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PubMed1994

Differential expression of immediate early genes in distinct layers of rat cerebral cortex after selective immunolesion of the forebrain cholinergic system.

The aim of this study was to show whether reduction or loss of cortical cholinergic activity results in any particular change in the expression of the proto-oncogenes c-fos and/or c-jun. To produce cortical cholinergic hypofunction, the monoclonal antibody, 192IgG, to the low-affinity nerve growth factor receptor p75NGFR coupled to a cytotoxin, saporin, was used as an efficient and selective immunotoxin for cholinergic neurons in rat basal forebrain. Brain sections of adult rats that had received an intracerebroventricular injection of 4 micrograms of the 192IgG-saporin were subjected to in situ hybridization using oligonucleotides to detect c-fos and c-jun mRNA. Autoradiographs obtained were evaluated by quantitative image analysis. Seven days following injection of the immunotoxin there was a dramatic loss in acetylcholinesterase staining in frontal, parietal, piriform, temporal, and occipital cortices, hippocampus, and olfactory bulb, but not in the striatum and cerebellum. In situ hybridization revealed a considerable increase in the level of c-fos mRNA in the lateral septum following the cholinergic lesion, whereas in the medial septum both c-fos and c-jun mRNA were elevated. Immunolesioning led to a distinct and specific increase in the level of c-jun but not c-fos mRNA in the parietal and occipital cortex that was restricted to cortical layer IV. These data suggest that reduced cortical cholinergic activity differentially regulates expression of c-fos/c-jun genes in distinct cortical regions of the rat brain.

Acetylcholinesterase↗
PubMed1995

Efferent projections of the paraventricular thalamic nucleus in the rat.

The paraventricular nucleus of the thalamus (PVT) receives input from all major components of the circadian timing system, including the suprachiasmatic nucleus (SCN), the intergeniculate leaflet and the retina. For a better understanding of the role of this nucleus in circadian timing, we examined the distribution of its efferent projections using the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L). The efferent projections of the PVT are loosely organized along its dorsal-ventral and anterior-posterior axes. The anterior PVT sends projections to the SCN; the dorsomedial and ventromedial hypothalamic nuclei; the lateral septum; the bed nucleus of the stria terminalis; the central and basomedial amygdaloid nuclei; the anterior olfactory nucleus; the olfactory tubercle; the nucleus accumbens; the infralimbic, piriform, and perirhinal cortices; the ventral subiculum; and the endopiriform nucleus. A small PHA-L injection, restricted to the ventral portion of the anterior PVT, produces a similar pattern of labeling, except for a marked decrease in the number of labeled fibers in the hypothalamus, cortex, and lateral septum and an increase in labeling in the endopiriform nucleus and basolateral amygdaloid nucleus. The posterior PVT has a more limited efferent distribution than the anterior PVT, terminating in the anterior olfactory nucleus; the olfactory tubercle; the nucleus accumbens; and the central, basolateral, and basomedial nuclei of the amygdala. Our results show that the anterior PVT is ideally situated to relay circadian timing information from the SCN to brain areas involved in visceral and motivational aspects of behavior and to provide feedback regulation of the SCN.

Amygdala↗
PubMed1995

Prolactin binding sites in rat brain and liver: effects of long-term ovariectomy and ovarian steroids.

The effects of long-term ovariectomy on the levels of brain and liver lactogenic binding sites as well as plasma and liver prolactin (PRL) have been investigated in sham-operated and ovariectomized rats receiving either 17 beta estradiol (OVX-E), progesterone (OVX-P), or vehicle (OVX-V). The levels of lactogenic binding sites in the parietal and piriform cortices, amygdala, thalamus, hypothalamus, as well as in the liver were significantly decreased after long-term ovariectomy. Moreover, the levels of plasma and liver PRL were also significantly decreased. Exogenous estradiol and progesterone replacement restored the levels of lactogenic binding sites in the parietal cortex and hypothalamus as well as in the liver. However, plasma and liver PRL levels were significantly increased by estradiol but only restored by progesterone. These results suggest that ovarian steroids influence the levels of lactogenic binding sites and prolactin.

Animals↗
PubMed1990

Induction of c-fos mRNA and protein in neurons and glia after traumatic brain injury: pharmacological characterization.

Focal brain injury in mice induced c-fos mRNA and protein in neurons throughout the damaged neocortex, including the piriform and the entorhinal cortices, as well as in nonneural brain cells (e.g., glia, pia, ependyma). The pattern of c-fos induction after injury suggested that injury led to spreading depression which then led to c-fos induction in neurons. Human neurons in the temporal cortex and hippocampus also showed c-fos protein induction after neurosurgical trauma. The c-fos mRNA and protein induction in mouse neurons was prevented by the noncompetitive NMDA antagonist ketamine but only partially inhibited by the voltage-dependent calcium channel antagonist nifedipine and the calmodulin antagonist trifluoperazine. The c-fos protein induction in nonneural brain cells after injury was not affected by these drugs. Thus, induction of c-fos in neocortical neurons after focal brain injury is partly NMDA receptor mediated.

Animals↗
PubMed1988

Specific [3H]SCH23390 binding to dopamine D1 receptors in cerebral cortex and neostriatum: evidence for heterogeneities in affinity states and cortical distribution.

The tritiated antagonist SCH23390 was used to identify dopamine D1 receptors in the cerebral cortex and neostriatum. The kinetic properties of binding were investigated in parallel experiments with membrane preparations from both tissues. The densities of receptors (Bmax) and the dissociation constants (KD) were determined from saturation curves, and the specificity of binding verified in competition experiments using agonists and antagonists. The cortical D1 receptor displays the same pharmacological selectivity (including stereospecificity) and kinetic properties as the neostriatal D1 receptor. From both the dissociation kinetics by dilution and the competition curves, it could be established that there is an heterogeneity of binding probably due to high- and low-affinity states. Endogenous dopamine, 4-hydroxy-3-methoxyphenylacetic acid, 3,4-dihydroxyphenylacetic acid, and 3-methoxytyramine contents, as well as D1 receptor distribution, were measured for the neostriatum and four localized cortical areas: anterior cingulate, primary somatosensory, primary visual, and piriform-entorhinal. For the regions examined, the distribution of D1 receptors is heterogeneous, but correlates very well (r greater than 0.98) with the endogenous levels of dopamine and its major metabolites.

Animals↗
PubMed2003

fMRI of emotional responses to odors: influence of hedonic valence and judgment, handedness, and gender.

Previous positron emission tomography studies of right-handed individuals show that the left orbitofrontal cortex is dominant during emotional processing of odors. We collected functional magnetic resonance imaging data from 28 subjects to study this network as a function of odor hedonic valence (pleasant vs. unpleasant), active hedonic judgments versus passive sensation of hedonically charged odors, handedness, and gender. Two functional runs were performed, with pleasant and unpleasant odors presented in different epochs. In the first run, subjects passively smelled odorants, whereas in the second run they rated degree of odor pleasantness or unpleasantness by using a "finger-span" technique that simulated a visual rating scale. Electrodermal and plethysmography responses were simultaneously recorded to control for covert, physiological manifestations of the emotional response. The piriform-amygdala area and ventral insula were activated more for unpleasant than pleasant odors. More extreme ratings were also associated with higher electrodermal amplitude, suggesting that activation stemmed more from emotional or hedonic intensity than valence, and that unpleasant odors induced more arousal than pleasant odors. Unpleasant odors activated the left ventral insula in right-handers and the right ventral insula in left-handers, suggesting lateralized processing of emotional odors as a function of handedness. Active decisions about odor pleasantness induced specific left orbitofrontal cortex activation, implicating the role of this area in the conscious assessment of the emotional quality of odors. Finally, left orbitofrontal cortex was more active in women than men, potentially in relation to women's well-documented advantage in odor identification.

Adult↗
PubMed1987

Organization of amygdaloid projections to the mediodorsal thalamus and prefrontal cortex: a fluorescence retrograde transport study in the rat.

Previous studies have shown that the amygdala projects to both the mediodorsal thalamic nucleus (MD) and its cortical projection area, the prefrontal cortex (PFC). In this investigation rats received injections of different fluorescent retrograde tracers (true blue and diamidino yellow) into MD and either the lateral, polar, or medial PFC in order to examine the relationship of amygdaloid neurons with cortical and/or thalamic projections. PFC injections labeled neurons in the basolateral (BL), basomedial (BM), ventral endopiriform (EnV), and rostral lateral nuclei as well as the periamygdaloid cortex (PAC) and the medial part of the amygdalohippocampal area (AHA). In BL, which contained the great majority of neurons projecting to PFC, most labeled cells were concentrated in particular parts of the nucleus and were topographically organized. The overwhelming majority of labeled neurons in BL were large pyramidal or piriform cells that correspond to class I neurons described in Golgi studies. Occasional small neurons with thin dendrites were also observed; these cells may be class II neurons. MD injections labeled numerous cells in the anterior division of the cortical nucleus, medial nucleus, and caudomedial part of the central nucleus. Moderate numbers of labeled cells were found in caudal portions of BM and PAC, whereas scattered cells were observed throughout the rest of the amygdala with the exception of the lateral nucleus. In BL and AHA many MD-projecting neurons were observed along nuclear boundaries and in the adjacent white matter. Neurons in BL, BM, and AHA usually had large elongated or irregular somata and two to four primary dendrites that branched sparingly. Other cells had smaller ovoid somata. The morphology and distribution of MD-projection cells in the basolateral amygdala indicate that they are primarily large class II neurons. Double-labeled amygdaloid neurons, labeled by both cortical and thalamic injections, were observed only in a small number of animals. Control experiments suggest that most of the double-labeled cells in these cases were artifacts caused by spread of the thalamic injectate into the third ventricle with subsequent uptake by fibers in the anterior commissure. Thus the findings of this study suggest that different neuronal populations in the amygdala project to the two poles of the MD-PFC system. In the basolateral amygdala class I neurons are the predominant cell type involved in PFC projections, whereas a subpopulation of class II neurons, hitherto thought to be primarily local-circuit neurons, project to MD.

Amidines↗
PubMed1999

Different nitric oxide synthase inhibitors cause rapid and differential alterations in the ligand-binding capacity of transmitter receptors in the rat cerebral cortex.

Inhibitors of nitric oxide (NO) synthesis reduce postlesional neuronal death during reperfusion injury by reducing the NO-mediated increase in excitatory neurotransmitter-release. The protective effects of various NO-synthase (NOS) inhibitors differ due to their isoform selectivity. The effects of NO-mediated excessive neurotransmitter supply are transmitted via specific neurotransmitter receptors expressed by the target cells. We report changes in the ligand-binding of different excitatory and inhibitory neurotransmitter-receptors studied by in vitro receptor autoradiography after in vivo-application of NOS-inhibitors. Since the constitutively expressed neuronal NOS-I is area-specifically distributed within the rat cortex, numerous cortical areas were studied in non-lesioned rats, in order to analyze the area-specific effects of NOS-inhibitors. The results showed that the NOS-I-specific inhibitor 7-nitroindazole increased binding of 3H-muscimol, 3H-pirenzepine and 3H-kainate, whereas the less isoform-specific, general NOS-inhibitor L-nitroarginine increased binding of 3H-muscimol and 3H-AMPA in most cortical areas, leaving 3H-kainate binding almost unchanged. The water soluble L-nitroarginine-methylester caused similar effects to those of L-nitroarginine which changed over a period of chronic treatment. The inhibitory GABAA-receptors were increased after NOS-inhibition in most cortical areas, whereas binding of 3H-Oxotremorine-M (acetylcholine receptors), 3H-MK-801 (NMDA-receptors) and 3H-AMPA (AMPA receptors) was affected differently among the cortical areas. Strongest alterations of ligand-binding capacity after administration of NOS-inhibitors were seen in cortical areas known to contain the highest packing densities of NOS-I-positive interneurons such as the piriform and entorhinal cortices, indicating that, in normal animals, neurotransmission and probably cognitive information processing would be affected by the pharmacological modulation of nitric oxide production.

Animals↗
PubMed1994

A theoretical and neurophysiological consideration on the pathogenesis of positive symptoms of schizophrenia: implications of dopaminergic function in the emotional circuit.

The implications of the emotional circuit and the gating mechanism by dopamine (DA) proposed by Maeda in the pathogenesis of positive symptoms of schizophrenia were reconsidered based upon recent advances and findings in the fields of neurophysiology and neuropharmacology and in biological studies of schizophrenia. The gating mechanism by DA was partly supported by new evidence that glutamatergic or GABAergic neurotransmission, which mediates the hippocampo-lateral septal or the piriform cortico-amygdaloid neuronal connections, is likely to be modulated by DA. The compensation-facilitating or gating functions of DA was considered again to play an important role in producing positive symptoms in schizophrenics, who have been suggested to have morphological abnormalities in the limbic system or in the prefrontal cortex prior to the appearance of positive symptoms.

Brain↗
PubMed2003

Rhythmically discharging basal forebrain units comprise cholinergic, GABAergic, and putative glutamatergic cells.

The basal forebrain plays important roles in arousal, learning, and memory by stimulating cortical activation characterized by rhythmic slow theta and high-frequency beta-gamma activities. Although cholinergic neurons play a significant part in these roles, other, including GABAergic, neurons appear to contribute. Using juxtacellular labeling with neurobiotin of neurons recorded within the magnocellular preoptic-substantia innominata area in urethan-anesthetized rats, we show that in addition to cells that are cholinergic or GABAergic, other cells that are neither fire rhythmically in correlation with stimulation-induced rhythmic slow activity on the cortex. Neurons with the characteristics of the noncholinergic/nonGABAergic cells contain phosphate-activated glutaminase (PAG), the synthetic enzyme for transmitter glutamate and may thus be glutamatergic. Within their oscillatory spike trains, putative glutamatergic neurons fire at a lower frequency (~20 Hz) than the GABAergic neurons (~40 Hz) and the cholinergic neurons (average: 75 Hz), whose spike trains include high-frequency bursts. The three groups all discharge rhythmically at a slow frequency in correlation with rhythmic slow activity recorded on the prefrontal, entorhinal, piriform and olfactory bulb cortices. The predominant slow frequency corresponds to the respiratory-olfactory rhythm, which is commonly slower than, yet can be as fast as, the hippocampal theta rhythm during certain coordinated behaviors, such as sniffing-whisking. While stimulating higher frequency beta-gamma activities, putative glutamatergic together with GABAergic and cholinergic cells may thus collectively modulate rhythmic slow activity and thereby promote coherent processing and plasticity across distributed cortical networks during coordinated behaviors and states.

Acetylcholine↗
PubMed1976

Fiber trajectories of olfactory bulb efferents in the hamster.

Olfactory bulb efferents sweep caudally over the surface of the piriform lobe in a broad fiber sheet. The internal organization of this axon population was analysed by topologically transforming the cortical surface from its in situ cylindrical form into an unrolled (flattened) map. The distribution of degeneration elicited by restricted bulb lesions and fiber transections was then reconstructed onto this map. Most of the projection cortex of the main olfactory bulb is innervated in a widespread, non-topographic manner by axons that collect in the compact bundle of the lateral olfactory tract (LOT). LOT collateral branches bound for the prepiriform cortex veer laterally off the main trajectory of the tract at an angle of 50 degrees or less. Thus, transection of discrete fiber populations leaves only a small wedge-shaped pocket of totally denervated cortex distal to the cut. The medial half of the olfactory tubercle and the hippocampal rudiment receive their bulbar input along medially disposed fibers that do not join the LOT proper. The lateral half of the olfactory tubercle, however, receives an input from LOT fiber collaterals as well as these medial bulb efferents. Finally, much of the corticomedial amygdaloid complex receives fibers from the accessory olfactory bulb along a specialized subdivision of the LOT, the accessory olfactory tract. These observations are expressed in a schematic summary of the trajectories of olfactory bulb efferents as they appear in the unrolled map and in the more standard ventral view of the hamster brain.

Animals↗
PubMed1995

Stimulation of glucose utilization in the rat claustrum by pain.

The involvement of the claustrum in processing of somatosensory information was investigated using the formalin test as an established pain test. The metabolic activity of the claustrum and other brain structures belonging to the somatosensory system was assessed by autoradiographic method of the uptake of (3H)-labelled 2-deoxyglucose (2-DG). Glucose utilization in the claustrum was stimulated by subcutaneous injection of formalin into the front paw. The increase of radioactivity was observed not only in the claustrum, but also in the anterior pretectum, the ventral thalamic nucleus, the somatosensory, insular and piriform cortices on the contralateral side to formalin stimulation. After stereotactical injection of morphine into the contralateral pretectum to stimulation side, uptake of 2-DG in the claustrum was abolished. These results indicate that the claustrum is an important relay nucleus in the somatosensory system, which may convey somatosensory information from the pretectum to the cerebral cortex, thus by-passing the thalamus, throughout the pretecto-claustro-cortical pathways.

Animals↗
PubMed2001

Prenatal cocaine exposure produces consistent developmental alterations in dopamine-rich regions of the cerebral cortex.

Administration of cocaine to pregnant rabbits produces robust and long-lasting anatomical alterations in the dopamine-rich anterior cingulate cortex of offspring. These effects include increased length and decreased bundling of layer III and V pyramidal neuron dendrites, increases in parvalbumin expression in the dendrites of interneurons, and increases in detectable GABAergic neurons. We have now examined multiple cortical regions with varying degrees of catecholaminergic innervation to investigate regional variations in the ability of prenatal cocaine exposure to elicit these permanent changes. All regions containing a high density of tyrosine hydroxylase-immunoreactive fibers, indicative of prominent dopaminergic input, exhibited alterations in GABA and parvalbumin expression by interneurons and microtubule-associated protein-2 labeling of apical dendrites of pyramidal neurons. These regions included the medial prefrontal, entorhinal, and piriform cortices. In contrast, primary somatosensory, auditory and motor cortices exhibited little tyrosine hydroxylase staining and no measurable cocaine-induced changes in cortical structure. From these data we suggest that the presence of dopaminergic afferents contributes to the marked specificity of the altered development of excitatory pyramidal neurons and inhibitory interneurons induced by low dose i.v. administration of cocaine in utero.

Animals↗
PubMed1999

Progressive parenchymal deposition of beta-amyloid precursor protein in rat brain following global cerebral ischemia.

In addition to producing acute neuronal necrosis within selectively vulnerable brain regions, our recent studies have shown that global cerebral ischemia may also be followed by protracted degenerative changes occurring over the course of 10 weeks. Chronic brain pathology may be associated with the abnormal deposition of beta-amyloid precursor protein (betaAPP). In the present study, we used a monoclonal antibody to the N-terminal portion of betaAPP to characterize the brains of rats surviving 1-10 weeks following 10 min of global brain ischemia produced by bilateral carotid artery occlusions plus systemic hypotension. After ischemia, increased betaAPP immunolabeling emerged in several brain regions. In the hippocampus, granular deposits appeared in the damaged CA1 area by 2 weeks, and by 4-10 weeks the remnants of necrotic CA1 neurons were also immunolabeled. In striatum and thalamus, regions with necrotic cell death also revealed granular betaAPP deposits. The neocortex was devoid of overt ischemic neuronal damage but revealed prominent betaAPP immunoreactivity. Large ovoid deposits of low-density betaAPP immunostaining occurred in cortical neurons at 1-2 weeks. At 4-10 weeks, large round or oval deposits immunoreactive for betaAPP appeared in several cortical regions. The highest density of deposits was seen in the temporal and piriform cortices. Our results indicate that abnormal betaAPP deposition may result from ischemic as well as chronic neurodegenerative processes.

Amyloid beta-Protein Precursor↗
PubMed2004

Zac1 is up-regulated in neural cells of the limbic system of mouse brain following seizures that provoke strong cell activation.

Zac1, a new zinc-finger protein that regulates both apoptosis and cell cycle arrest, is abundantly expressed in many proliferative/differentiation areas during brain development. In the present work, we studied Zac1 gene expression and protein in experimental seizure models following i.p. injection of pentylenetetrazole (PTZ) or kainic acid (KA). Following KA treatment, an early and intense up-regulation of Zac1 is detected in the limbic areas, such as the hippocampus, cortex and amygdaloid and hypothalamic nuclei. Pre-treatment with MK-801, an antagonist of the NMDA receptors, fully blocks the effect of KA in the hippocampus, whereas it only attenuates KA-induced Zac1 up-regulation in the other areas of the limbic system. A reduced induction is obtained with PTZ-treated animals, specifically in the entorhinal and piriform cortices as well as in amygdaloid and hypothalamic nuclei. Thus, Zac1 is highly induced in the seizure models that generate strong neuronal stimulation and/or extensive cell damage (cell death), reinforcing its putative role in the control of the cell cycle and/or apoptosis. Moreover, strong induction is observed in the granular cells of the dentate gyrus (which are resistant to neurodegeneration) and in some glial cells of the dentate gyrus and subventricular zone, suggesting that Zac1 may be implicated in the mechanisms of neural plasticity following injury.

Animals↗
PubMed2001

Early-generated preplate neurons in the developing telencephalon: inward migration into the developing striatum.

Specialized subsets of early-generated neurons provide the cellular cues that are necessary for the establishment of characteristic cell and fiber interactions in each brain region. During the development of the mammalian cerebral cortex, the early-generated cells line up in the most superficial part of the telencephalic pallium forming the preplate. It has been generally thought that the preplate derivatives are exclusively located in the cortical region and govern the early histogenetic phase of cortical development. However, we here disclose an unexpected evidence that a subset of early-generated neurons of the piriform preplate migrate inward into and disperse within the subcortical structure striatum during the embryonic stage. Their migratory route is unique and its direction is opposite to the ordinary migration of neuronal precursors directed outward from the periventricular germinal zone. After immigrating into the developing striatum, these early-generated cells are closely associated with the intrastriatal fascicules of axons. The majority of these cells are eliminated by apoptotic cell death during the early postnatal stage. Based on these findings, we propose a new concept: the preplate neurons may not only direct cortical histogenesis but also change their location to play a role in the development of subcortical structures.

Animals↗
PubMed1998

Inducibility of c-Fos protein in visuo-motor system and limbic structures after acute and repeated administration of nicotine in the rat.

To identify neuroanatomical substrates affected by nicotine, we have studied its effects after acute and repeated administration through the c-Fos protein inducibility in various brain structures. Ninety minutes after acute nicotine (0.35 mg/kg, s.c.) the number of c-Fos-like immunoreactive nuclei was consistently increased in visuo-motor structures such as the superior colliculus, the medial terminal nucleus of accessory optic tract, and the nucleus of the optic tract. The anteroventral and lateroposterior thalamic nuclei, connected with the retina and involved in limbic processing, showed a c-Fos induction. c-Fos was preferentially induced in terminal fields of neurons of the ventral tegmental area such as the nucleus accumbens, the central amygdala, the lateral habenula, the lateral septum, as well as the cingulate, medial prefrontal, orbital and piriform cortices. In chronically treated rats (0.35 mg/kg s.c., 3 x day for 14 days), the last nicotine injection given on the 15th day was still able to induce 90 minutes later c-Fos protein in visuo-motor, retino-limbic, subcortical, and cortical limbic structures. Moreover, this chronic treatment produced an additional recruitment of c-Fos-positive nuclei in the cingulate cortex, the core and the ventral shell of the nucleus accumbens. c-Fos induction after nicotine differs from that reported after other addictive drugs in terms of pattern and chronic inducibility, indicating that different mechanisms are involved for maintaining this transcription factor. In addition to a preferential sensitivity of mesolimbic dopaminergic neurons to nicotine, activation of visuo-limbic and limbic regions could be relevant for understanding some context-dependent and addictive behaviors produced by nicotine.

Aged↗
PubMed2005

Afferent connections of the amygdalopiriform transition area in the rat.

The amygdalopiriform transition area (APir) is often considered part of the lateral entorhinal cortex (Entl). However, in contrast to Entl, APir densely innervates the central extended amygdala (EAc) and does not project to the dentate gyrus. In order to gain a more comprehensive understanding of these territories, the afferent connections of APir were examined in the rat with retrograde (cholera toxin B subunit or FluoroGold) and anterograde tracers (Phaseolus vulgaris leucoagglutinin) and compared to those of the neighboring Entl. The results suggest that APir and Entl are interconnected and receive topographically organized hippocampal projections. Both are targeted by the olfactory bulb, the piriform, posterior agranular insular and perirhinal cortices, the ventral tegmental area, dorsal raphe nucleus, and locus coeruleus. Most importantly, the data reveal that APir and Entl also have specific inputs and should be viewed as separate anatomical entities. The APir receives robust projections from structures affiliated with the EAc, including the anterior basomedial and posterior basolateral amygdaloid nuclei, the gustatory thalamic region, parasubthalamic nucleus, and parabrachial area. The Entl is a major recipient for amygdaloid projections from the medial part of the lateral nucleus and the caudomedial part of the basolateral nucleus. Moreover, the medial septum, subicular complex, nucleus reuniens, supramammillary region, and nucleus incertus, which are associated with the hippocampal system, preferentially innervate the Entl. These data underscore that APir processes olfactory and gustatory information and is tightly linked to EAc operations, suggesting that it may play a role in reward mechanisms, particularly in hedonic aspects of feeding.

Afferent Pathways↗