Laminar and region-specific cell surface markers in the entorhinal cortex and hippocampus.
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Animals↗
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Comparative anatomy of the entorhinal cortex and hippocampus in mammals.
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Animals↗
Ontogeny of the entorhinal cortex.
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Cerebral Cortex↗
Neuronal cell types in entorhinal cortex and hippocampal formation of man and other mammalia: an interspecies comparison.
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Animals↗
Morphological and functional correlates of borders in the entorhinal cortex and hippocampus.
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Animals↗
Ultrastructural analysis of tryptophan hydroxylase immunoreactive nerve terminals in the rat cerebral cortex and hippocampus: their associations with local blood vessels.
Physiological evidence has indicated that serotonin (5-hydroxytryptamine) could be a regulator of cerebral blood flow in various regions of the brain. In the present study, tryptophan hydroxylase immunocytochemistry was used to characterize, both at the light and electron microscopic levels, serotonergic nerve terminals and primarily their relationships with intraparenchymal microarterioles and capillaries in the rat frontoparietal cortex, entorhinal cortex and hippocampus. Irrespective of the brain area, serotonergic varicosities were primarily apposed to either dendrites or nerve terminals, were on average 0.37 micron2 in surface area (0.69 micron calculated diameter) and 12-22% of them engaged in synaptic junctions, mostly with dendritic elements. Perivascular terminals (defined as immunolabelled varicosities located within a 3 micron perimeter around the vessel basal lamina) in the frontoparietal cortex represented 8-11% of all immunoreactive terminals counted, as determined by light and electron microscopy, respectively. In the entorhinal cortex and hippocampus, the proportion of perivascular terminals was only determined at the ultrastructural level and corresponded to 10% and 4%, respectively. In the frontoparietal cortex, serotonergic varicosities were located significantly closer (n = 250, 0.98 +/- 0.05 micron; P < 0.001) to the blood vessels than those of the entorhinal cortex (n = 116, 1.41 +/- 0.08 microns) or hippocampus (n = 105, 1.31 +/- 0.08 microns). Of all perivascular serotonergic terminals in the frontoparietal cortex, 26% were in the immediate vicinity (0-0.25 micron) of the vessel wall, with 2.8% directly abutting on the basement membrane, while 11.6% were separated from it only by a thin astrocytic leaflet. This situation contrasts with that observed in the entorhinal cortex and hippocampus, where no immunoreactive varicosity was ever seen directly contacting the vessel basal lamina and with only 10-13% of the terminals being within 0.25 micron from the vessels. The surface area of perivascular serotonergic terminals was comparable in all regions studied and corresponded to 0.22 micron2; these virtually never engaged in synaptic contacts with adjacent neuronal structures. Our results indicate that tryptophan hydroxylase-immunolabelled terminals are identical to previously characterized serotonin-containing varicosities. Furthermore, the present data show intimate associations between serotonergic terminals and microvessels in the three regions examined. However, perivascular terminals in the frontoparietal cortex were more frequent and/or located much closer to local microvessels than those in the other regions, and might be more directly involved in neurogenic control of local cerebral blood flow.
Animals↗
Differential neuronal encoding of novelty, familiarity and recency in regions of the anterior temporal lobe.
Activity of 2072 neurones was recorded in the anterior temporal lobe--in area TE, perirhinal cortex, entorhinal cortex and hippocampus--during performance of a visual recognition task by monkeys. In area TE, perirhinal cortex and entorhinal cortex, 454 neurones (38% of the 1162 visually responsive neurones) responded differentially on the basis of the relative familiarity or recency of presentation of the stimuli; in the hippocampus only one (3%) of its 40 visually responsive neurones) did so. The differentially responsive neurones were classified into those signalling information concerning the recency (19%), familiarity (37%) or novelty (38%) of stimuli. For 98% of these neurones a decreased response signalled that stimuli had occurred previously: no large response increments were observed. The mean differential latency of each of these types of neurone was shorter (approximately 75 ms) in area TE than in the other areas. Examples of each of these types of neurone with memory spans of approximately 24 h were found in each region. The mean memory span of recency neurones was significantly longer in perirhinal cortex than area TE. For familiarity neurones a significant mean response decrement took 4-8 min to develop, indicating a slow underlying plastic change, in contrast to the rapid change seen for recency and novelty neurones. The implications of these results are discussed in relation to the neuronal basis of recognition memory.
Analysis of Variance↗
Distribution of estrogen target sites in the 2-day-old mouse forebrain and pituitary gland during the 'critical period' of sexual differentiation.
The present study provides a detailed anatomical description of estrogen target cells in the mouse forebrain and pituitary gland during the sexual imprinting stage of the brain. Six 2-day-old mice (3 males and 3 females) were s.c. injected with 16 alpha-[125I]iodo-11 beta-methoxy-17 beta-estradiol ([125I]MIE2) and two additional mice (one male and one female) were s.c. injected with 1000x unlabeled 17 beta-estradiol 1 h before [125I]MIE2 to check the specificity of estradiol binding. Two hours after injection the mice were decapitated, the brains dissected, frozen sectioned, and processed for thaw mount autoradiography. The highest intensity of nuclear labeling was observed in the preoptic-anterior hypothalamic area, amygdala and cortex entorhinalis. Strong labeling was present in the cerebral cortex and moderate to strong labeling in the lateral septum, bed nucleus of stria terminalis and pituitary gland. Weak to moderate labeling was observed in the bulbus olfactorius, circumventricular organs, basal ganglia, ventral striatum, thalamus, hippocampus and pineal gland. No sex differences were observed in the intensity of labeling and distribution of the estrogen target sites. The topographic distributions of estrogen-concentrating cells in the hypothalamus of the 2-day-old mouse forebrain was similar to the adult pattern but differed prominently in the cerebral cortex, entorhinal cortex and thalamus: the cerebral cortex showed an extensive and intensive labeling, the intensity of labeling in the entorhinal cortex greatly exceeded that observed in the adult and the nucleus anterior medialis thalami was distinctly labeled.
Animals↗
Efferent connections of the nucleus reuniens and the rhomboid nucleus in the rat: an anterograde PHA-L tracing study.
Direct projections from the nucleus reuniens (Re) and the rhomboid nucleus (Rh) in the midline of the thalamus were examined in the rat by utilizing anterograde axonal transport of Phaseolus vulgaris leukoagglutinin (PHA-L). The Re projected axon terminals densely to the anterior cingulate cortex, infralimbic area of the medial frontal cortex, agranular insular cortex, entorhinal cortex, and parasubiculum. Labeled terminals in these cerebral cortices were distributed mainly in layer I, except for the entorhinal cortex where labeled terminals were distributed in layers I-IV. On the other hand, labeled terminals of projection fibers from the Rh to the cerebral cortex were distributed in layers II-VI of the anterior cingulate cortex, frontal cortex, parietal cortex, and agranular insular cortex. In the nucleus accumbens, caudate putamen, and basolateral amygdaloid nucleus, labeled terminals from the Rh were more dense than those from the Re. In the hypothalamus, labeled terminals from the Re were more dense than those from the Rh. The septal nuclei and field CA1 of Ammon's horn received labeled axon terminals from the rostral portion of the Re, but not from the caudal portion of the Re or the Rh. The patterns of distribution of axon terminals from the Re and Rh were similar in other subcortical target regions. To confirm the PHA-L results, wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) was injected into two projection sites of PHA-L-labeled axons. After injection into the agranular insular cortex, WGA-HRP-labeled neurons were found in the Re, but only a few were present in the Rh. In contrast to this, after WGA-HRP injection into the nucleus accumbens, WGA-HRP-labeled neurons were found in the Rh, but only a few were seen in the Re.
Animals↗
Repeated episodic exposure to ethanol affects neurotrophin content in the forebrain of the mature rat.
Chronic exposure to ethanol can cause deficits in learning and memory. It has been suggested that withdrawal is potentially more damaging than the ethanol exposure per se. Therefore, we explored the effect of repeated episodic exposure to ethanol on key regulators of cortical activity, the neurotrophins. Rats were exposed to ethanol via a liquid diet for 3 days per week for 6-24 weeks. Control rats were pair-fed an isocaloric liquid diet or ad libitum fed chow and water. The concentrations of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) were determined using enzyme-linked immunosorbant assays (ELISAs). Five telencephalic structures were examined: parietal cortex, entorhinal cortex, hippocampus, the basal nucleus, and the septal nuclei. All five areas expressed each of the three neurotrophins; BDNF was most abundant and NGF the least. The parietal cortex was susceptible to ethanol exposure, NGF and BDNF content increased, and NT-3 content fell, whereas no changes were detectable in the entorhinal cortex. In the hippocampus, the amount all three neurotrophins increased following episodic ethanol exposure. Neurotrophin content in the two segments of the basal forebrain was affected; NGF and NT-3 content in the basal forebrain was reduced and NGF and BDNF content in the septal nuclei was increased by ethanol exposure. In many cases where ethanol had an effect, the change was transient so that by 24 weeks of episodic exposure, no significant changes were evident. Thus, the effects of ethanol are site- and time-dependent. This pattern differs from changes caused by chronic ethanol exposure, hence, neurotrophins must be vulnerable to the effects of withdrawal. Furthermore, the ethanol-induced changes do not appear to fit a model consistent with retrograde regulation, rather they suggest that neurotrophins act through autocrine/paracrine systems.
Animals↗
Abeta deposition is associated with neuropil changes, but not with overt neuronal loss in the human amyloid precursor protein V717F (PDAPP) transgenic mouse.
The PDAPP transgenic mouse overexpresses human amyloid precursor protein V717F (PDAPP minigene) and develops age-related cerebral amyloid-beta protein (Abeta) deposits similar to senile plaques in Alzheimer's disease. We find age-related cortical and limbic Abeta deposition that begins at 8 months and progresses to cover 20-50% of the neuropil in cingulate cortex, entorhinal cortex, and hippocampus of 18-month-old heterozygotic animals. The regional patterns of transgene expression and amyloid deposition suggest that Abeta deposits occur at the terminals of overexpressing neurons. Amyloid deposition is associated with dystrophic neurites and extensive gliosis. However, stereological analysis shows that there is no overt neuronal loss in entorhinal cortex, CA1 hippocampal subfield, or cingulate cortex through 18 months of age. In addition, there is no apparent loss of mRNA encoding neuronal synaptic, cytoskeletal, or metabolic proteins. Thus, widespread Abeta deposition in 18-month-old heterozygotic mice produces neuritic alterations and gliosis without widespread neuronal death.
Aging↗
Localization of pontine PGO wave generation sites and their anatomical projections in the rat.
A number of experimental and theoretical reports have suggested that the ponto-geniculo-occipital (PGO) wave-generating cells are involved in the generation of rapid eye movement (REM) sleep and REM sleep dependent cognitive functions. No studies to date have examined anatomical projections from PGO-generating cells to those brain structures involved in REM sleep generation and cognitive functions. In the present study, pontine PGO wave-generating sites were mapped by microinjecting carbachol in 74 sites of the rat brainstem. Those microinjections elicited PGO waves only when made in the dorsal part of the nucleus subcoeruleus of the pons. In six rats, the anterograde tracer biotinylated dextran amine (BDA) was microinjected into the physiologically identified cholinoceptive pontine PGO-generating site to identify brain structures receiving efferent projections from those PGO-generating sites. In all cases, small volume injections of BDA in the cholinoceptive pontine PGO-generating sites resulted in anterograde labeling of fibers and terminals in many regions of the brain. The most important output structures of those PGO-generating cells were the occipital cortex, entorhinal cortex, piriform cortex, amygdala, hippocampus, and many other thalamic, hypothalamic, and brainstem nuclei that participate in the generation of REM sleep. These findings provide anatomical evidence for the hypothesis that the PGO-generating cells in the pons could be involved in the generation of REM sleep. Since PGO-generating cells project to the entorhinal cortex, piriform cortex, amygdala, and hippocampus, these PGO-generating cells could also be involved in the modulation of cognitive functions.
Action Potentials↗
Long-latency event-related potentials in rats: effects of task and stimulus parameters.
Animal models of event-related potentials have recently been developed in rats in order to gain further understanding of the psychobiological variables which underlie these waveforms. In the present study, unanesthetized male Wistar rats, chronically implanted with electrodes, were utilized in order to: (i) compare event-related potentials recorded following the presentation of passively presented auditory stimuli from different neocortical, hippocampal and perihippocampal sites; (ii) test the effects of changes in stimulus probability and loudness on event-related potentials recorded from those sites; and (iii) record event-related potentials from rats who were actively performing in a tone discrimination task. The results of these studies showed that in all electrode sites (frontal cortex, parietal cortex, entorhinal cortex, hippocampus) a series of large amplitude potentials in the 10-200 ms latency range could be recorded in response to passively presented stimuli. Late positive potentials in the 300-400 ms range were only identified in recordings from the posterior cortex, entorhinal area, and dorsal hippocampus. Some of these late positive components were also found to be sensitive to changes in stimulus probability. A similar series of waves were detected in a paradigm where rats were required to actively discriminate between two tones; however, the morphologies of the waveforms were found to be more distinct. These studies suggest that rats may be good subjects for the exploration of the neural origins of event-related potentials. These studies demonstrate that rats performing in an auditory discrimination task can generate electrophysiological potentials which are time locked to the onset of a "cognitively relevant" stimulus (event-related potentials). These potentials can be recorded in limbic (hippocampus and amygdala) and cortical (parietal cortex) brain sites. The event-related potentials recorded in rats respond to changes in stimulus parameters in a similar fashion to those previously described in monkeys and human subjects. The identification of a rat model of event-related potentials provides an opportunity to further explore the neural origins of event-related potentials, to estimate the role of genetics in determining individual variation in waveforms, as well as to provide electrophysiological assays of the effects of various drugs on neurosensory and cognitive processing.
Acoustic Stimulation↗
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↗
Kindling alters entorhinal cortex-hippocampal interaction by increased efficacy of presynaptic GABA(B) autoreceptors in layer III of the entorhinal cortex.
We studied the effect of kindling, a model of temporal lobe epilepsy, on the frequency-dependent information transfer from the entorhinal cortex to the hippocampus in vitro. In control rats repetitive synaptic activation of layer III projection cells resulted in a frequency dependent depression of the synaptic transfer of action potentials to the hippocampus. One-to-two-days after kindling this effect was strongly reduced. Although no substantial change in synaptic inhibition upon single electrical stimulation was detected in kindled rats, there was a significant depression in the prolonged inhibition following high frequency stimulation. In kindled animals, paired-pulse depression (PPD) of stimulus-evoked IPSCs in layer III neurons was significantly stronger than in control rats. The increase of PPD is most likely caused by an increased presynaptic GABA(B) receptor-mediated autoinhibition. In kindled animals activation of presynaptic GABA(B) receptors by baclofen (10 microM) suppressed monosynaptic IPSCs significantly more than in control rats. In contrast, activation of postsynaptic GABA(B) receptors by baclofen was accompanied by comparable changes of the membrane conductance in both animal groups. Thus, in kindled animals activation of the layer III-CA1 pathway is facilitated by an increased GABA(B) receptor-mediated autoinhibition leading to an enhanced activation of the monosynaptic EC-CA1 pathway.
Action Potentials↗
FMRI brain activation in response to odors is reduced in primary olfactory areas of elderly subjects.
Olfactory function is affected by aging and deficits often result in decreasing quality of life, health and safety. The present study investigated the cortical substrate of olfactory deficits related to aging with functional Magnetic Resonance Imaging (fMRI), with a retronasal olfactory stimulation protocol using flavored aqueous solutions presented to the mouth. Activation was found in young subjects in the piriform/amygdalar region and in the orbitofrontal cortex and in other areas previously found activated in neuroimaging studies using odorized air, including insula and cerebellum. Activation was seen in similar areas in old subjects but the degree of activation was significantly lower in regions receiving primary olfactory projections (piriform cortex, entorhinal cortex, and amygdala). This result supports the hypothesis of dysfunction and/or degeneration in areas critical to olfactory processing as a major cause of olfactory deficits in the older population.
Adult↗
Age-related changes in [3H]MK-801 binding in the Fischer 344 rat brain.
In this study we tested the hypothesis that the efficacy of L-glutamate to stimulate [3H]MK-801 binding to the NMDA receptor/channel complex is altered as a function of aging. L-Glutamate, or related excitatory amino acid (EAA), is the endogenous neurotransmitter of the NMDA receptor/channel complex. These studies examined the efficacy and potency with which L-glutamate produces receptor activation, channel opening and subsequent MK-801 binding as a function of increasing age by comparing dose-response curves (EC50 and Emax) from 6-, 12-, and 24-month-old F-344 rats. The number of NMDA receptors, as determined by [3H]MK-801 binding in the presence of a saturating concentration of L-glutamate, was reduced in the inner frontal cortex, entorhinal cortex and the lateral striatum in aged rats when compared with young adults. When a range of L-glutamate concentrations were used, differences in Emax were noted in the same brain regions in addition to several others in aged and middle-aged animals when compared with young-adult animals. No changes in EC50 values were noted in any of the brain regions at either age when compared with young-adults.
Aging↗
Amygdala kindling and c-fos protein(s).
c-fos protein was visualized immunohistochemically in the brains of rats after partial amygdala seizures and generalized amygdala-kindled seizures and in seizure-free amygdala-kindled rats. Four hours following partial amygdala seizures there was a massive induction of c-fos protein in the ipsilateral piriform cortex, entorhinal cortex, and amygdala. Following generalized amygdala-kindled seizures there was a massive bilateral induction of c-fos in the entire cerebral cortex, amygdala, piriform and entorhinal cortices, hippocampus, and dentate gyrus. However, there did not appear to be any change in the basal levels of c-fos in the brains of amygdala-kindled rats that had been seizure free for 7 days. These results show that kindled seizures induce c-fos in neurons, but that the permanence of kindling is not related to altered basal c-fos levels.
Amygdala↗