[Brain topometry in man; red nucleus, Luy's nucleus, amygdaloid nucleus].
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Amygdala↗
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Dynorphinergic GABA neurons are a target of both typical and atypical antipsychotic drugs in the nucleus accumbens shell, central amygdaloid nucleus and thalamic central medial nucleus.
Administration of typical and atypical antipsychotic drugs leads to activation of cells in the nucleus accumbens shell, central amygdaloid nucleus, and midline thalamic central medial nucleus, implicating important shared effects of these drugs. However, the exact cell types responding to antipsychotic drugs in the nucleus accumbens shell, central amygdaloid nucleus, and midline thalamic central medial nucleus are unclear. We report here that, in a rat model, the results of studies using double immunofluorescence labeling with antibodies directed against markers specific to candidate cell types suggest that the cells responding to haloperidol and clozapine in all three sites are: 1) neurons, rather than astrocytes; 2) inhibitory GABA neurons, but not acetylcholinergic neurons; and 3) dynorphin-containing GABA neurons, but not M-enkephalin-containing GABA neurons. The present study provides pharmacological evidence, at the cellular level in vivo, that the shared effects of antipsychotic drugs, whether typical and atypical, is activation of dynorphinergic GABA neurons in the nucleus accumbens shell, central amygdaloid nucleus, and midline thalamic central medial nucleus. Alternative ways to modulate dynorphinergic GABA neuronal activity or its target receptors might present an important new avenue for the treatment of schizophrenia and other psychotic disorders.
Acetylcholine↗
Centrally administered orexin-A activates corticotropin-releasing factor-containing neurons in the hypothalamic paraventricular nucleus and central amygdaloid nucleus of rats: possible involvement of central orexins on stress-activated central CRF neurons.
We examined the effects of centrally administered orexin-A on corticotropin-releasing factor (CRF)-containing neurons in the hypothalamic paraventricular nucleus (PVN) and the central amygdaloid nucleus (CeA) of rats, using dual immunostaining for CRF and Fos. Ninety minutes after intracerebroventricular administration of orexin-A, approximately 96% and 45% of CRF-containing neurons expressed Fos-like immunoreactivity (LI) in the PVN and the CeA, respectively. We also examined the effects of immobilized stress and cold exposure on orexin-A-containing neurons in the rat hypothalamus using dual immunostaining for orexin-A and Fos. After immobilized stress for 20 min and cold exposure at 4 degrees C for 30 min, approximately 24% and 15% of orexin-A-containing neurons expressed Fos-LI, respectively. These results suggest that orexins in the central nervous system may be involved in the activation of central CRF neurons induced by stress.
Amygdala↗
Coexistence of peptides (corticotropin releasing factor/neurotensin and substance P/somatostatin) in the bed nucleus of the stria terminalis and central amygdaloid nucleus of the rat.
Coexistence of corticotropin releasing factor and neurotensin and also of substance P and somatostatin was demonstrated in the lateral bed nucleus of the stria terminalis and the central amygdaloid nucleus of the rat, by means of a light microscopic mirror method or immunofluorescent double staining. Using the former technique, a major proportion of corticotropin releasing factor-like immunoreactive cells were found to display neurotensin-like immunoreactivity in the dorsal subdivision of the lateral bed nucleus of the stria terminalis and the lateral subdivision of the central amygdaloid nucleus. On the other hand, the immunofluorescent method showed that a significant number of neurons with both substance P- and somatostatin-like immunoreactivity were located in the ventral subdivision of the lateral bed nucleus of the stria terminalis and the medial subdivision of the central amygdaloid nucleus. Distribution patterns of such co-localized peptides may indicate that there are morphological and biochemical similarities between the dorsal subdivision of the lateral bed nucleus of the stria terminalis and the lateral subdivision of the central amygdaloid nucleus, as well as between the ventral subdivision of the lateral bed nucleus of the stria terminalis and the medial subdivision of the central amygdaloid nucleus. Previous studies have demonstrated that peptide-containing neurons in the lateral bed nucleus of the stria terminalis and central amygdaloid nucleus, such as corticotropin releasing factor-, neurotensin-, substance P- and somatostatin-like immunoreactive cells, project to the lower brainstem. The results of the present study suggest that corticotropin releasing factor/neurotensin and substance P/somatostatin neurons may be part of the lateral bed nucleus of the stria terminalis/central amygdaloid nucleus-lower brainstem pathways.
Amygdala↗
Synaptic reorganization in the medial amygdaloid nucleus after lesion of the accessory olfactory bulb of adult rat. II. New synapse formation in the medial amygdaloid nucleus by fibers from the bed nucleus of the stria terminalis.
The rearrangement of terminations from the bed nucleus of stria terminalis (BST) was examined in the medial amygdaloid nucleus (MAN) at 2 months following the lesion of the accessory olfactory bulb (AOB) using an electron microscopy and degeneration study. At 2 days following a BST lesion, the number of degenerating synapses was 0.7 +/- 0.1 (mean +/- S.E.M.) per unit area (2500 microns2) in the molecular layer, and 3.0 +/- 0.3 in the cellular part. At 2 months after an AOB lesion, the degenerating synapses from the AOB had completely disappeared from the MAN. The BST was then lesioned at 2 months after the AOB lesion and, at 2 days following this BST lesion, the degenerating synapses were counted in MAN. The numbers observed were 3.3 +/- 0.6 per unit area in the molecular layer and 4.5 +/- 0.4 in the cellular part. Therefore, the number of these degenerating synapses increased significantly within the molecular layer, though, in the cellular part the number of synapses was not significantly elevated over control. No differences in postsynaptic profiles (ratio of synapses on dendritic spine to dendritic shaft) were observed after the AOB lesion. These results indicate that the BST fibers formed new synapses in the molecular layer following the denervation of AOB fibers. The possibility of new synapse formation by other afferent fibers in addition to the AOB fibers is discussed as is the relationship between lesion induced synaptic reorganization and functional recovery after injury.
Amygdala↗
Topographic organization of collateral projections from the basolateral amygdaloid nucleus to both the prefrontal cortex and nucleus accumbens in the rat.
The basolateral amygdaloid nucleus, a limbic/autonomic center in the basal forebrain, has been known to send projection fibers to the prelimbic and dorsal agranular insular areas in the prefrontal cortex, as well as to the nucleus accumbens. In the present study, we investigated single basolateral amygdaloid nucleus neurons sending their axons to both the prefrontal cortex and nucleus accumbens. The fluorescent retrograde double-labeling technique was employed in the rat; True Blue was injected into the prelimbic or dorsal agranular insular cortex, and Diamidino Yellow into the medial or lateral part of the nucleus accumbens. The majority of basolateral amygdaloid nucleus neurons projecting to the dorsal agranular insular cortex or prelimbic cortex were located, respectively, in the rostral two-thirds or caudal two-thirds of the nucleus, while those projecting to the medial or lateral part of the nucleus accumbens were diffusely distributed in the nucleus. Almost 50% of basolateral amygdaloid nucleus neurons projecting to the prelimbic cortex sent their axon collaterals to the medial part of the nucleus accumbens. About 30-40% of basolateral amygdaloid nucleus neurons projecting to the dorsal agranular insular cortex or prelimbic cortex issued their axon collaterals to the lateral part of the nucleus accumbens. The axons bifurcating to both the dorsal agranular insular cortex and lateral part of the nucleus accumbens, those bifurcating to both the prelimbic cortex and lateral part of the nucleus accumbens, or those bifurcating to both the prelimbic cortex and medial part of the nucleus accumbens arose preferentially from the rostral, middle or caudal parts of the basolateral amygdaloid nucleus, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Amidines↗
Colocalization of peptide and glucocorticoid receptor immunoreactivities in rat central amygdaloid nucleus.
The central amygdaloid nucleus (ACe) is part of the amygdaloid complex that participates in adrenocorticotrophin secretion, stress-related reactions and behavioral functions. The ACe contains numerous glucocorticoid receptor (GR)-immunoreactive (IR) neurons, and in addition it has been shown to contain several neuropeptide-IR somata and nerve terminals. In order to study the relationship between the GR- and neuropeptide-IR structures we mapped the distribution of GR-like immunoreactivity (LI) in amygdaloid complex and colocalized the neuropeptide- and GR-LIs in the ACe. In the amygdaloid complex the central, medial and cortical nuclei contained a high number of GR-IR neurons, whereas a moderate number of GR-IR neurons were observed in the basolateral and basomedial nuclei. Only a few GR-IR neurons were seen in the lateral nucleus. In the ACe, the majority of corticotrophin-releasing factor (CRF)-, met-enkephalin (met-ENK)-, neurotensin (NT)- and somatostatin (SOM)-IR neurons contained also GR-IR. About half of the substance P (SP)-IR neurons were seen to contain GR-IR, whereas only some of the few vasoactive intestinal polypeptide and cholecystokinin-IR neurons showed GR-LI. Nerve terminals containing calcitonin gene-related peptide and the above mentioned peptides were seen in close contact with the GR-IR neurons. These results suggest that the glucocorticoids may modulate directly the neurotransmitter synthesis of the CRF-, met-ENK, NT-, SOM- and SP-IR cells in the ACe.
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Role of the central amygdaloid nucleus in shaping the discharge of gustatory neurons in the rat parabrachial nucleus.
The central amygdaloid nucleus (CeA) receives projection from the parabrachial nucleus (PBN) gustatory neurons and descendingly projects to the PBN. To assess if the CeA is involved in modulating the activity of gustatory neurons in the PBN, the effects of electrical stimulation and electrolytic lesion of CeA on PBN gustatory neurons were observed. Of 60 neurons observed, 30 were classified as NaCl-best, 18 as HCl-best, 5 as Quinine HCl (QHCl)-best, and 7 as sucrose-best. During CeA stimulation, the responses to at least one effective stimulus were inhibited in most PBN neurons, with the response magnitudes to HCl and QHCl significantly decreased (P<0.01). In contrast, bilateral lesions of CeA facilitated the responses to HCl and QHCl (P<0.01). According to the best-stimulus category, the effects on the responses to HCl and QHCl were similarly subjected to these modulations either during electrical stimulation or after electrolytic lesions of CeA. Analyses of across-unit patterns indicated that the CeA stimulation increased the chemical selection of PBN taste neurons while the CeA lesions depressed the effect on the chemical selection between NaCl and QHCl. These findings suggest that the CeA may be involved in mediating feeding behavior via modulating the activity of gustatory neurons of PBN.
Action Potentials↗
Serotonergic and nonserotonergic neurons in the dorsal raphe nucleus send collateralized projections to both the vestibular nuclei and the central amygdaloid nucleus.
Using a combination of double retrograde tracing and serotonin immunofluorescence staining, we examined whether individual serotonergic and nonserotonergic neurons in the dorsal raphe nucleus are sources of collateralized axonal projections to vestibular nuclei and the central amygdaloid nucleus in the rat. Following unilateral injections of Diamidino Yellow into the vestibular nuclei and Fast Blue into the central amygdaloid nucleus, it was observed that approximately one-fourth of the dorsal raphe nucleus neurons projecting to the vestibular nuclei send axon collaterals to the central amygdaloid nucleus. Immunofluorescence staining for serotonin revealed that more than half of the dorsal raphe nucleus neurons from which these collateralized projections arise contain serotonin-like immunoreactivity. These findings indicate that a subpopulation of serotonergic and nonserotonergic dorsal raphe nucleus cells may act to co-modulate processing in the vestibular nuclei and the central amygdaloid nucleus, regions implicated in the generation of emotional and affective responses to real and perceived motion.
Amidines↗
Testosterone effects on development of vasopressin messenger RNA expression in the bed nucleus of the stria terminalis and medial amygdaloid nucleus in male rats.
To study whether testicular secretions in development have a permanent influence on vasopressin (AVP) messenger RNA expression in the bed nucleus of the stria terminalis (BST) and medial amygdaloid nucleus (MA), male rats that were castrated neonatally or in adulthood were compared after both were similarly treated with testosterone. Males castrated neonatally had fewer cells that were labeled for AVP mRNA and a less density of grains per labeled cell in the BST and MA than males castrated in adulthood. These data indicate that testicular secretions in early development have an organizational effect on AVP mRNA expression in the BST and MA, and this effect was accomplished not only by determining the number of cells that produce AVP, but also by influencing the ability of each individual cell to produce AVP.
Amygdala↗
Species differences in the vasopressin-immunoreactive pathways in the bed nucleus of the stria terminalis and medial amygdaloid nucleus in prairie voles (Microtus ochrogaster) and meadow voles (Microtus pennsylvanicus).
Vasopressin-immunoreactive (AVP-ir) cells in the bed nucleus of the stria terminalis (BST) and medial amygdaloid nucleus (MA) and their AVP-ir projections to the lateral septum were studied in monogamous prairie voles (Microtus ochrogaster) and promiscuous meadow voles (M. pennsylvanicus). A sexually dimorphic AVP-ir pathway was found in both species; males had more AVP-ir cells in the BST and MA, as well as denser AVP-ir fibers in the lateral septum, than did females. A significant species difference was also found. Overall, meadow voles had more AVP-ir cells in the BST and MA than did prairie voles. Male prairie voles, however, had a higher density of AVP-ir fibers in the lateral septum than male meadow voles. The species difference in the sexually dimorphic AVP-ir projections in the BST and MA is implicated in the rodents' different life strategy and behavior.
Amygdala↗
Sexual differentiation of vasopressin projections of the bed nucleus of the stria terminals and medial amygdaloid nucleus in rats.
The vasopressin-immunoreactive (AVP-ir) projections of the bed nucleus of the stria terminalis (BST) and medial amygdaloid nucleus (MA) are much denser in males than in females even if males and females are treated with similar amounts of testosterone. Previous studies have established that testosterone influences AVP-ir projections during development, but not whether these effects of testosterone were permanent. This study tested the effects of various hormonal manipulations during development on the ability of testosterone to influence the AVP immunostaining in cells of the BST and MA and of fibers in the lateral septum of adult rats. In the first experiment, male rats that were castrated at 3 months of age (control males) had more AVP-ir cells in the BST and a higher density of AVP-ir fibers in the lateral septum than neonatally castrated male rats, whose cell numbers and fiber density did not differ from female rats that were ovariectomized neonatally or at 3 months of age (control females). This suggested that testicular secretions influence sexual differentiation of AVP-ir fiber pathways after birth. The second experiment showed that males castrated at the day of birth or at 1 week after birth had less AVP-ir cells in the BST and MA and a lower AVP-ir fiber density in the lateral septum than male rats castrated at the third week after birth or control males. This indicated that testicular secretions influenced the differentiation of AVP-ir pathways around postnatal day 7. This was further confirmed in the third experiment, in which testosterone propionate treatment at the seventh postnatal day significantly raised AVP-ir fiber density in the lateral septum of neonatally gonadectomized male and female rats and fully restored the number of AVP-ir cells in the BST of neonatally castrated males. Combined, these data suggest that testosterone levels around the seventh postnatal day determine the sexual differentiation of AVP-ir projections to the lateral septum.
Amygdala↗
Fiber outgrowth from fetal vasopressin neurons of the suprachiasmatic nucleus, bed nucleus of the stria terminalis, and medial amygdaloid nucleus transplanted into adult Brattleboro rats.
Outgrowth of fibers from different types of vasopressin (AVP) neurons was compared in the brains of AVP-deficient Brattleboro rats. Fetal grafts of the suprachiasmatic nucleus (SCN), the bed nucleus of the stria terminalis (BST), and the medial amygdaloid nucleus (MA) were implanted into the lateral ventricle. AVP-immunoreactive fibers from all grafts entered the host tissue in the lateral septum. SCN fibers were confined to the lateral margin of the septum. In contrast, MA and BST fibers formed equally dense networks spanning the width of the lateral septum. The data suggest that these transplanted neurons show specific outgrowth, and that the phylogenetically related BST and MA neurons follow similar cues to reach their targets.
Amygdala↗
Projections from the parvocellular part of the posteromedial ventral nucleus of the thalamus to the lateral amygdaloid nucleus in the cat.
It was shown in the cat by anterograde and retrograde WGA-HRP methods that the medial portion of the parvocellular part of the posteromedial ventral nucleus of the thalamus (VPMpc-m) sent fibers ipsilaterally to the rostrodorsal part of the lateral amygdaloid nucleus (Al-rd). The regions of the orbital gyrus (OG), which were connected reciprocally with the VPMpc-m, were also observed to send fibers to the Al-rd. Thus the VPMpc-m was assumed to project to the Al-rd directly, and indirectly via the OG.
Amygdala↗
Interrelations between monoaminergic afferents and corticotropin-releasing factor-immunoreactive neurons in the rat central amygdaloid nucleus: ultrastructural evidence for dopaminergic control of amygdaloid stress systems.
Ample evidence implicates corticotropin-releasing factor (CRF)-producing neurons of the central amygdaloid nucleus (CeA) in vegetative, endocrine, and behavioral responses to stress and anxiety in laboratory rats. Monoaminergic systems are involved in modulating these responses. In the present paper, interrelations between CRF-immunoreactive (ir) neurons, and noradrenergic, serotonergic, and dopaminergic afferents were studied using single and double immunolabeling for light and electron microscopy in the rat CeA. Dopaminergic axons formed dense plexus in the CeA overlapping with the localization of CRF-ir neurons, and their terminals formed frequent associations with CRF-ir somata. Contacts of serotonergic axons on CRF-ir neurons were few, and contacts of noradrenergic axons were the exception. Ultrastructurally, symmetric synapses of dopaminergic terminals on CRF-ir somata and dendrites were found. More than 83% of CRF-ir somata were contacted in single ultrathin sections. About half of these possessed two or more contacts. Of non-ir somata, 37% were contacted by dopaminergic terminals, and only 13% of these had two or more contacts. Correlative in situ hybridization indicated that CeA CRF-ir neurons may express receptor subtype dopamine receptor subtype 2. In conclusion, dopaminergic afferents appear to specifically target CeA CRF neurons. They are thus in a position to exert significant influence on the rat amygdaloid CRF stress system.
Amygdala↗
Direct projections from the central amygdaloid nucleus to the hypothalamic paraventricular nucleus: possible role in stress-induced adrenocorticotropin release.
The amygdala, particularly the central amygdaloid nucleus, is important for the expression of adrenocorticotropin and corticosterone responses during stress. The aim of the present study was to determine if the central amygdaloid nucleus directly innervated the hypothalamic paraventricular nucleus. To accomplish this aim, the Phaseolus vulgaris leucoagglutinin lectin anterograde tracing method was used. Injections of the tracer into the medial central amygdaloid nucleus resulted in axonal and terminal labeling within the medial and lateral parvocellular parts of the caudal paraventricular nucleus. A dense patch of labeling was observed within the lateral wing of the lateral part of the parvocellular paraventricular nucleus. Only a few labeled axons were observed within the paraventricular nucleus of animals that had lectin injections localized to the lateral part of the central nucleus. Tracer injections localized to the medial amygdaloid nucleus resulted in axonal and terminal labeling primarily within the anterior parvocellular and periventricular regions of the paraventricular hypothalamic nucleus. Sparse to moderate axonal and terminal labeling was observed within the magnocellular parts of the paraventricular nucleus in animals that had injections of tracer into either the medial central nucleus or the medial nucleus. No labeling was observed within the paraventricular nucleus of animals that had injections of lectin within other amygdaloid nuclei or adjacent regions of the striatum. The results demonstrated a topographically organized projection from the amygdala to the hypothalamic paraventricular nucleus. The central nucleus mainly innervates the caudal lateral and medial parvocellular paraventricular nucleus. The medial nucleus innervates the rostral parvocellular parts of the paraventricular nucleus. These pathways could form the anatomical substrates of amygdaloid modulation of neuroendocrine responses to stressors.
Adrenocorticotropic Hormone↗
Fine structure and possible origins of nerve fibers with corticotropin-releasing factor-like immunoreactivity in the rat central amygdaloid nucleus.
The fine structure of nerve fibers with corticotropin-releasing factor (CRF)-like immunoreactivity in the central amygdaloid nucleus and CRF-containing afferents to the nucleus were investigated by pre-embedding immunoelectron microscopy and by the combination of fluoro-gold tracing and the indirect immunofluorescence method. Significant numbers of CRF nerve endings and dendrites formed synapses with non-immunoreactive dendrites and axon terminals, respectively. Axon terminals devoid of CRF frequently made synapses with the soma of immunoreactive and non-immunoreactive neurons; CRF nerve endings in contact with the soma were fewer in number. Occasionally, CRF was localized to both pre- and postsynaptic structures in the central amygdaloid nucleus. After fluoro-gold injection into the central amygdaloid nucleus and adjacent areas, double-labeled cells with the tracer and CRF were observed mainly in the lateral hypothalamic area and occasionally in the dorsal raphe nucleus, and they were less numerous than single-labeled cells. These findings suggest that part of the CRF axon terminals identified in the electron micrographs arises from neurons in the lateral hypothalamic area and the dorsal raphe nucleus and the others from intra-amygdaloid CRF neurons. The immunoreactive dendrites are likely to derive from neurons in the central amygdaloid nucleus, which are shown to send axons to the lower brainstem. Thus, this study demonstrates that CRF structures constitute a more complex neuronal network in the central amygdaloid nucleus than previously considered.
Amygdala↗
Direct projections from the central amygdaloid nucleus to the globus pallidus and substantia nigra in the cat.
Employing both anterograde and retrograde axonal tracing, we investigated direct projections from the central amygdaloid nucleus to the basal ganglia in the cat. The anterograde axonal tracing of Phaseolus vulgaris-leucoagglutinin revealed that projection fibers from the central amygdaloid nucleus to the basal ganglia ended in the globus pallidus (the feline homolog to the external segment of the globus pallidus of primates) and substantia nigra. The amygdalopallidal fibers terminated chiefly in the medial most part of the globus pallidus at its caudal level. The amygdalonigral fibers terminated densely in the substantia nigra pars lateralis, and moderately in the dorsolateral part of the substantia nigra pars reticulata; none of them were found to end in the substantia nigra pars compacta. Both of the amygdalopallidal and amygdalonigral projections were ipsilateral. These neuronal connections were confirmed by retrograde axonal tracing of cholera toxin B subunit in the second set of the experiments: The cells of origin of the amygdalopallidal and amygdalonigral projections were located predominantly in the lateral part of the central amygdaloid nucleus, and additionally in the intercalated cell islands of the amygdala. Most of them were of small bipolar or multipolar type. The cells projecting to the globus pallidus were preferentially distributed at the rostral levels of the central nucleus and intercalated cell islands of the amygdaloid complex, while those projecting to the substantia nigra were mainly located at the caudal levels of these amygdaloid subdivisions. In the third set of the experiments, sequential double-antigen immunofluorescence histochemistry for transported cholera toxin B subunit and horseradish peroxidase showed that some single neurons in the lateral part of the central amygdaloid nucleus, particularly at its middle level, issued axon collaterals to both the globus pallidus and substantia nigra pars lateralis. The results of the present study indicate that the central amygdaloid nucleus sends projection fibers to the globus pallidus and substantia nigra possibly to exert a limbic influence upon forebrain motor mechanisms.
Amygdala↗