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PubMed1981

Olfactory bulb projections to the parahippocampal area of the rat.

Recent evidence suggests that the main olfactory bulb projects caudally beyond the prepiriform cortex and the cortical amygdaloid nuclei to the region of the piriform lobe called the parahippocampal area. Included within this area is the entorhinal cortex, which is composed of six major subdivisions. Since questions remain as to which of these subdivisions receives centripetal fibers from the bulb, we reexamined these projections using autoradiography and HRP histochemistry and correlated the sites of termination with the cytoarchitecture of the entorhinal cortex. The results indicate that olfactory bulb axons reach all parts of the parahippocampal area, including the cortex which forms the medial and lateral banks of the amygdaloid sulcus (area TR), and both subdivisions of the laterally located entorhinal cortex (28L' and 28L). Also, label is observed over the more medially located fields of the entorhinal cortex, including the cortex posterior to the cortical amygdaloid nucleus (28M'), as well as the ventrolateral parts of medial entorhinal cortex (28M). In addition, evidence of label occurs over the full extent of the transition zone (28i) which separates areas 28L and 28M. These results suggest that the olfactory bulb has a more extensive projection to the parahippocampal area in the rat than previously thought, and may provide at least some input to all of the parahippocampal areas which project to the hippocampal formation.

Animals↗
PubMed1999

Perirhinal cortex projections to the amygdaloid complex and hippocampal formation in the rat.

The differential efferent projections of the perirhinal cortex were traced by using anterograde and retrograde tracing techniques. The dorsal bank cortex (area 36) projected lightly to the lateral entorhinal cortex and more strongly to the lateral, posterolateral cortical, and posterior basomedial amygdaloid nuclei and amygdalostriatal transition zone. The ventral bank (dorsolateral entorhinal cortex) projected to the lateral entorhinal cortex, dorsal subiculum, and subfield CA1 and mainly targeted the basolateral amygdaloid nucleus. Corticocortical projections from the dorsal and ventral banks targeted different cortical areas. The fundus of the rhinal sulcus (area 35) projected to both lateral and medial entorhinal cortices, ventral subiculum, lateral and basolateral nuclei, and amygdalostriatal transition zone. Corticocortical projections targeted areas projected to by both dorsal and ventral banks and also by second somatosensory area, first temporal cortical area, and striate cortex. Neurons projecting to the lateral nucleus were distributed in all layers of the dorsal bank, wheras those projecting to CA1 and subiculum were found in superfical layers (mostly layer III) of the ventral bank. Projections to the basolateral nucleus arose from superfical layers (mostly layer II) of the fundus and deep layers of the ventral bank. Furthermore, projections to the amygdala mostly arose from rostral levels, whereas hippocampal projections primarily originated caudally. The rat perirhinal cortex is heterogeneous in its efferent connectivity, and distinct projections arise from the dorsal and ventral banks and fundus of the rhinal sulcus. The widespread cortical connectivity of the fundus suggests that only this part of the perirhinal cortex is similar to area 35 of the primate brain.

Amygdala↗
PubMed1991

Regional and time dependent variations of low Mg2+ induced epileptiform activity in rat temporal cortex slices.

In order to study spatial interactions during low magnesium induced epileptiform activity, changes in extracellular potassium concentration ([K+]0) and associated slow field potentials (f.p.'s) were recorded in thin rat temporal cortex slices (400 microns) containing the neocortical temporal area 3 (Te3), the entorhinal cortex (EC) and the hippocampal formation with the dentate gyrus, area CA3 and CA1 and the subiculum (Sub). The epileptiform activity was characterized by short recurrent epileptiform discharges (40 to 80 ms, 20/min) in areas CA3 and CA1 and by interictal discharges and tonic and clonic seizure like events (SLE's) (13-88s) in the EC, Te3 and Sub. While interictal discharges occurred independent of each other in the different subfields, the three areas became synchronized during the course of a SLE. The EC, Te3 and Sub all could represent the "focus" for generation of the SLE's. This initiation site for SLE's sometimes changed from one area to another. The characteristics of the rises in [K+]0 and subsequent undershoots were comparable to previous observations in in vivo preparations. Interestingly, rises in [K+]0 could start before actual onset of seizure like activity in secondarily recruited areas. The epileptiform activity could change its characteristics to either a state of recurrent tonic discharge episodes or to a continuous clonic discharge state reminiscent of various forms of status epilepticus. We did not observe, in any of these states, active participation by area CA3 in the epileptiform activity of the EC in spite of clear projected activity to the dentate gyrus. Even after application of picrotoxin (20 microM), area CA3 did not actively participate in the SLE's generated in the entorhinal cortex. When baclofen (2 microM) was added to the picrotoxin containing medium, SLE's occurred both in the entorhinal cortex and in area CA3, suggesting that inhibition of inhibitory interneurons by baclofen could overcome the "filtering" of projected activity from the entorhinal cortex to the hippocampus.

Animals↗
PubMed2003

Activation of metabotropic glutamate 5 and NMDA receptors underlies the induction of persistent bursting and associated long-lasting changes in CA3 recurrent connections.

The aim of this study was to describe the induction and expression mechanisms of a persistent bursting activity in a horizontal slice preparation of the rat limbic system that includes the ventral part of the hippocampus and the entorhinal cortex. Disinhibition of this preparation by bicuculline led to interictal-like bursts in the CA3 region that triggered synchronous activity in the entorhinal cortex. Washout of bicuculline after a 1 hr application resulted in a maintained production of hippocampal bursts that continued to spread to the entorhinal cortex. Separation of CA3 from the entorhinal cortex caused the activity in the latter to become asynchronous with CA3 activity in the presence of bicuculline and disappear after washout; however, in CA3, neither the induction of bursting nor its persistence were affected. Associated with the CA3 persistent bursting, a strengthening of recurrent collateral excitatory input to CA3 pyramidal cells and a decreased input to CA3 interneurons was found. Both the induction of the persistent bursting and the changes in synaptic strength were prevented by antagonists of metabotropic glutamate 5 (mGlu5) or NMDA receptors or protein synthesis inhibitors and did not occur in slices from mGlu5 receptor knock-out mice. The above findings suggest potential synaptic mechanisms by which the hippocampus switches to a persistent interictal bursting mode that may support a spread of interictal-like bursting to surrounding temporal lobe regions.

Animals↗
PubMed2003

Activation of perforant path neurons to field CA1 by hippocampal projections.

Previous evidence showed that single-shock stimulation of dorsal hippocampal commissure (PSD) fibers to the entorhinal cortex led to sequential activation of perforant path neurons to the dentate gyrus, dentate granule cells, pyramidal neurons of hippocampal fields CA3 and CA1, and, through reentrant hippocampal impulses, neurons of deep and superficial layers of the entorhinal cortex. The aim of the present study was to ascertain whether perforant path neurons to CA1 are activated by the PSD input and/or by the reentrant hippocampal impulses in this model. Field potentials evoked by single-shock (0.1-Hz) or repetitive (1-4 Hz) PSD stimulation were recorded in anesthetized guinea pigs from the entorhinal cortex, dentate gyrus, fields CA1 and CA3, and subiculum. A current source-density analysis of the evoked potentials was used to localize the input to field CA1 and dentate gyrus. After either single-shock or repetitive PSD stimulation, an early current sink was found in the molecular layer of the dentate gyrus, but no sink was present in CA1. With low-frequency PSD stimulation, a late (approximately 40-ms) surface positive wave occurred in field CA1 alone. During this wave, a current sink was found in the stratum lacunosum-moleculare of CA1, but no sink was present in the dentate gyrus. The late wave had threshold and magnitude related to the building up of the response evoked by reentrant hippocampal impulses in layer III of the entorhinal cortex and was abolished by selective interruption of the perforant path to CA1. The results show that the commissural input to the entorhinal cortex activates perforant path neurons to the dentate gyrus, but not those to field CA1 which are recruited by repetitive hippocampal impulses. These findings show different frequency-dependent patterns of loop operation that might be related to different behaviors.

Algorithms↗
PubMed2000

Cellular and molecular neuropathology of the parahippocampal region in schizophrenia.

The entorhinal cortex, subiculum, and hippocampus have been regions of great interest in both clinical and neuropathological investigations of schizophrenia. Postmortem studies have identified numerous abnormalities, although many remain controversial or unconfirmed. Among the cellular and molecular neuropathological findings are (1) abnormal cytoarchitecture of the entorhinal cortex characterized by poorly formed layer II neuron clusters and laminar disorganization; (2) normal neuron density but smaller neuron size in the superficial lamina of the entorhinal cortex and subiculum; (3) abnormal expression of the microtubule-associated protein MAP2 in the entorhinal cortex and subiculum; (4) aberrant glutamatergic and catecholaminergic innervation of the entorhinal cortex; (5) abnormal mRNA expression of various transcription factors, ion channels, and neurosecretory pathway-related proteins in entorhinal stellate neurons; and (6) an absence of any neurodegeneration. Altogether, these findings suggest that aberrant neurodevelopmental processes play a key role in the pathobiology of schizophrenia and provide a neuroanatomic basis for understanding many of the clinical and neuropsychological abnormalities in the disorder.

Animals↗
PubMed1993

An in vitro study of focal epileptogenesis in combined hippocampal-parahippocampal slices.

Brain slices from adult rats that included ventral hippocampus and adjacent parahippocampal areas were studied at various sites for the appearance of epileptiform discharges as extracellular potassium ([K+]o) was systematically varied over the range of 3 mM to 10 mM. The development of evoked epileptiform discharges (EEDs) and spontaneous epileptiform discharges (SEDs) was monitored in areas CA1, CA3, the hilus of the dentate gyrus (dentate hilus), the granule cell layer of the dentate gyrus (dentate gyrus), subiculum and entorhinal cortex. Increasing [K+]o elicited EEDs in a concentration-dependent manner. The entorhinal cortex and CA1 areas were most susceptible to this effect; the dentate gyrus was least susceptible. Increasing [K+]o also caused an increase in SEDs in all hippocampal areas. Separating entorhinal cortex from the rest of the slice by transections did not abolish discharges in any location. Lesions of the Schaeffer collaterals abolished discharges in CA1 but not in CA3. These findings demonstrate that changes in the extracellular milieu that are associated with epileptiform discharges in vivo are capable of eliciting paroxysmal discharges at multiple loci in the hippocampus and adjacent regions. Further, these findings demonstrate for the first time the intrinsic capacity of the entorhinal cortex to generate epileptiform discharges under in vitro ionic conditions known to occur in the intact brain during seizures.

Action Potentials↗
PubMed2005

Glycogen phosphorylase reactivity in the entorhinal complex in familiar and novel environments: evidence for labile glycogenolytic modules in the rat.

Active and total glycogen phosphorylase were measured histochemically in the entorhinal complex of male Sprague-Dawley rats. Rats were sacrificed from their home cage, or after 5 min in a novel holeboard. Hemispheres from each group were paired, sectioned and processed together. Glycogen phosphorylase reactivity highlighted entorhinal cortex in contrast to less densely stained perirhinal cortex or neocortex. The presubiculum, but not parasubiculum, was strongly reactive for glycogen phosphorylase. Within medial and lateral entorhinal cortex, modularity of active glycogen phosphorylase reactivity was apparent. In inner Layer I there were small ( approximately 50 microm) intense patches of active glycogen phosphorylase. In Layer III there were both small and larger ( approximately 200 microm), patches of active glycogen phosphorylase. Lamina dessicans was reactive. Layers V and VI were relatively unreactive. Exposure to a holeboard intensified the small patches of active glycogen phosphorylase in inner Layer I, while attenuating active glycogen phosphorylase reactivity in Layer III. Total glycogen phosphorylase was unaffected by exposure to the novel environment and exhibited a pattern of continuous dense reactivity suggesting enzyme reserves, particularly in superficial layers of entorhinal cortex. These patterns confirm earlier evidence that glycogenolytic demand in Layers I and III of rat entorhinal cortex is organized in a modular fashion and show that such demand can be modified by brief exposure to a novel holeboard.

Animals↗
PubMed1996

Direct connection between perirhinal cortex and hippocampus is a major constituent of the lateral perforant path.

Single-pulse stimulation of the perirhinal cortex (PRC) evoked field responses in the dorsal hippocampal CA1 region in urethane-anesthetized rats. In depth profiles conducted by moving the PRC stimulating electrode, the largest amplitude hippocampal potential was generated when the stimulating electrode was located within the perirhinal region. More dorsal (temporal cortex) or more ventral (lateral entorhinal cortex) stimulating sites elicited minimal hippocampal potentials. The hippocampal response was maintained during 100 Hz stimulation of the PRC, suggesting that it was monosynaptic, and high-frequency stimulation (400 Hz) of the PRC produced a significant potentiation of hippocampal CA1 field potentials (46.73 +/- 4.14%). When the PRC and the lateral perforant path (LPP) were stimulated separately, the depth/amplitude profiles obtained from a roving recording electrode located within the dorsal hippocampus were similar. In order to determine if fibers from PRC project to the hippocampus via the LPP, the PRC-CA1 and LPP-CA1 potentials were recorded prior to and during procaine (20%, 0.5 microliter) blockade of the LPP. A simultaneous loss of both potentials was observed immediately following procaine infusion, while a commissural control potential was unaffected. Both LPP and PRC potentials returned approximately 30-40 min later. Electrolytic lesions of PRC produced a significant decrease in the amplitude of LPP-hippocampal potentials when testing was conducted 4-5 days postlesion. Lesions of lateral entorhinal cortex or temporal cortex did not produce such effects. These data suggest that a direct pathway from perirhinal cortex to the dorsal hippocampal CA1 field can undergo long-term potentiation (LTP) and that this pathway makes a major contribution to the lateral perforant path.

Animals↗
PubMed1996

Distribution of substance P-immunoreactive neurons and fibers in the monkey hippocampal formation.

Substance P containing neurons was visualized by immunocytochemistry in the monkey hippocampus, subicular complex, and entorhinal cortex. Immunoreactive neurons were found solely in the hilar region of the dentate gyrus, and in strata oriens and pyramidale of Ammon's horn. In the subicular complex, immunoreactive neurons were located in those layers which were close to the alveus, whereas in the entorhinal cortex most of the substance P-positive neurons appeared in the second and third layers above the lamina dissecans. The majority of substance P-containing neurons were large multipolar cells, but small bipolar and multipolar cells also occurred in Ammon's horn, subiculum and entorhinal cortex. Dendrites of immunoreactive cells were smooth and displayed a few small, faintly stained spines which were hard to identify in the light microscopic preparations, but were visible with electron microscopy. Substance P-positive dendrites were exclusively found in the hilar region and never observed in the upper two-thirds of the molecular layer of the dentate gyrus. Moreover, immunoreactive dendrites rarely penetrated the stratum lacunosum-moleculare of Ammon's horn. In the electron microscopic preparations, somal and dendritic features of substance P-positive neurons were similar to those observed for GABAergic local circuit neurons. Axons of the substance P-immunoreactive local circuit neurons were thin and richly arborized in the upper two-thirds of the molecular layer of the dentate gyrus, in the stratum lacunosum-moleculare of Ammon's horn as well as in the subpial layers of the subicular complex and entorhinal cortex. Their terminals formed exclusively symmetric synapses with dendrites and spines. However, substance P-immunoreactive boutons were not found to make symmetric, axosomatic synapses on the granule cells of the dentate gyrus and very few were present on the pyramidal neurons of Ammon's horn, subicular complex, and entorhinal cortex. Hippocampal neurons, which were immunoreactive for substance P, also contained the neuropeptide somatostatin. However, not all of the somatostatin-containing neurons were substance P-immunoreactive. Thus, substance P-positive neurons are a subpopulation of somatostatin immunoreactive, GABAergic neurons. In conclusion, substance P-immunoreactive neurons are ideally suited for feed-back dendritic inhibition which may control the effectiveness of the main excitatory cortical input to the granule cells of the dentate gyrus and pyramidal neurons of the Ammon's horn.

Animals↗
PubMed1998

Transplanted embryonic entorhinal neurons make functional synapses in adult host hippocampus.

Grafts of embryonic entorhinal cortex (EC) or non-entorhinal cortex (NEC) were placed into the hippocampus of adult rats with transection of the perforant paths. Graft-host connectivity was investigated at 4-6 months post-transplantation by recording extracellular evoked responses in hippocampal slice preparations. Electrical stimulation of the grafts evoked excitatory postsynaptic potentials (EPSPs) in the outer molecular layer of the dentate gyrus, and the stratum lacunosum moleculare of CA1, CA3, and elicited population spikes in the granule cell layer and the pyramidal cell layer of CA1, but not CA3. While the latencies and the forms of these evoked response were similar to those in matched control slices from the normal animals, the amplitudes were smaller than normal controls. However, in the slices with NEC grafts, no such responses were recorded when stimulus was applied in similar position in the grafts. The findings suggest that grafted entorhinal neurons make viable synaptic connections with the host hippocampus.

Animals↗
PubMed2005

Gene expression correlates of neurofibrillary tangles in Alzheimer's disease.

Neurofibrillary tangles (NFT) constitute one of the cardinal histopathological features of Alzheimer's disease (AD). To explore in vivo molecular processes involved in the development of NFTs, we compared gene expression profiles of NFT-bearing entorhinal cortex neurons from 19 AD patients, adjacent non-NFT-bearing entorhinal cortex neurons from the same patients, and non-NFT-bearing entorhinal cortex neurons from 14 non-demented, histopathologically normal controls (ND). Of the differentially expressed genes, 225 showed progressively increased expression (AD NFT neurons > AD non-NFT neurons > ND non-NFT neurons) or progressively decreased expression (AD NFT neurons < AD non-NFT neurons < ND non-NFT neurons), raising the possibility that they may be related to the early stages of NFT formation. Immunohistochemical studies confirmed that many of the implicated proteins are dysregulated and preferentially localized to NFTs, including apolipoprotein J, interleukin-1 receptor-associated kinase 1, tissue inhibitor of metalloproteinase 3, and casein kinase 2, beta. Functional validation studies are underway to determine which candidate genes may be causally related to NFT neuropathology, thus providing therapeutic targets for the treatment of AD.

Aged, 80 and over↗
PubMed2004

Postnatal maturation of cortical serotonin lateral asymmetry in gerbils is vulnerable to both environmental and pharmacological epigenetic challenges.

Long-term effects of postnatal differential rearing conditions and/or early methamphetamine (MA) application on serotonin (5-HT) fibre density were investigated in several cortical areas of both hemispheres of gerbils. The aim of this study was twofold: (1) Is the 5-HT fibre innervation of the cerebral cortex lateralised, and (2) if so, do postnatal environmental conditions and/or an early drug challenge interfere with development of 5-HT cerebral asymmetries? For that purpose, male gerbils were reared either under semi-natural or restricted environmental and social conditions, under both conditions once (on postnatal day 14) being treated with either a single dose of MA (50 mg/kg, i.p.) or saline. On postnatal day 110, 5-HT fibres were immunohistochemically stained and innervation densities quantified in prefrontal cortex, insular cortex, frontal cortex, parietal cortex, and entorhinal cortex. It was found that (1) 5-HT innervation in the cerebral cortex was clearly lateralised; (2) direction and extent of this asymmetry were not uniformly distributed over the different areas investigated; (3) both early methamphetamine challenge and rearing condition differentially interfered with adult 5-HT cerebral asymmetry; (4) combining MA challenge with subsequent restricted rearing tended to reverse the effects of MA on 5-HT cerebral asymmetry in some of the cortical areas investigated; and (5) significant responses in 5-HT cerebral asymmetry only occurred in prefrontal and entorhinal association cortices. The present findings suggest that the ontogenesis of cortical laterality is influenced by epigenetic factors and that disturbances of the postnatal maturation of lateralised functions may be associated with certain psychopathological behaviours.

Adrenergic Agents↗
PubMed1999

Regional distribution of tau, beta-amyloid and beta-amyloid precursor protein in the Alzheimer's brain: a quantitative immunolabelling study.

Regional variation in the distribution of SP and NFT within the brain is well documented. Consideration of such variation is potentially of help in formulating models of disease progression. Several models propose that pathological changes in Alzheimer's disease (AD) progress in a step-wise fashion along neuronally connected regions. In this study, we measured tau, Abeta and betaAPP load in different brain regions and examined our results against models of AD progression. Blocks of brain tissue from 45 AD and 15 control cases were immunolabelled for tau, Abeta and betaAPP. Immunolabelled areas were measured as a proportion of the area of the field. Tau load was almost twice as great in the entorhinal cortex than elsewhere in the brain and was least in the cingulate gyrus. In contrast, Abeta was greatest in the cingulate gyrus and least in the entorhinal cortex. BetaAPP rankings were similar to those of tau. Thus the site with the greatest Abeta load (cingulate cortex) had the least tau and the site with the greatest tau load (entorhinal cortex) had the least Abeta. The entorhinal and cingulate cortex are neuronally interconnected. Our results might be explained on the basis that a neurone with its cell body in the entorhinal cortex and axonal terminals in the cingulate cortex shows predominately tau pathology in relation to the cell body and predominately Abeta pathology in relation to its axonal terminals. We conclude that our observations are consistent with previously described models of AD progression. It is possible that tau-rich neurones are associated through their projections to Abeta rich sites. Further work of this kind analysing differential pathological profiles in interconnected brain regions may contribute to refining this model.

Aged↗
PubMed1989

A brain regional analysis of morphologic and cholinergic abnormalities in Alzheimer's disease.

In the brains of 21 patients with Alzheimer's disease (AD) and 10 nondemented controls, senile plaques (SPs), neurofibrillary tangles (NFTs), and three indexes of cholinergic function were quantified in the middle frontal (MF) and superior temporal (ST) cortex, the entorhinal cortex (HEN), and the prosubiculum (HPR) of the hippocampus. Control brains contained few SPs without preferential distribution in any of the brain regions examined, while NFTs were found almost exclusively in the HPR. In brains from patients with AD, an inverse relationship of SPs and NFTs was found in the brain regions examined; SPs were preferentially in the neocortex and NFTs preferentially in the hippocampus. The specific activities of choline acetyltransferase and acetylcholinesterase were reduced in all regions examined, while no significant change in the density of muscarinic binding sites was observed in any region. Numerous NFTs were associated with an earlier age at onset, while the presence of SPs was related to the cholinergic deficit in AD. Earlier-onset (less than 67 years) AD was also associated with a qualitative difference in the regional distribution of NFTs compared with cases with a later onset. In the latter group, most NFTs were observed in the hippocampus, a distribution pattern similar to that observed with normal aging. In AD cases with an earlier onset, NFTs were more globally distributed in the neocortex and allocortex.

Acetylcholinesterase↗
PubMed1985

Alterations in regional brain concentrations of neurotensin and bombesin in Parkinson's disease.

Frozen samples of postmortem human brain tissue from patients with Parkinson's disease (n = 25) and control patients who died without neurological disease (n = 25) were assayed for neurotensin and bombesin by specific radioimmunoassay. Twelve brain regions were examined: substantia nigra, ventral tegmental area, periaqueductal gray matter, caudate nucleus, putamen, globus pallidus, amygdala, hippocampus, nucleus accumbens, frontal cortex, cingulate cortex, and entorhinal cortex. In patients with Parkinson's disease, the concentration of bombesin was significantly decreased in the caudate nucleus and globus pallidus, and the concentration of neurotensin was significantly reduced in the hippocampus. The concentration of neither peptide was significantly altered in the substantia nigra or ventral tegmental area, two regions known to exhibit reductions in other neurotransmitter substances.

Aged↗
PubMed1993

Dementia in Parkinson's disease: biochemical evidence for cortical involvement using the immunodetection of abnormal Tau proteins.

In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti-paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55, 64, and 69, which are known to be specific and reliable biochemical markers of Alzheimer-type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer-type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.

Adult↗
PubMed1992

Regional distribution of DARPP-32 (dopamine- and adenosine 3',5'-monophosphate-regulated phosphoprotein of Mr = 32,000) mRNA in mouse brain.

DARPP-32 (dopamine- and adenosine 3',5'-monophosphate-regulated phosphoprotein of Mr = 32,000) mRNA distribution was examined in adult mouse central nervous system by in situ hybridization. In general, DARPP-32 mRNA was found in regions of brain where cells express the dopamine D1 subtype receptor. Cells of the olfactory tubercle, caudate-putamen, and nucleus accumbens had the highest levels of DARPP-32 mRNA, as did choroid plexus and Purkinje cells. Relatively high levels were found in medial habenula and lateral piriform cortex. Moderate levels were seen in cerebral cortex layer VI, medial piriform cortex, lateral entorhinal cortex, tenia tecta, anterior olfactory nucleus, and lateral bed nucleus of the stria terminalis. Low levels were observed in hippocampus, cerebral cortex layers II and III, olfactory bulb, and the nucleus of the lateral olfactory tract. DARPP-32 mRNA levels in the amygdaloid nuclei varied greatly.

Animals↗