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PubMed1998

Down-regulated NPY receptor subtype-5 mRNA expression in genetically obese mouse brain.

Brain neuropeptide Y (NPY) subtype-5 (Y5 receptor) mRNA expression in lean (+/+) and obese (ob/ob) C57Bl/6 mice was examined using a non-radioactive in situ hybridization detection method. Significant decreases in Y5 receptor mRNA expression were found in the ventromedial, dorsomedial and arcuate hypothalamic nuclei, midline thalamic nuclei, piriform, cingulate and retrosplenial granular cortices of the obese mouse brain. There were minor changes in the amount of Y5 receptor mRNA expression in the hippocampal formation and medial habenular nucleus. Results indicated that Y5 receptor mRNA expression is downregulated in hereditary obese (ob/ob) mice. This is possibly due to over-expression of hypothalamic NPY which occurs in this phenotype.

Animals↗

PubMed1991

[3H]paroxetine binding and serotonin content of rat and rabbit cortical areas, hippocampus, neostriatum, ventral mesencephalic tegmentum, and midbrain raphe nuclei region.

The high-affinity binding of [3H]paroxetine to membranes was measured in different regions of the rat and rabbit brain: cingulate, frontal, parietal, piriform, entorhinal, and visual cortical areas; dorsal and ventral hippocampus; rostral and caudal halves of neostriatum (rat) or caudate nucleus and putamen (rabbit); ventral mesencephalic tegmentum; and midbrain raphe nuclei region. The tissue concentrations of serotonin (5-HT), 5-hydroxyindole-3-acetic acid (5-HIAA) and 5-hydroxy-l-tryptophan (5-HTP) were also determined by high-performance liquid chromatography (HPLC) in the same brain samples. The regional density of [3H]paroxetine binding varied in both species; the highest values (Bmax) were found in the midbrain raphe region and ventral mesencephalic tegmentum. The cortical values ranged from moderate to low, with a significantly higher density in the cingulate cortex of the rat compared with rabbit. In the rat, there was also a higher density in the ventral than dorsal hippocampus, and the caudal than rostral neostriatum. In the rabbit, the hippocampal and neostriatal values were generally lower and more uniform. In both species, there was an excellent correlation between regional 5-HT levels and specific [3H]paroxetine binding (r = 0.87 in the rat and 0.96 in the rabbit). Considering the available quantitative data on the number of 5-HT nerve cell bodies and axon terminals in different regions of the rat brain, it appears likely that the high amount of [3H]paroxetine binding in the midbrain raphe region and ventral mesencephalic tegmentum reflects the presence of 5-HT uptake sites on 5-HT nerve cell bodies and dendrites as well as axon terminals. In other brain regions, the heterogeneous distribution of [3H]paroxetine binding parallels that of the number of 5-HT axon terminals, emphasizing the potential usefulness of this radioligand as a marker of 5-HT innervation density.

5-Hydroxytryptophan↗

PubMed2000

[Spatial organization of the corticopalladial projection system of dog brain].

Spatial organization of corticopallidal projectional system was studied in 11 outbred dogs by method based on horse radish peroxidase transport. It was demonstrated that globus pallidum receives projections predominantly from neocortical zones (motor, premotor, somatosensory, parietal and auditory and from insular field of mesocortex. Mesocortical (prelimbic, orbital and insular) and allocortical (entorhinal, piriform and periamygdalar) including archicortex (subicular part of hippocampal formations) fields project onto ventral pallidum. Entopeduncular nucleus receives projections from neocortical zones (motor, premotor, somatosensory, parietal and auditory), mesocortex (prelimbic, orbital, insular and cingular fields) and allocortex (entorhinal and periamygdalar fields). The data obtained indicate specificity of distribution of cortical afferent projectional fibres in each of nuclei studied which allows to consider globes pallidum as motor zone and ventral pallidum as limbic zone of paladial complex. As projections from functionally different cortical fields were revealed in entopeduncular nucleus it may be suggested that this is the exact site for interaction of functionally different information, including the one received from the cortex.

Animals↗

PubMed1997

Alterations in glutamate transporter protein levels in kindling-induced epilepsy.

There is increasing evidence that levels of glutamate are elevated in certain brain regions immediately prior to and during induction and propagation of seizures. Modulation of high-affinity glutamate uptake is a potential mechanism responsible for the elevated levels observed with Seizures. To date, three distinct Na(+)-dependent glutamate transporters have been cloned from rat and rabbit: GLT-1, GLAST, and EAAC-1. We performed a series of experiments to determine whether levels of these transporters are altered in amygdala-kindled rats. Levels of GLT-1, GLAST, and EAAC-1 were examined in three brain regions (hippocampus, piriform cortex/amygdala, and limbic forebrain) by quantitative immunoblotting using subtype-specific antibodies. GLAST protein was down-regulated in the piriform cortex/amygdala region of kindled rats as early as 24 h after one stage 3 seizure and persisting through multiple stage 5 seizures. In contrast, kindling induced an increase in EAAC-1 levels in piriform cortex/amygdala and hippocampus once the animals had reached the stage 5 level. NO changes in GLT-1 were observed in any region examined. Changes in transporter levels could contribute to the changes in glutamate levels seen with kindling.

ATP-Binding Cassette Transporters↗

PubMedDate not supplied

[Prionic neuroinvasion and cerebellar lesion in Creutzfeldt-Jakob disease].

Examining the histological brain sections of patients with Creutzfeldt-Jakob disease (CJD) showed the accumulation of PrP(CJD) in the cerebellar cortical layers. In nCJD, the prion accumulated mainly in the granular layer in the area of synapses of moss fibers with granular cell dendrites in the cerebellar glomeruli and in the molecular layer in the area of the synapses formed by granular cell axons and great stellate neurons of the granular layer with the dendrites of Purkinje's piriform cells of busket cells and Golgi's cells. PrP(CJD) amyloid plaques were formed in these regions. In sporadic CJD, PrP(CJD) accumulated only in the cerebellar molecular layer in the area of the synapses formed by climbing fibers with the dendrites of Purkinje cells. The findings lead to the conclusion that prion spreads along different nerve fibers through the synapses. The preserved Purkinje cells contacting the plaques suggest that prion is not itself highly neurotoxic.

Cerebellar Cortex↗

PubMed1996

Inhibitory effects of dextromethorphan on c-fos protein expression during focal cerebral ischemia in rats.

AIM: To study the effect of dextromethorphan (DM) in focal cerebral ischemia. METHODS: The c-fos protein was detected immunohistochemically in the brain of rats after focal cerebral ischemia (induced by placing a nylon thread in the lumen of the internal carotid artery) with and without treatment with DM. RESULTS: Focal cerebral ischemia induced c-fos protein expression outside the core territory of the middle cerebral artery (MCA) and neuronal damage in the core territory of the MCA. There was an evident expression of c-fos protein in the ipsilateral regions outside the MCA territory (e.g. cingulate cortices, piriform cortices and entorhinal cortices), and in the contralateral regions of hippocampus after 4-h reperfusion following 1-h MCA occlusion. But morphological results showed severe edema and neuronal damage in the core territory and the ipsilateral hippocampus. DM blocked both the c-fos protein induction and neuronal damage in all regions. CONCLUSION: DM reduced c-fos protein expression and blocked the neuronal damage after focal cerebral ischemia.

Animals↗

PubMed1983

The neuronal architecture of the dorsal division of the medial geniculate body of the cat. A study with the rapid Golgi method.

The neurons in the nuclei of the dorsal division of the medial geniculate body were studied with the rapid Golgi method in kittens and young adult cats. The dorsal nuclei contain two principal cell types: a large stellate neuron with radiate dendrites and a bushy neuron with tufted dendrites, each with extensive dendritic fields. Two sizes of cells with locally arborizing axons (local circuit neurons) were found. The small and commonly observed one is stellate in shape, has a limited dendritic domain, and an axon with multiple, often profuse collaterals ending in the vicinity of the cell. A second, and much less common variety (large local circuit neuron) is somewhat larger and has fewer axon collaterals. Subtle, but distinct variations in these cell types distinguish the deep and superficial dorsal nuclei and also the anterior tier of nuclei (deep dorsal and superficial). These functional differences may correlate with the relative morphological homogeneity of the ventral nucleus compared to the extremely heterogeneous medial division. The dorsal division should be regarded as part of the pulvinar-lateralis posterior complex both structurally and functionally. In the suprageniculate nucleus, the principal neurons are stellate cells with large perikarya and numerous and extensive dendrites covered with appendages. The large axon is devoid of collaterals. A small local circuit cell with several axon collaterals, and sparse, restricted dendrites has also been observed. In the adjacent posterior limitans nucleus, the principal neuron has a medium-sized, piriform or somewhat elongated perikaryon, a few very long radiating dendrites, which may span the depth of the nucleus, and a long, poorly branched axon. Small neurons are also seen here. A comparison of the structure, connections, and function of the medial geniculate body suggests that the dorsal division is predominantly, but probably not exclusively auditory, while the ventral nucleus is entirely auditory and relatively homogeneous, and the medial division, polymodal and heterogeneous with respect to input.

Animals↗

PubMed1995

Quantitative autoradiographic localization in rat brain of alpha 2-adrenergic and non-adrenergic I-receptor binding sites labelled by [3H]rilmenidine.

alpha 2A-Adrenergic receptor (AR) and non-adrenergic imidazoline receptor (I-R) binding sites have been previously characterized in rat cerebral cortex membranes using the N-substituted oxazoline, [3H]rilmenidine ([3H]Ril) [King, P.R. et al., Eur. J. Pharmacol., 218 (1992) 101-108]. In the present study, in vitro autoradiography was used to quantify the regional distribution of these receptors throughout the rat neuroaxis. The distribution and relative density (fmol/mg tissue) of I-Rs was examined in the presence of 1 microM adrenaline to block the adrenergic component of 40 nM [3H]Ril binding and non-specific binding was measured in the presence of another oxazoline, Bay a6781 (10 microM). Both alpha 2A-ARs and I-Rs were broadly, but heterogeneously, distributed. In forebrain, high levels of [3H]Ril-labelled alpha 2A-AR sites were observed in the anterior olfactory nucleus, the piriform, entorhinal and perirhinal cortices, lateral septum, bed nucleus of the stria terminalis, several thalamic nuclei, the amygdala and the arcuate, dorsomedial and posterior hypothalamic nuclei. In hindbrain, alpha 2A-AR sites were concentrated in locus coeruleus, lateral parabrachial nucleus, nucleus of the solitary tract and area postrema. I-R sites accounted for 50% or more of specific [3H]Ril binding (40 nM) in most cortical and hypothalamic nuclei, nucleus of the solitary tract, cranial motor nuclei and most spinal cord layers. The highest densities of I-Rs were found in the arcuate, dorsomedial and posterior hypothalamic nuclei, the locus coeruleus, the area postrema, the cranial motor nuclei and associated with spinal motor neurones. A very high concentration of I-Rs was also detected in the pineal gland. The distribution of alpha 2-AR sites determined resembled that reported with [3H]p-aminoclonidine which appears to specifically label alpha 2-ARs and not I1-R sites in rat brain sections, and [3H]methoxyidazoxan which is a selective alpha 2-AR antagonist. The regional and cellular distribution of I-R binding sites was unlike the distribution of putative I1-R sites labelled by [3H]clonidine in human brain, although comparable autoradiographic mapping studies in rat brain have not been done using this ligand. The regional and cellular distribution of [3H]-labelled I-R binding sites had both similarities and differences to that reported using the imidazoline ligand, [3H]idazoxan, with common labelling of areas such as area postrema, arcuate and interpeduncular nuclei and pineal gland with the two ligands, and differential relative binding levels ([3H]Ril > [3H]idazoxan) associated with hippocampal pyramidal cells and brainstem and spinal motor neurones.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-2 Receptor Agonists↗

PubMed1993

Neuropathology of herpes simplex virus encephalitis in a rat seizure model.

Herpes simplex virus type 1 (HSV-1) is the cause of a serious and often fatal encephalitis. Patients who survive herpes simplex encephalitis (HSE) experience behavioral abnormalities including profound cognitive dysfunctions. We have developed a rat model of acute HSE to investigate the cognitive impairments caused by HSV-1 central nervous system (CNS) infection. Following intranasal inoculation of Lewis rats with a neurovirulent strain of HSV-1, animals shed virus in both ocular and nasal secretions and developed clinical signs of infection, including partial complex motor seizures that eventually generalized. Homogenization assays demonstrated infectious virus in the trigeminal ganglia, olfactory bulbs, and the piriform and entorhinal cortices. Histopathological assessment revealed inflammatory and hemorrhagic lesions in the trigeminal ganglia, olfactory bulbs, amygdala, hippocampus, the piriform and entorhinal cortices, and the spinal trigeminal nuclei. Viral antigens and nucleic acids were also detected within these structures by immunofluorescence microscopy and in situ hybridization, respectively. Viral-induced astrocytic hypertrophy in the CNS was demonstrated by glial fibrillary acidic protein immunoreactivity. Together, these results indicate that HSV-1 has the ability to invade, replicate, and induce site-specific CNS damage in the Lewis rat.

Animals↗

PubMed1991

Lithium modifies convulsions and brain phosphoinositide turnover induced by organophosphates.

Inositol-1-phosphate (Ins1P), an index of phosphoinositide (PI) turnover, was measured in frontal and piriform cortices, caudate, thalamus, hippocampus and cerebellum in saline or LiCl (5 m Eq./kg) pretreated rats 60 min. after graded doses of DFP, paraoxon, or soman. DFP only produced bursts of convulsive activity whereas both paraoxon and soman produced prolonged tonic-clonic convulsions. All three organophosphates (OP) produced convulsions at a lower dose in LiCl than in saline pretreated rats. Regional Ins1P correlated better with the presence or absence of convulsions than with the dose of paraoxon or soman. This was true both in saline and LiCl pretreated rats. In saline pretreated non-convulsing rats, there was a cholinergic increase (1.5-2.0 X) in Ins1P in all brain regions except cerebellum after OP injection. In saline pretreated convulsing rats, there was a marked seizurogenic further increase in Ins1P; highest in caudate (8 X) and cortex (6 X). In LiCl pretreated nonconvulsing rats, the OP-induced cholinergic increase in Ins1P was significant only in caudate, thalamus and hippocampus. In LiCl pretreated convulsing rats, the further seizurogenic increase in Ins1P was less than in saline pretreated rats except in thalamus and hippocampus. Thus, OP produce both a cholinergic and a seizurogenic increase in PI turnover. These data suggest that increased PI turnover in the hippocampus may indicate a lithium-induced lowering of the seizure threshold for OP in limbic regions.

Animals↗

PubMed1988

Efferent connections of the substantia innominata in the rat.

The efferent connections of the substantia innominata (SI) were investigated employing the anterograde axonal transport of Phaseolus vulgaris leucoagglutinin (PHA-L) and the retrograde transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). The projections of the SI largely reciprocate the afferent connections described by Grove (J. Comp. Neurol. 277:315-346, '88) and thus further distinguish a dorsal and a ventral division in the SI. Efferents from both the dorsal and ventral divisions of the SI descend as far caudal as the ventral tegmental area, substantia nigra, and peripeduncular area, but projections to pontine and medullary structures appear to originate mainly from the dorsal SI. Within the amygdala and hypothalamus, which receive widespread innervation from the SI, the dorsal SI projects preferentially to the lateral part of the bed nucleus of the stria terminalis; the lateral, basolateral, and central nuclei of the amygdala; the lateral preoptic area; paraventricular nucleus of the hypothalamus; and certain parts of the lateral hypothalamus, prominently including the perifornical and caudolateral zones described previously. The ventral SI projects more heavily to the medial part of the bed nucleus of the stria terminalis; the anterior amygdaloid area; a ventromedial amygdaloid region that includes but is not limited to the medial nucleus; the lateral and medial preoptic areas; and the anterior hypothalamus. Modest projections reach the lateral hypothalamus, with at least a slight preference for the medial part of the region, and the ventromedial and arcuate hypothalamic nuclei. Both SI divisions appear to innervate the dorsomedial and posterior hypothalamus and the supramammillary region. In the thalamus, the subparafascicular, gustatory, and midline nuclei receive a light innervation from the SI, which projects more densely to the medial part of the mediodorsal nucleus and the reticular nucleus. Cortical efferents from at least the midrostrocaudal part of the SI are distributed primarily in piriform, infralimbic, prelimbic, anterior cingulate, granular and agranular insular, perirhinal, and entorhinal cortices as well as in the main and accessory olfactory bulbs. The cells of origin for many projections arising from the SI were identified as cholinergic or noncholinergic by combining the retrograde transport of WGA-HRP with histochemical and immunohistochemical procedures to demonstrate acetylcholinesterase activity or choline acetyltransferase immunoreactivity. Most of the descending efferents of the SI appear to arise primarily or exclusively from noncholinergic cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2001

Brain activation during odor perception in males and females.

Several studies indicate that women outperform men in olfactory identification tasks. The psychophysical data are more divergent when it comes to gender differences at levels of odor processing which are cognitively less demanding. We therefore compared cerebral activation with H2(15)O PET in 12 females and 11 males during birhinal passive smelling of odors and odorless air. The odorous compounds (odorants) were pure olfactory, or mixed olfactory and weakly trigeminal. Using odorless air as the baseline condition, activations were found bilaterally in the amygdala, piriform and insular cortices in both sexes, irrespective of the odor. No gender difference was detected in the pattern of cerebral activation (random effect analysis SPM99, corrected p < 0.05) or in the subjective perception of odors. Males and females seem to use similar cerebral circuits during the passive perception of odors. The reported female superiority in assessing olfactory information including odor identification is probably an effect of a difference at a cognitive, rather than perceptive level of olfactory processing.

Adult↗

PubMed1998

Zinc-containing afferent projections to the rat corticomedial amygdaloid complex: a retrograde tracing study.

The mammalian amygdaloid complex is densely innervated by zinc-containing neurons. The distribution of the terminals throughout the region has been described, but the origins of these zinc-containing fibers have not. The present work describes the origins of one major component of the zinc-containing innervation of the amygdaloid complex, namely, the component that innervates the corticomedial complex. Selective labeling of zinc-containing axons was accomplished by intracerebral microinfusion of selenium anions (SeO3(2-)), a procedure that produces a ZnSe precipitate in zinc-containing axonal boutons with subsequent retrograde transport to the neurons of origin. After infusions of SeO3(2-) into combinations of cortical, medial, or amygdalohippocampal regions, retrogradely labeled zinc-containing somata were found in all amygdaloid nuclei except for the medial and central nuclei, the bed nucleus of the accessory olfactory tract, the nucleus of the lateral olfactory tract, and the anterior amygdaloid area. Extrinsic zinc-containing projections to the same amygdaloid terminal fields were found to originate from the infralimbic, cingulate, piriform, perirhinal and entorhinal cortices, and from the prosubiculum and CA1. Commissural zinc-containing projections were found to originate from the posterolateral and posteromedial cortical nuclei and from the posterior part of the basomedial nucleus. Zinc-containing neurons have been implicated in the pathophysiology of epilepsy, in cell death after seizure or stroke, and in Alzheimer's disease, all clinical conditions that involve the amygdaloid complex. Identification of the zinc-containing pathways is a prerequisite to the elucidation of zinc's role in these disorders.

Alzheimer Disease↗

PubMed1999

Peripheral administration of novel anti-inflammatories can attenuate the effects of chronic inflammation within the CNS.

In the present study we investigated whether nitroflurbiprofen (NFP) or nitro-aspirin can reduce the inflammatory response induced by continuous infusion of lipopolysaccharide (LPS) into the fourth ventricular space of the rat's brain for 30 days. The chronic LPS infusion produced an extensive inflammation that was particularly evident in the hippocampus, subiculum and entorhinal and piriform cortices. Daily peripheral administration of NFP dose-dependently, and significantly, attenuated the brain inflammation as indicated by the decreased density and reactive state of microglial cells. Daily peripheral administration of nitro-aspirin also attenuated the brain inflammation, but to a much lesser degree than NFP. The results demonstrated that nonsteroidal anti-inflammatory drugs (NSAIDs) could reduce brain inflammation and that NFP is an effective anti-inflammatory agent.

Animals↗

PubMed1999

Relationship between seizure-induced transcription of the DNA damage-inducible gene GADD45, DNA fragmentation, and neuronal death in focally evoked limbic epilepsy.

We investigated the temporal and spatial profile of mRNA transcription for the growth arrest and DNA damage-inducible gene GADD45, DNA fragmentation, and neuronal death in rat brain following focally evoked limbic seizures. GADD45 mRNA was detected by in situ hybridization, whereas fragmented DNA was detected using in situ nick end-labeling by the large (Klenow) fragment of DNA polymerase I. Kainic acid (0.1 microg) was injected into the right amygdala of rats to induce seizures for 45 min, after which diazepam (30 mg/kg) was administered. GADD45 mRNA, DNA fragmentation, and cell death were quantified bilaterally within six limbic brain regions 0-96 h following seizure cessation. All animals underwent seizures of equivalent severity and duration as determined electrographically. In situ hybridization detected bilateral up-regulation of GADD45 mRNA throughout the CA1, CA3, and dentate gyrus of the hippocampus, the piriform and retrosplenial cortices, and the thalamus within 1 h of seizure termination. GADD45 mRNA levels remained elevated for up to 6 h, declining to baseline within all structures by 16 h. Klenow-positive cells were only found within the CA3 pyramidal layer of the ipsilateral hippocampus and appeared 16-72 h following seizure cessation. Morphologic cell death was also restricted to the CA3 subfield. These data demonstrate that focally evoked limbic seizures trigger early bihemispheric GADD45 mRNA transcription within connected limbic structures, whereas subsequent DNA fragmentation and cell death are restricted to selectively vulnerable brain regions.

Amygdala↗

PubMed1998

Expression of VGF mRNA in the adult rat central nervous system.

VGF is a secretory peptide precursor that is expressed and processed by neuronal cells in a cell type-specific fashion. In addition, VGF transcription and secretion are rapidly and relatively selectively induced by neurotrophins and depolarization in vitro. To gain insight into the possible function(s) of VGF in the nervous system, we have carried out a detailed examination of the distribution of VGF mRNA in the adult rat central nervous system by using in situ hybridization. Robust expression was detected in many neurons throughout the brain and spinal cord, in several types of neurons in the retina, and in presumptive chromaffin cells of the adrenal medulla. In the brain, prominent expression of VGF mRNA was observed in neurons of the main and accessory olfactory bulbs; in the anterior olfactory nucleus; in the induseum griseum and taenia tecta; in the olfactory tubercle; in CA1-CA3, the hilus of the dentate gyrus, and the subicular complex of the hippocampal formation; in the piriform, periamygdaloid, transitional, and lateral entorhinal cortices; in the endopiriform nucleus; in the hypothalamus, particularly the preoptic, periventricular, supraoptic, suprachiasmatic, and arcuate nuclei; and in a number of septal, thalamic, amygdaloid, and brainstem nuclei. Labeling was also seen in neurons of the neocortex and transitional cortical areas, particularly in layer V, and in basal ganglia and cerebellum. These data demonstrate that VGF mRNA is expressed much more extensively in the brain than has been described in previous RNA or immunohistochemical studies, and, furthermore, that VGF is widely expressed in the spinal cord and retina.

Amygdala↗

PubMed1992

Haloperidol prevents induction of the hsp70 heat shock gene in neurons injured by phencyclidine (PCP), MK801, and ketamine.

The non-competitive NMDA receptor antagonists, PCP (phencyclidine), MK801, and ketamine produce psychosis in humans and abnormal vacuoles in posterior cingulate and retrosplenial rat cortical neurons. We show that PCP (> or = 5 mg/kg), MK801 (> or = 0.1 mg/kg), and ketamine (> 20 mg/kg) induce hsp70 mRNA and HSP70 heat shock protein in these vacuolated, injured neurons, and PCP also induces hsp70 in injured neocortical, piriform, and amygdala neurons. The PCP, MK801, and ketamine drug induced injury occurs in 30 day and older rats, but not in 0-20 day old rats, and is prevented by prior administration of the antipsychotic drugs haloperidol and rimcazole. Since haloperidol and rimcazole block dopamine and sigma receptors, and since M1 muscarinic cholinergic receptor antagonists also prevent the injury produced by PCP, MK801, and ketamine, future studies will be needed to determine whether dopamine, sigma, M1, or other receptors mediate the injury.

Amygdala↗

PubMed1991

A PHA-L analysis of ascending projections of the dorsal raphe nucleus in the rat.

Ascending projections from the dorsal raphe nucleus (DR) were examined in the rat by using the anterograde anatomical tracer, Phaseolus vulgaris leucoagglutinin (PHA-L). The majority of labeled fibers from the DR ascended through the forebrain within the medial forebrain bundle. DR fibers were found to terminate heavily in several subcortical as well as cortical sites. The following subcortical nuclei receive dense projections from the DR: ventral regions of the midbrain central gray including the 'supraoculomotor central gray' region, the ventral tegmental area, the substantia nigra-pars compacta, midline and intralaminar nuclei of the thalamus including the posterior paraventricular, the parafascicular, reuniens, rhomboid, intermediodorsal/mediodorsal, and central medial thalamic nuclei, the central, lateral and basolateral nuclei of the amygdala, posteromedial regions of the striatum, the bed nucleus of the stria terminalis, the lateral septal nucleus, the lateral preoptic area, the substantia innominata, the magnocellular preoptic nucleus, the endopiriform nucleus, and the ventral pallidum. The following subcortical nuclei receive moderately dense projections from the DR: the median raphe nucleus, the midbrain reticular formation, the cuneiform/pedunculopontine tegmental area, the retrorubral nucleus, the supramammillary nucleus, the lateral hypothalamus, the paracentral and central lateral intralaminar nuclei of the thalamus, the globus pallidus, the medial preoptic area, the vertical and horizontal limbs of the diagonal band nuclei, the claustrum, the nucleus accumbens, and the olfactory tubercle. The piriform, insular and frontal cortices receive dense projections from the DR; the occipital, entorhinal, perirhinal, frontal orbital, anterior cingulate, and infralimbic cortices, as well as the hippocampal formation, receive moderately dense projections from the DR. Some notable differences were observed in projections from the caudal DR and the rostral DR. For example, the hippocampal formation receives moderately dense projections from the caudal DR and essentially none from the rostral DR. On the other hand, virtually all neocortical regions receive significantly denser projections from the rostral than from the caudal DR. The present results demonstrate that dorsal raphe fibers project significantly throughout widespread regions of the midbrain and forebrain.

Animals↗