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PubMed1996

Expression of the neural adhesion molecule L1 in the deafferented dentate gyrus.

Expression of the neural adhesion molecule L1 and its potential involvement in axonal sprouting were examined in the deafferented rat dentate gyrus. We focused on the dentate gyrus because of its well-defined cytoarchitecture and well-characterized neuronal degeneration and sprouting response following entorhinal cortex lesions. In the molecular layer of the dentate gyrus, a trilaminar staining pattern was observed, with the middle molecular layer exhibiting slightly denser immunolabeling compared to both inner and outer molecular layers. Two to 12 days after a unilateral entorhinal cortex lesion, a progressive loss of L1 immunolabeling was noted in the ipsilateral middle and outer molecular layers, followed by a substantial reappearance of immunostaining 65 days after lesion incidence. The width of the immunostained ipsilateral inner molecular layer revealed a progressive widening and by postlesion day 65 occupied about 50% of the total width of the molecular layer. Immunoelectron microscopy localized L1 to the surface of unmyelinated axons in both normal and deafferented dentate gyrus. In situ hybridization revealed L1 messenger RNA confined to neurons throughout the hippocampal formation, but did not indicate changes in L1 messenger RNA levels in the hippocampus, dentate gyrus, entorhinal cortex or basal forebrain in response to unilateral entorhinal cortex lesions. Changes in L1 immunolabeling in the deafferented dentate gyrus corresponded in a spatial and temporal manner to changes of the synaptic marker synaptophysin and axonal marker phosphorylated tau. Results of the present study are most consistent with the view that L1 is expressed on reinnervating fibers after they make synaptic contacts with other structures. Thus, L1 appears to be involved in the maturation and stabilization of reinnervating fibers and consequently may play an important role in the repair process of the lesioned adult CNS.

Animals↗
PubMed1997

Cholinergic sprouting in the rat fascia dentata after entorhinal lesion is not linked to early changes in neurotrophin messenger RNA expression.

After unilateral entorhinal cortex lesion cholinergic septohippocampal fibres sprout in the denervated fascia dentata. This process is dependent on neurotrophin changes following the lesion. Thus, there is an up-regulation of nerve growth factor and brain-derived neurotrophic factor messenger RNA expression in the denervated granule cells which is detectable 4 h postlesion and returns to control levels by 24 h. Here, using a competitive polymerase chain reaction and in situ hybridization, a transient neurotropin messenger RNA increase could be demonstrated bilaterally following unilateral electrolytic entorhinal cortex lesion. Treatment of the animals with the N-methyl-D-aspartate receptor antagonist dizocilpine maleate blocked this messenger RNA increase, suggesting an involvement of this receptor type in the neurotrophin changes. However, in spite of this blockade, the typical cholinergic sprouting response as visualized with acetylcholinesterase histochemistry was present in animals four weeks after entorhinal cortex lesion. These data suggest that brief initial changes in neurotrophin messenger RNA expression in dentate granule cells are not responsible for the induction of the cholinergic sprouting. Changes in neurotrophin messenger RNA expression occurring immediately postlesion may be linked to glutamate release from entorhinal terminals resulting from the electrolytic lesion of the projection cells in the entorhinal cortex. We hypothesize that later changes in neurotrophin expression, for example in glial cells, are more likely to be related to the cholinergic sprouting process.

Acetylcholinesterase↗
PubMed1996

Entorhinal-hippocampal interactions revealed by real-time imaging.

The entorhinal cortex provides the major cortical input to the hippocampus, and both structures have been implicated in memory processes. The dynamics of neuronal circuits in the entorhinal-hippocampal system were studied in slices by optical imaging with high spatial and temporal resolution. Reverberation of neural activity was detected in the entorhinal cortex and was more prominent when the inhibition due to gamma-aminobutyric acid was slightly suppressed. Neural activity was transferred in a frequency-dependent way from the entorhinal cortex to the hippocampus. The entorhinal neuronal circuit could contribute to memory processes by holding information and selectively gating the entry of information into the hippocampus.

Animals↗
PubMed1999

Functional coupling in rat central olfactory pathways: a coherence analysis.

This experiment determined the importance of functional coupling between structures of central olfactory pathways: the olfactory bulb (OB), anterior (APC), posterior (PPC) parts of the piriform cortex and lateral entorhinal cortex (EC). From local field potential signals obtained in awake rats, coupling during spontaneous activity was estimated with variables reflecting level of coherence computed with a dynamical method. Results revealed a clear hierarchy in the strength of coupling between structures with dissociation within the piriform cortex: PPC was more tightly coupled with the EC than with APC. Systemic injection of a cholinergic antagonist, scopolamine, suggested that tonic coupling is strongly mediated by cortico-cortical connections and not by an external synchronizer, except between OB and APC.

Action Potentials↗
PubMed2002

Retrograde tracing of zinc-enriched (ZEN) neuronal somata projecting to the olfactory bulb.

Zinc ions seem to be important to several neurological functions and have been connected to the pathophysiology of epilepsy, neuronal cell death after seizure or stroke, and Alzheimer's disease. Both epilepsy and Alzheimer's disease are clinical conditions believed to involve the olfactory bulb. The mammalian olfactory bulb is densely innervated by zinc-enriched (ZEN) neurons, and the distribution of the ZEN terminals in the mouse olfactory bulb has previously been described. The aim of this study was to describe the origins of ZEN terminals projecting into the main olfactory bulb of the rat. Selective labeling of ZEN terminals was accomplished by intracerebral infusion of sodium selenide, whereby zinc selenium clusters are created in the ZEN terminals. Some of these clusters move by retrograde axonal transport to the somata where they can be silver-enhanced by autometallography (AMG). After infusion of sodium selenide into the main olfactory bulb, retrogradely labeled ZEN somata were found (1) ipsilaterally in all anterior olfactory nuclei, taenia tecta, piriform cortex and lateral entorhinal cortex, and (2) contralaterally in anterior olfactory nuclei except the external division. The ipsilateral anterior olfactory nucleus had the densest population of ZEN somata, and it was found that these somata originated mainly from pyramidal neurons in layers II and III of each area. The olfactory-related centrifugal afferents to the main olfactory bulb are discussed.

Afferent Pathways↗
PubMed2000

Dissociating entorhinal and hippocampal involvement in latent inhibition.

This study used anatomical cues to suggest a functional dissociation between the roles of the entorhinal cortex and the hippocampus in learning. The authors proposed that the highly convergent inputs to the entorhinal cortex indicate this region may be particularly important for selecting or compressing information. This hypothesis was tested in rabbits (Oryctolagus cunniculus) trained on an associative learning task that is a common index of stimulus selection. In this task, known as latent inhibition, preexposure to a stimulus (such as a tone) leads to slowed learning when the same tone is subsequently paired with an outcome (such as an airpuff to the eye). As hypothesized, rabbits with neurotoxic lesions of the entorhinal cortex failed to show slowed learning following preexposure (no latent inhibition) and learned the association faster than control rabbits. In contrast, hippocampal-lesioned animals showed normal (slowed) learning.

Animals↗
PubMed1998

Perirhinal cortex contributions to performance in the Morris water maze.

Rats with bilateral, electrolytic lesions of perirhinal cortex (PRC), lateral entorhinal cortex (LEC), or combined lesions (PRLE) were impaired relative to controls (sham) during initial acquisition in the Morris water maze, although all groups were eventually able to learn to locate the platform. A further deficit in the performance of PRC and PRLE, but not LEC groups, was evident, however, when a probe trial was conducted 2 min (but not 24 hours) after training. When the performance of sham- and PRC-lesioned rats was tested with variable memory delays inserted between training and probe trials, lesioned rats displayed an increase in the rate of forgetting for information made available during the training trial. This finding suggests that the PRC normally stores information regarding the cue-platform relationship and transfers this information to related structures during water maze performance.

Analysis of Variance↗
PubMed1975

Some connections of the entorhinal (area 28) and perirhinal (area 35) cortices of the rhesus monkey. I. Temporal lobe afferents.

In this investigation the efferent projections from ventral temporal neocortical and limbic cortical areas to the entorhinal and perirhinal cortices have been investigated in the rhesus monkey using silver impregnation methods. It was observed that virtually all ventral temporal neocortical areas contribute some afferents to the transitional zones of periallocortex (perirhinal and prorhinal cortices) forming the walls of the rhinal sulcus. These areas in turn project medially to the entorhinal cortex and hippocampus. Additional direct sources of afferent input to the entorhinal cortex were found to originate in Brodmann's areas 51, 49 and 27, and Bonin and Bailey's areas TF and TH. These connections have been characterized as final relays in multisynaptic cortico-cortical pathways linking the entorhinal cortex and, ultimately, hippocampus to the association areas of the frontal, parietal, temporal, and occipital lobes.

Animals↗
PubMed1998

Comparison of effects of valproate and trans-2-en-valproate on different forms of epileptiform activity in rat hippocampal and temporal cortex slices.

PURPOSE: Reducing the extracellular magnesium or calcium or increasing the extracellular potassium induces different patterns of epileptiform activity in the hippocampus and the entorhinal cortex. Although in the low Ca2+ and K+ models, seizure-like events (SLEs) develop in area CA1 of the hippocampus, only short recurrent discharges develop in the low Mg2+ model. In contrast, in low Mg2+, SLEs and late recurrent discharges (LRDs) are observed in the entorhinal cortex. METHODS: We compared the effects of valproate (VPA) and its major metabolite, trans-2-en-VPA (TVPA), on all these different model activities using extracellular field potential measurements. We also investigated the equilibration time course of VPA in the slice by using VPA-sensitive microelectrodes. RESULTS: Both drugs reversibly blocked most forms of epileptiform activity. The only exception was the LRDs in the entorhinal cortex. In paired experiments, TVPA appeared to be more effective than VPA bath applied with the same concentration to the same slice. With our measurements of the VPA concentrations in slices, we showed that the concentrations used were close to therapeutic drug levels. CONCLUSIONS: If TVPA stands the toxicological tests, it might be a useful alternative in the treatment of seizures.

Action Potentials↗
PubMed1997

Stereotactic amygdalohippocampotomy and mesial temporal spikes.

PURPOSE: To investigate the mechanism of mesial temporal spike generation, we sought to determine whether amygdalohippocampotomy by radiofrequency lesions altered spike rates in patients with medically intractable temporal lobe epilepsy. METHODS: The subjects were 14 patients whose ictal semiology, ictal and interictal EEGs, and neuropsychological profile were compatible with seizure origin from MRI-demonstrated unilateral mesial temporal sclerosis. Mesial temporal spikes were recorded by a multicontact electrode line stereotactically placed in the temporal horn of the lateral ventricle. A recording and lesioning electrode was also stereotactically advanced to multiple amygdala and hippocampal targets. Several confluent (9 patients) or discrete (5 patients) radiofrequency lesions were made in the amygdala and anterior hippocampus. Scalp and invasive recordings were performed before lesioning, between each lesioning process, and for 48 postoperative h. RESULTS: As compared to prelesion recordings, no consistent change in anterior and total mesial temporal spike rates occurred intraoperatively or postoperatively. Postlesion: prelesion spike ratios failed to correlate with effectiveness of lesionectomy for seizure control. In contrast, complex partial seizures improved in 13 of 14 patients. CONCLUSIONS: Amygdala and hippocampal destructive lesions had no consistent effect on meisal temporal spike quantity, but reduced temporal lobe CPS in 13 of 14 patients. This dichotomy suggests that CPS may result from concerted epileptogenesis of the hippocampus, entorhinal cortex, and possibly the amygdala, while the entorhinal cortex alone can produce interictal spikes.

Adolescent↗
PubMed2000

Differential c-Fos and caspase expression following kainic acid excitotoxicity.

Caspases play crucial roles in the inflammatory response and in the cell pathway leading to apoptosis. Caspase 1 (ICE), 2 (Nedd2), 3 (CPP32), 6 (Mch2) and 8 (Mch5, FLICE) expression was examined using immunohistochemistry in the brains of rats and gerbils following systemic administration of kainic acid (KA). The distribution of caspase expression was compared with the distribution of c-Fos expression, a transcription factor that is produced in response to the excitotoxic insult. Strong caspase 2 immunoreactivity was found in microglia up to 6 h following KA administration. Focal strong expression of caspases 1, 2, 3, 6 and 8 was observed in astrocytes and neurons, from 12 to 48 h after KA injection, in areas in which a number of neurons were committed to die. This distribution was in contrast with the generalised distribution of c-Fos expression following KA administration. Only a minority of neurons in the entorhinal cortex, amygdala and hilus, but a majority of neurons in selected thalamic nuclei, exhibited strong caspase expression in KA-treated rats. Similar findings, although minimised, were observed in KA-treated gerbils. Double-labelling caspase immunohistochemistry and in situ end-labelling of nuclear DNA fragmentation disclosed co-localisation of strong caspase expression and nuclear DNA breaks in a small percentage of neurons but no co-localisation in astrocytes. Western blots of entorhinal cortex and neocortex homogenates showed cleavage of certain caspase substrates in KA-treated rats. The intensity of the bands corresponding to lamin B and protein kinase C-delta was decreased in the entorhinal cortex following KA administration. Several bands appeared in the entorhinal cortex and neocortex paragraph signin Western blots processed for the demonstration of poly(ADP-ribose) polymerase (PARP), thus indicating that other proteases, in addition to caspases, cleaved PARP following KA administration. Taken together, these findings indicate that KA excitotoxicity triggers caspase expression which, although predominant in regions subjected to irreversible cell damage, has only a weak association with the presence of nuclear DNA breaks and neuron cell death. Although these results suggest caspase activation, further studies have to be performed to elucidate whether caspase activation plays a crucial role in KA excitotoxicity.

Animals↗
PubMed1986

Connections of the parahippocampal cortex in the cat. II. Subcortical afferents.

The organization of subcortical inputs to the parahippocampal cortex, which in the present study in the cat is considered to comprise the entorhinal and perirhinal cortices, was studied by using retrograde and anterograde tracing techniques. The results of the retrograde tracer horseradish peroxidase (HRP), HRP conjugated with wheat germ agglutinine (WGA-HRP), Fast Blue (FB) or Nuclear Yellow (NY] injections indicate that the entorhinal and perirhinal cortices receive inputs from the magnocellular basal forebrain and from distinct portions of the amygdaloid complex, the claustrum, and the thalamus. The two cortices are further projected upon by fibers from the supramamillary region of the hypothalamus, the ventral tegmental area of the mesencephalon, the dorsal raphe nucleus, the nucleus centralis superior, and the locus coeruleus. The entorhinal cortex, in addition, receives projections from the medial septum. As regards the projections from the amygdaloid complex, it was observed that the entorhinal cortex receives its heaviest input from the basolateral amygdaloid nucleus, whereas the perirhinal cortex receives a strong projection from the lateral nucleus and a weaker projection from the basomedial nucleus of the amygdala. Of the thalamic nuclei that project to the parahippocampal cortex, the nucleus reuniens is only connected with the entorhinal cortex, while fibers from the medial geniculate nucleus and the lateral posterior nucleus terminate in the perirhinal cortex. Injections of tritiated amino acid (3H-leucine) were placed in the medial septum, the dorsal and ventral claustrum, the basolateral and basomedial amygdaloid nuclei, and the nucleus reuniens of the thalamus. The results of these experiments demonstrate that, with the exception of the claustrum, these subcortical areas project mainly to the superficial layers I-III and the lamina dissecans of the parahippocampal cortex, and to a lesser degree to the deep layers V and VI.

Amidines↗
PubMed1990

The process of reinnervation in the dentate gyrus of adult rats: time course of increases in mRNA for glial fibrillary acidic protein.

The present study evaluates the time course of increased expression of the mRNA for glial fibrillary acidic protein (GFAP) within the dentate gyrus and hippocampus after unilateral lesions of the entorhinal cortex. Levels of GFAP mRNA were evaluated by dot blot hybridization of mRNA isolated from the hippocampus and quantitative in situ hybridization. For dot blot hybridization, RNA was isolated from pooled hippocampi obtained from animals killed at 12 hr, 1, 2, 4, 6, 8, 10, 14, and 30 d postlesion. A separate set of animals killed at 2, 4, 6, 8, 10, 12, 14, and 32 d were prepared for in situ hybridization. The dot blot analyses of mRNA isolated from the hippocampus revealed that on the side ipsilateral to the lesion, the levels of GFAP mRNA increased rapidly, reaching a peak at 2 d postlesion. The increases were not evident by 12 hr postlesion, but by 24 hr, levels of GFAP mRNA were 5-fold higher than control, and by 48 hr, the levels were over 6-fold higher than control. The levels of GFAP mRNA decreased after 2 d postlesion. At 4 and 6 d postlesion the levels were about 2-fold higher than control. At later postlesion intervals, mRNA levels were comparable to the control. At 2 d postlesion, the levels of GFAP mRNA were also increased about 2-fold over control levels on the contralateral side. After 2 d, the levels of GFAP mRNA on the contralateral side were comparable to the control. In situ hybridization revealed a complex pattern of changes in the levels of GFAP. At 2 d postlesion, the levels of GFAP mRNA increased dramatically throughout the hippocampus bilaterally. The increases were most pronounced in the denervated portions of the neuropil; however, the levels of GFAP mRNA were also substantially elevated in laminae that do not receive direct projections from the entorhinal cortex. GFAP mRNA levels were also increased in other areas that receive projections from the entorhinal cortex, including the septum, lateral-dorsal thalamus, and entorhinal cortex contralateral to the lesion. In addition, GFAP mRNA levels were increased in regions bordering the ventricles throughout the brain, and over the surface of the tectum. After 2 d postlesion, the increases in the levels of GFAP mRNA were for the most part restricted to areas containing terminal degeneration. The generalized increases throughout the hippocampus were no longer apparent. Areas bordering the ventricles continued to exhibit higher labeling than in control animals, but this effect was not as prominent as at 2 d postlesion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Parahippocampal pathology in Creutzfeldt-Jakob disease.

BACKGROUND: The hippocampal lesions in Creutzfeldt-Jakob disease (CJD) have been reported to be characteristically mild, but it has not been well known how the lesions change pathologically from the entorhinal cortex to the hippocampus. MATERIAL AND METHODS: This study was designed to clarify the ambiguity attending the parahippocampal lesions in CJD. Fourteen cases with pathologically diagnosed CJD were studied. They were classified into 2 groups: group I, which did not have cortical status spongiosus (SS) and included 5 cases; and group II, which had cortical SS and included 9 cases. Neuronal loss, astrocytosis, and spongiform change were studied in lesions in the entorhinal cortex, parasubiculum, presubiculum (external and internal principal laminae), subiculum, and prosubiculum, respectively. RESULTS: The results of this study showed that in group I neuronal loss and astrocytosis were more severe in the parasubiculum and the external principal lamina of the presubiculum than in the other regions including the entorhinal cortex, and in group II the lesions in the entorhinal cortex, parasubiculum, and the external principal lamina of the presubiculum were more severe than in the other regions. In both groups in this study the lesions from the internal principal lamina of the presubiculum through the prosubiculum in the direction of the hippocampus were mild, which could be the least vulnerable in the parahippocampal gyrus in CJD. CONCLUSION: On the contrary, our findings also raise the possibility that the parasubiculum and the external principal lamina of the presubiculum may be the structures most vulnerable to early lesions in the parahippocampal gyrus in CJD. To know the pathogenesis of these lesions may be the clue to delineate the mechanisms by which the neurons could be spared.

Aged↗
PubMed2007

Postnatal development of entorhinodentate projection of the Reeler mutant mouse.

We anterogradely labeled entorhinodentate axons by the injection of biotin dextran amine into the entorhinal cortex of adult wildtype and reeler mice to clarify whether the course and terminal endings of the reeler entorhinal projection are normal or not. We found that in the reeler mouse, biotin dextran amine-labeled entorhinodentate fibers arising from the entorhinal cortex curved around the hippocampal fissure instead of crossing it, whereas in the wildtype mouse, they crossed the fissure as a perforant pathway. Next, we examined carbocyanine dye (DiI) labeling of the immature entorhinodentate projection and the developmental changes of the hippocampal fissure during early postnatal days based on the laminin and glial fibrillary acidic protein (GFAP) immunohistochemistry. Injection of DiI into the entorhinal area of the wildtype and reeler mice at postnatal day 1 resulted in anterograde labeling of pioneer axons passing through the hippocampal fissure. However, follower axons could not penetrate through the hippocampal fissure in reeler mice, whereas in the normal controls, many DiI-labeled axons continued to pass through the fissure. GFAP immunohistochemistry demonstrated that GFAP-immunopositive astrocytes were abundant along the hippocampal fissure both in the wildtype and reeler mice at birth. In the wildtype mouse, GFAP-positive neurons nearby the fissure were decreasing in number during the early postnatal days, whereas in the reeler mouse, many GFAP-positive astrocytes were continuing to accumulate there. This barrier made of astrocytes in the reeler mouse may obstruct the ingrowth of the follower axons arising from the entorhinal cortex through the hippocampal fissure, resulting in the abnormal course of the entorhinodentate axons in this mutant.

Animals↗
PubMed2004

Early complement activation increases in the brain in some aged normal subjects.

Complement activation is increased in Alzheimer's disease (AD) and may contribute to the development and progression of this disorder. To compare early complement activation between normal and AD brain specimens, C4d and iC3b concentrations were measured in hippocampus, entorhinal cortex, temporal cortex, parietal cortex, and cerebellum from aged normal and AD subjects n=10-14 for both), and in hippocampus and entorhinal cortex from younger normal subjects (n=5-6). C4d and iC3b levels increased 2.3- to 4.6-fold in AD versus aged normal specimens (all P <0.05), with lowest concentrations of these activation proteins generally in cerebellum. No significant differences were present between aged and younger normal C4d and iC3b levels in hippocampus or entorhinal cortex. However, the concentrations of these proteins were markedly increased in several aged normal specimens. Normal subject age was moderately associated with both C4d (r=0.49) and iC3b (r=0.53) concentrations in the hippocampus. Increased brain complement activation in some elderly individuals may promote the subsequent development of AD.

Adult↗
PubMedDate not supplied

Substance P neurons in the human hippocampus: an immunohistochemical analysis in the infant and adult.

An analysis of the distribution of substance P immunoreactive nerve cell bodies and fibres is given for infant and adult human hippocampus by using the peroxidase-antiperoxidase technique of Sternberger. The description covers the substance P distribution in the area dentata, the Ammon's horn, the subicular complex and the entorhinal cortex. Each region shows a specific pattern in its substance P immunoreactivity. In general, the hippocampal neurons occur in three major classes of interneurons: large (20-35 microns) horizontal bipolar or multipolar neurons in the alveus, in the deep part of the subicular complex, the entorhinal cortex, and in the white matter of the angular bundle; small (10-20 microns) and large (20-35 microns) vertically oriented bipolar or multipolar neurons in the stratum oriens, in the stratum pyramidale of the Ammon's horn, and in the deep part of the subicular complex and the entorhinal cortex; large (20-35 microns) multipolar neurons in the hilus. Substance P immunoreactive fibres are particularly abundant around pyramidal cells of the CA2 and CA3 subfields of the Ammon's horn and around granule cells of the area dentata. They are also detected in the fimbria and angular bundle. Comparative study of the infant and adult hippocampus reveals no variation in the area dentata and Ammon's horn except that substance P immunoreactive fibres are more abundant in the molecular layer of the area dentata in adults. In contrast, a far more extensive number of substance P immunoreactive cell bodies are detected in the deep layers of the subicular complex and the entorhinal cortex, as well as in the white matter of the angular bundle in infants aged between three and 12 months old. This rich substance P immunoreactive network raises questions concerning its function within the human hippocampus.

Adult↗
PubMed1995

Quantitative autoradiographic characterisation of the binding of [3H]WAY-100635, a selective 5-HT1A receptor antagonist.

The binding characteristics of [3H]WAY-100635 ([O-methyl 3H]-N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl) cyclohexane carboxamide trihydrochloride), a potent and selective 5-HT1A antagonist radioligand, were examined in the rat brain using in vitro quantitative receptor autoradiography. The regional distribution of specific [3H]WAY-100635 binding sites was heterogeneous and demonstrated a strong correlation with that of [3H]8-OH-DPAT binding. The highest concentrations of [3H]WAY-100635-labelled sites were found in the lateral septal areas, dorsal raphe n., entorhinal cortex and the hippocampal formation (CA1, CA3 and dentate gyrus). Scatchard transformation of saturation isotherms revealed saturable [3H]WAY-100635 binding sites of high-affinity: in the hippocampal formation, Kd was approximately 1 nM and Bmax ranged between 187 and 243 fmol/mg tissue wet weight, in the entorhinal cortex, Kd = 0.44 nM and Bmax = 194 fmol/mg tissue wet weight, and in the rostral portion of the dorsal raphe n., Kd = 0.52 nM and Bmax = 157 fmol/mg tissue wet weight. The affinity of [3H]WAY-100635 for the 5-HT1A binding site tended to be higher in the dorsal raphe n. and entorhinal cortex compared with that of the hippocampal formation. In contrast, the binding affinity of [3H]8-OH-DPAT in the hippocampal formation was between 1.1 and 2.3 nM and the Bmax was 137 to 183 fmoles/mg tissue wet weight; in the entorhinal cortex, Kd = 3.2 nM and Bmax = 141 fmoles/mg tissue wet weight, and in the rostral portion of the dorsal raphe n., Kd = 3.4 nM and Bmax = 163 fmol/mg tissue wet weight.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗