Flip angle = 45 deg., Field of View = 240 mm, Matrix 256 x 256, Pixel 0.9375 x 0.9375, Slice thickness 1.5 mm, Gapless. MR image data were analyzed by SPM using an imaging analysis software MEDx (Sensor Systems Inc.) running on UNIX workstation (Sun SPARC Solaris 7, Sun Microsystems, Inc.). Volumetry was performed by automatic segmentation technique using SPM for the whole brain and the gray matter, and manual tracing using ROI based quantitative methods for the prefrontal cortex, the hippocampus and the entorhinal cortex. Local volumes were normalized by the intracranial volume and the gray matter volume. Correlation to age was determined by Pearson's correlation coefficient. Volumetric MRI was performed under blinded conditions. RESULTS: Volumetric MRI of normal brain in healthy elderly subjects showed age-related changes. The whole brain (r = -0.568, p < 0.01), the gray matter (r = -0.406, p < 0.01), the prefrontal cortex (r = -0.470, p < 0.01), the hippocampus (r = -0.305, p < 0.05), and the entorhinal cortex (r = -0.455, p < 0.01) volume significantly decreased with age. The age-related hippocampal volume reduction was similar to the gray matter reduction, but the age-related prefrontal cortex and entorhinal cortex volume reductions were greater than the gray matter volume reduction. The prefrontal cortex and the hippocampal volumes differed by sex, being greater in females (p < 0.05). The hippocampal volume was lateralized: right side was greater than the left (p < 0.01). The entorhinal cortex volume was lateralized so that the left side was greater than the right (p < 0.01). CONCLUSION: As a result of volumetric MRI using SPM, age-related changes of normal brain in healthy elderly persons did not always show unified atrophy. The ratio of atrophy was different by a local area. Our findings suggested that the most marked age-related brain volume reductions were seen in the prefrontal cortex and the entorhinal cortex. The age-related hippocampal volume reduction was similar to the gray matter reduction.

Aged↗
PubMed2002

The entorhinal cortex-nucleus accumbens pathway and latent inhibition: a behavioral and neurochemical study in rats.

Latent inhibition (LI) refers to the decrease in conditioned response produced by the repeated nonrein-forced preexposure to the to-be-conditioned stimulus. Experiment I investigated the effects of electrolytic lesions of the entorhinal cortex on LI in a conditioned emotional response procedure. Entorhinal cortex lesions attenuated LI. Experiments 2 and 3 investigated whether this attenuation of LI could result from a modification in nucleus accumbens (NAcc) dopamine (DA) release. Rats with entorhinal cortex lesions displayed normal spontaneous and amphetamine-induced locomotor activity, as well as normal basal and amphetamine-induced release of DA within the NAcc (assessed by microdialysis). Taken together, these results show that entorhinal cortex lesions disrupt LI in a way that is unlikely to be due to an alteration of DA release within the NAcc.

Animals↗
PubMed1998

Effects of new valproate derivatives on epileptiform discharges induced by pentylenetetrazole or low Mg2+ in rat entorhinal cortex-hippocampus slices.

The effects of four valproic acid derivatives were studied on pentylenetetrazole-induced epileptiform discharges in combined entorhinal cortex hippocampus slices. The two new sugar-esters of valproic acid, dimethylenexylitol valproate (VDMX, 0.5 mM) and glucose valproate (VG, 2 mM) abolished the epileptiform activity. These two new derivatives were compared to two clinically used anticonvulsant drugs, valpromide (2 mM) which suppressed the activity and valproic acid (2 mM), which was ineffective. The new drugs VDMX and VG were also tested on different patterns of epileptiform activity induced by lowering of [Mg2+]0. A 1 mM concentration of VDMX and 2 mM VG, reversibly suppressed the recurrent short discharges in area CA1 and the seizure-like events in the entorhinal cortex. A concentration of 2 mM VDMX was required to abolish the late recurrent discharges in entorhinal cortex. VG at 2 mM reduced the frequency of these discharges by 58.5+/-9.5%.

Animals↗
PubMed2000

Restoration of latent inhibition by olanzapine but not haloperidol in entorhinal cortex-lesioned rats.

RATIONALE: Latent inhibition (LI) refers to the decrease in conditioned response induced by the repeated non-reinforced pre-exposure to the conditioned stimulus before its pairing with the unconditioned stimulus during the conditioning stage. LI has been considered as a relevant animal model for the study of the biological bases of schizophrenia. LI has recently been demonstrated to depend on the integrity of the entorhinal cortex, as lesioning of this area disrupted LI. OBJECTIVES: The present study aimed to verify whether the classical neuroleptic haloperidol and/or the atypical antipsychotic olanzapine would prevent the effect of entorhinal cortex lesioning. METHODS: LI was studied in an off-baseline conditioned emotional response (CER) paradigm in which a tone is paired with a footshock. Entorhinal cortex lesions were produced by the electrolytic method. After a recovery period, both lesioned and control rats received either haloperidol (0.3 mg/kg), olanzapine (0.3 mg/kg) or vehicle before both the pre-exposure and conditioning stages of the experiment. RESULTS: In control rats, pre-exposure to the tone induced LI, which was affected by neither haloperidol nor olanzapine. Lesioning of the entorhinal cortex produced a deficit of LI, which was restored by olanzapine but not by haloperidol. CONCLUSIONS: This result suggests a dissociation of the anatomical and pharmacological targets of the two drugs. The possible involvement of dopamine D3 receptors in the effects of olanzapine is discussed.

Animals↗
PubMed2003

Binge ethanol treatment causes greater brain damage in alcohol-preferring P rats than in alcohol-nonpreferring NP rats.

BACKGROUND: Genetics is a known risk factor for alcoholism, and human alcoholics are known to suffer from a loss of brain function and mass. A 4 day rat binge drinking model is known to cause brain region-specific damage. To investigate the role of genetics in binge-drinking-induced brain damage, we studied bidirectionally selected rat lines, the alcohol-preferring P and the alcohol-nonpreferring NP rat lines. METHOD: P and NP rats were treated with a 4 day binge ethanol protocol. Animals were killed, transcardially perfused, and fixed, and their brains were removed, sectioned, and stained by using the amino cupric silver stain of de Olmos or by using immunohistochemistry for phospho-extracellular signal regulated kinases and other antigens. RESULTS: Significant brain damage was found in the olfactory bulbs, posterior perirhinal cortex, and entorhinal cortex in both P and NP rats. P rats were found to have significantly greater brain damage, compared with NP rats, in the posterior perirhinal and posterior entorhinal cortexes, 239% +/- 50% (p < 0.02) and 219% +/- 46% (p < 0.01), respectively. Phospho-extracellular signal regulated kinase immunohistochemistry stained prominently in damaged brain areas. CONCLUSIONS: The P rat line, a genetic model of alcoholism, shows greater region-specific brain damage due to binge ethanol treatment than its genetic counterpart, the NP rat line. These findings suggest that genetics contribute to susceptibility for binge-induced brain damage.

Alcohol Drinking↗
PubMed2000

Effects of standard anticonvulsant drugs on different patterns of epileptiform discharges induced by 4-aminopyridine in combined entorhinal cortex-hippocampal slices.

Application of 4-aminopyridine (4-AP) has previously been reported to produce different patterns of epileptiform discharges in entorhinal cortex (EC)-hippocampal slices: recurrent short discharges (RSDs) in hippocampal area CA1, seizure-like events (SLEs) and negative-going potentials (NGPs) in the medial entorhinal cortex (mEC). Using recordings of field potentials, we investigated the pharmacological effects of the clinically employed standard anticonvulsant drugs phenytoin (PHT), carbamazepine (CBZ), valproic acid (VPA) and phenobarbital (PHB) and those of pentobarbital (PB) on 4-AP-induced epileptiform activity. The anticonvulsant drugs showed different effects: SLEs were completely blocked by all tested drugs. Valproic acid, which suppressed all epileptiform activities, seemed to have the most fundamental effect of all drugs on 4-AP induced activity, because under phenytoin and carbamazepine, some epileptiform activity was still observable. The RSDs in hippocampal area CA1 of the hippocampus did not respond to the different anticonvulsants. In contrast, PB decreased the frequency of the RSDs in CA1 and enhanced the frequency of the NGPs in the EC. We propose that the activities induced by 4-AP in the combined entorhinal cortex-hippocampal slices may provide an in vitro model for the development of new drugs against difficult-to-treat focal epilepsy.

4-Aminopyridine↗
PubMed2005

Effect of early isolation on signal transfer in the entorhinal cortex-dentate-hippocampal system.

Deprivation of socio-sensory interactions during early life impairs brain function in adulthood. In previous investigations we showed that early isolation severely affects neuron development in several structures of the hippocampal region, including the entorhinal cortex. In the present study we investigated the effects of early isolation on signal processing along the entorhinal cortex-dentate-CA3-CA1 system, a major memory circuit of the hippocampal region. Male and female guinea-pigs were assigned at 6-7 days of age to either a social or an isolated environment. At 90-100 days of age the animals were anesthetized and field potentials were recorded from the entorhinal cortex-dentate-CA3-CA1 circuit, driven by dorsal psalterium commissural volleys. Analysis of the input-output function in the different structures showed that in isolated males there was a small reduction in the input-output function of the population excitatory postsynaptic potential and population spike evoked in layer II of the entorhinal cortex. No changes occurred in isolated females. In isolated males and females there was a reduction in the input-output function of the population excitatory postsynaptic potential and population spike evoked in the dentate gyrus, CA3 and CA1, but this effect was larger in males. In isolated males, but not in females, the population spike/population excitatory postsynaptic potential ratio was reduced in all investigated structures, indicating that in males the size of the discharged neuron population was reduced more than due to the decreased input. Results show that isolation reduces the synaptic function in the whole entorhinal cortex-dentate gyrus-CA3-CA1 system. While the entorhinal cortex was moderately impaired, the dentate-hippocampal system was more severely affected. The impairment in the signal transfer along the entorhinal cortex-dentate gyrus-CA3-CA1 system was heavier in males, confirming the larger susceptibility of this sex to early experience. This work provides evidence that malfunctioning of a major hippocampal network may underlie the learning deficits induced by impoverished surroundings during early life.

Animals↗
PubMedDate not supplied

Polysynaptic potentiation at different levels of rat olfactory pathways following learning.

This study was aimed at investigating the consequences of learning on late polysynaptic components of evoked field potential signals recorded in parallel at different levels of the olfactory pathways. For this, evoked field potentials induced by electrical stimulation of the olfactory bulb were recorded simultaneously in the anterior piriform cortex, the posterior piriform cortex, the lateral entorhinal cortex, and the dentate gyrus. The different parameters of late components were measured in each site before and after completion of associative learning in anesthetized rats. In the learning task, rats were trained to associate electrical stimulation of one olfactory bulb electrode with the delivery of sucrose (positive reward) and stimulation of a second olfactory bulb electrode with the delivery of quinine (negative reward). In this way, stimulation of the same olfactory bulb electrodes used for inducing field potentials served as a discriminative cue in the learning paradigm. The data confirmed previous observation that learning was associated with a lowering in late-component-1 intensity of induction in the posterior piriform cortex. The use of simultaneous recording allowed us to further specify the consequences of learning on late-component distribution in the studied network. Indeed the data showed that whereas before learning, late component 1 was rather uniformly distributed among the recorded sites; following learning, its expression was facilitated preferentially in the posterior piriform cortex and lateral entorhinal cortex. Furthermore, learning was accompanied by the emergence of a new late component (late component 2), which occurred simultaneously in the four recording sites. The possible involvement of potentiation of polysynaptic components in recognition and/or consolidation processes will be discussed.

Animals↗
PubMed2000

Expression of brain-derived neurotrophic factor, neurotrophin-3 and their receptor messenger RNAs in monkey rhinal cortex.

The primate rhinal cortex, consisting of areas 36 and 35 of the perirhinal cortex and the entorhinal cortex (area 28), plays a crucial role in perception and memory. We investigated the expression of messenger RNAs for brain-derived neurotrophic factor and neurotrophin-3, as well as those for their respective tyrosine kinase receptors, TrkB and TrkC, in the monkey rhinal cortex. Results from in situ hybridization revealed that each of these messenger RNAs was expressed in neurons with distinct laminar and areal patterns of distribution. Brain-derived neurotrophic factor messenger RNA was principally detected in layers V/ VI of area 36, and layers II/III and V of the entorhinal cortex. Some of the messenger RNA-positive cells in the deep layers of the rhinal cortex were confirmed to exhibit a pyramidal cell-like morphology. Neurotrophin-3 messenger RNA expression was confined to layers II/III of the entorhinal cortex. In contrast, trkB and trkC messenger RNAs were expressed rather homogeneously and abundantly throughout the rhinal cortex. The laminar and cellular distributions of brain-derived neurotrophic factor and neurotrophin-3 messenger RNAs indicate the predominant expression of these neurotrophins in projection neurons. These results suggest that brain-derived neurotrophic factor and neurotrophin-3 regulate neuronal connectivities of forward and backward projections from the rhinal cortex and contribute to functional reorganization underlying the formation and maintenance of long-term memory in primates.

Animals↗
PubMed1999

Cerebral glucose metabolism in unilateral entorhinal cortex-lesioned rats: an animal PET study.

To evaluate the effect of entorhinal cortical lesion on cerebral cortical function, we studied cerebral glucose utilization (CMRGlc) using a high resolution PET scanner after quinolinic acid lesion of the unilateral entorhinal cortex in rats. [18F]Fluorodeoxyglucose PET was performed at 4 days and 4 weeks after surgery, and CMRGlc in the bilateral frontal, parietal and temporal regions were analyzed. At 4 days, the entorhinal lesion induced a 12-15% decrease in CMRGlc of frontal, parietal and temporal regions ipsilateral to the lesion. The hypometabolism continued at 4 weeks in the temporal region. These findings suggest that entorhinal lesion induces cerebral cortical hypometabolism, which implies a pathogenetic role of entorhinal area on the cortical hypometabolism in Alzheimer's disease.

Analysis of Variance↗
PubMed2006

Anticonvulsant effects of N6-cyclohexyladenosine microinjected into the CA1 region of the hippocampus on entorhinal cortex-kindled seizures in rats.

In this study, the role of adenosine A1 receptors of the hippocampal CA1 region in entorhinal cortex-kindled seizures was investigated in rats. Animals were kindled by daily electrical stimulation of the entorhinal cortex. In fully kindled rats, N(6)-cyclohexyladenosine (CHA; a selective A1 receptor agonist) and 1, 3-dimethyl-8-cyclopenthylxanthine (CPT; a selective A1 receptor antagonist) were microinfused bilaterally into the hippocampal CA1 region. Rats were stimulated and seizure parameters were measured. Results obtained showed that CHA (10 and 50 micro moles) decreased the afterdischarge duration (ADD) in the hippocampal CA1 region and entorhinal cortex, stage 5 seizure duration (S5D) and seizure duration (SD) only at the dose of 50 micro moles, and significantly increased the latency to stage 4 (S4L). Intrahippocampal CPT increased ADD and S5D, and significantly reduced the latency to stage 4 (S4L) at the dose of 10 micromoles. Pretreatment of rats with CPT (5 micro moles) before CHA (50 micro moles), significantly reduced the effect of CHA on seizure parameters. The results suggest that the CA1 region of the hippocampus plays an important role in spreading seizure spikes from the entorhinal cortex to other brain regions and activation of adenosine A1 receptors in this region participates in the anticonvulsant effects of adenosine agonists.

Adenosine↗
PubMed1994

Lowering of extracellular pH suppresses low-Mg(2+)-induces seizures in combined entorhinal cortex-hippocampal slices.

Lowering [Mg2+]o induces epileptiform bursting in hippocampus and entorhinal cortex (EC), presumably by activation of N-methyl-D-aspartate (NMDA) receptors. Since increasing [H+]o has been shown to reduce NMDA receptor activation, we hypothesized that this could contribute to anticonvulsant actions of acidic pH. To test this, we studied the effects of raising extracellular PCO2 (20.6%, pH = 6.7) or lowering extracellular pH (6.7 or 6.2) on low-Mg(2+)-induced epileptiform discharges. Lowering the pH to 6.7 by either means increased the interval between seizure-like events (SLEs), decreased the maximal amplitude of SLEs, and if the site of seizure generation was at a distance from the recording site, acidification slowed the rate of seizure propagation. In contrast, the duration of SLEs was unaffected by acidic pH or high PCO2. Raising PCO2 or lowering pH to 6.7 also blocked early (8-10 min) but not late (> 20 min) phases of status-like discharges. All effects of the extracellular pH changes were fully reversible. Further lowering of extracellular pH to 6.2 completely and reversibly blocked both SLEs and status-like discharges. Our data show that the effects of high PCO2 and low pH on seizures in the EC in vitro may be dose-dependent and consistent with induction by proton blockade of NMDA receptors. Thus, blockade of NMDA currents by protons may be an important component of the anticonvulsant action of extracellular acidosis. The results also suggest that acidosis may be a desirable property for new antiepileptic treatments.

Acidosis↗
PubMed1997

Serotonin1A receptor autoradiography during alcohol-withdrawal kindling.

A series of autoradiography experiments were conducted in order to test the theory that the serotonin (5-HT) receptor subtype 5-HT(1a) is involved in alcohol-withdrawal kindled convulsive behaviour. Alcohol-withdrawal kindling was performed by subjecting male Wistar rats to multiple episodes consisting of 2 days of alcohol intoxication and 5 days of alcohol withdrawal. In the first episode alcohol intoxication led to focal downregulation of [3H]-8-hydroxy-2-(di-n-propylamino)tetralin ([3H]-8-OH-DPAT) binding sites in septum and subregions of frontal cortex, hippocampus, and entorhinal cortex. This alcohol-induced response was blunted in both alcohol-withdrawal kindled animals and in animals exposed to repeated alcohol dependence in which the previous withdrawal reactions were blocked by diazepam administration. A paradoxical upregulation of [3H]-8-OH-DPAT binding sites was found in septum and subregions of frontal cortex, hippocampus, and entorhinal cortex in control animals which were fed isocalorically with the alcohol-withdrawal kindled animals and subsequently exposed to 2 days of alcohol intoxication. It was concluded that the alterations in the alcohol induced 5-HT(1a) receptor regulation after multiple episodes of alcohol dependence were not caused by alcohol-withdrawal kindling processes per se, but were due to both alcohol specific and alcohol non-specific effects.

Animals↗
PubMed2001

Olfactory learning induces differential long-lasting changes in rat central olfactory pathways.

In the present work, we investigated lasting changes induced by olfactory learning at different levels of the olfactory pathways. For this, evoked field potentials induced by electrical stimulation of the olfactory bulb were recorded simultaneously in the anterior piriform cortex, the posterior piriform cortex, the lateral entorhinal cortex and the dentate gyrus. The amplitude of the evoked field potential's main component was measured in each site before, immediately after, and 20 days after completion of associative learning. Evoked field potential recordings were carried out under two experimental conditions in the same animals: awake and anesthetized. In the learning task, rats were trained to associate electrical stimulation of one olfactory bulb electrode with the delivery of sucrose (positive reward), and stimulation of a second olfactory bulb electrode with the delivery of quinine (negative reward). In this way, stimulation of the same olfactory bulb electrodes used for inducing field potentials served as a discriminative cue in the learning paradigm. The data showed that positively reinforced learning resulted in a lasting increase in evoked field potential amplitude restricted to posterior piriform cortex and lateral entorhinal cortex. In contrast, negatively reinforced learning was mainly accompanied by a decrease in evoked field potential amplitude in the dentate gyrus. Moreover, the expression of these learning-related changes occurred to be modulated by the animals arousal state. Indeed, the comparison between anesthetized versus awake animals showed that although globally similar, the changes were expressed earlier with respect to learning, under anesthesia than in the awake state. From these data we suggest that associative olfactory learning involves different neural circuits depending on the acquired value of the stimulus. Furthermore, they show the existence of a functional dissociation between anterior and posterior piriform cortex in mnesic processes, and stress the importance of the animal's arousal state on the expression of learning-induced plasticity.

Anesthetics↗
PubMed1990

Perforant path stimulation differentially alters prodynorphin mRNA and proenkephalin mRNA levels in the entorhinal cortex-hippocampal region.

The regulatory effect of the perforant path on opioid gene expression in the entorhinal cortex-hippocampal region was investigated. The left perforant path was electrically stimulated at the angular bundle under conditions which elicit wet dog shakes but no motor seizures in rats. Animals were given either an acute stimulation composed of several consecutive stimulation trials, or daily stimulations with a single trial every day for 6 days. Rats were then sacrificed at 24 h or 6 days after the last trial. The amounts of prodynorphin mRNA (DYN mRNA) and proenkephalin A mRNA (EK mRNA) in the hippocampus and entorhinal cortex were measured by RNA blot analysis. Dynorphin A(1-8) and [Met5]enkephalin immunoreactivities were determined by radioimmunoassay. A decrease in DYN mRNA level of approximately 50-80% was found on both sides of the hippocampus 24 h after both acute and daily stimulation. Hippocampal dynorphin A(1-8) immunoreactivity was also reduced at 24 h, and persisted for at least 6 days. In contrast, bilateral increases in EK mRNA level were observed in the hippocampus (54-101%) and entorhinal cortex (97-165%) 24 h after the acute stimulation. Also, [Met5]enkephalin immunoreactivity in the hippocampus tended to be increased at this time. These results indicate that activation of the perforant path inhibits the gene expression of prodynorphin, but enhances that of proenkephalin in the entorhinal cortex-hippocampal region.

Animals↗
PubMed1998

MR volumetric analysis of the human entorhinal, perirhinal, and temporopolar cortices.

PURPOSE: Our purpose was to investigate the normal volumes of the human entorhinal, perirhinal, and temporopolar cortices on MR imaging studies using a customized program. METHODS: We designed a protocol in which the volumes of the entorhinal, perirhinal, and temporopolar cortices were determined from coronal MR images using anatomic landmarks defined on the basis of cytoarchitectonic analyses of 49 autopsy cases. MR volumetry of these cortical areas was performed in 52 healthy volunteers. RESULTS: The overall mean volumes were 1768 +/- 328 mm3/1558 +/- 341 mm3 (right/left) for the entorhinal cortex, 2512 +/- 672 mm3/2572 +/- 666 mm3 for the perirhinal cortex, and 2960 +/- 623 mm3/3091 +/- 636 mm3 for the temporopolar cortex. The right entorhinal cortex was 12% larger than the left. The volume of the temporopolar cortex was reduced bilaterally by 13% in the older age group compared with younger subjects, while the volumes of the entorhinal and perirhinal cortices were unaffected by age. There were no differences between men and women in the volumes of any of the three cortices. CONCLUSION: Our method provides a tool by which to measure volumes of the entorhinal, perirhinal, and temporopolar cortices on coronal MR images.

Adolescent↗
PubMed2001

Fos imaging reveals differential neuronal activation of areas of rat temporal cortex by novel and familiar sounds.

To provide information about the possible regions involved in auditory recognition memory, this study employed an imaging technique that has proved valuable in the study of visual recognition memory. The technique was used to image populations of neurons that are differentially activated by novel and familiar auditory stimuli, thereby paralleling previous studies of visual familiarity discrimination. Differences evoked by novel and familiar sounds in the activation of neurons were measured in different parts of the rat auditory pathway by immunohistochemistry for the protein product (Fos) of the immediate early gene c-fos. Significantly higher counts of stained neuronal nuclei (266 +/- 21/mm2) were evoked by novel than by familiar sounds (192 +/- 17/mm2) in the auditory association cortex (area Te3; AudA). No such significant differences were found for the inferior colliculus, primary auditory cortex, postrhinal cortex, perirhinal cortex (PRH), entorhinal cortex, amygdala or hippocampus. These findings are discussed in relation to the results of lesion studies and what is known of areas involved in familiarity discrimination for visual stimuli. Differential activation is produced by novel and familiar individual stimuli in sensory association cortex for both auditory and visual stimuli, whereas the PRH is differentially activated by visual but not auditory stimuli. It is suggested that this latter difference is related to the nature of the particular auditory and visual stimuli used.

Acoustic Stimulation↗