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Distribution of galanin and galanin transcript in the brain of a galanin-overexpressing transgenic mouse.

The distribution of galanin mRNA-expressing cells and galanin-immunoreactive (IR) cell bodies and processes was studied in the brain of mice overexpressing galanin under the PDGF-B promoter (GalOE mice) and of wild type (WT) mice, both in colchicine-treated and non-treated animals. In this abstract, we only describe the results in GalOE mouse. A widespread ectopic expression of galanin (both mRNA and peptide) was found, that is a situation when neither transcript nor peptide could be seen in WT mice, not even after colchicine treatment. However, in some regions, such as claustrum, basolateral amygdala, thalamus, CA1 pyramidal cells, and Purkinje cells only galanin mRNA could be detected. In the forebrain galanin was seen in the mitral cells of the olfactory bulb, throughout the cortex, in the basolateral amygdaloid nucleus, claustrum, granular and pyramidal cell layers of the hippocampus, subiculum and presubiculum. In the thalamus, the anterodorsal, mediodorsal, intermediodorsal and mediodorsal lateral nuclei, the reuniens and reticular nuclei showed ectopic expression of galanin. Within the hypothalamus, neurons of the suprachiasmatic nucleus contained galanin. In the mesencephalon, the geniculate nucleus, nucleus ruber, the mesencephalic trigeminal and reticulotegmental nuclei ectopically expressed galanin. In the cerebellum, galanin was observed in the Purkinje cells and in the lateral and interposed cerebellar nuclei. In the pons, sensory and motor nuclei of the trigeminal nerve, the laterodorsal and dorsal tegmental nuclei, the pontine, reticulotegmental and gigantocellular reticular nuclei expressed galanin. Within the medulla oblongata, labeled cells were detected in the facial, ambiguus, prepositus, lateral paragigantocellular and lateral reticular nuclei, and spinal trigeminal nucleus. High densities of galanin-IR fibers were found in the axonal terminals of the lateral olfactory tract, the hippocampal and presumably the cerebellar mossy fibers system, in several thalamic and hypothalamic regions and the lower brain stem. Possible functional consequences of galanin overexpression are discussed.

Animals↗

Electrophysiological and morphological properties of rat basolateral amygdaloid neurons in vitro.

Electrophysiological and morphological properties of neurons in the rat basolateral amygdala (BLA) were assessed using intracellular recordings in brain slice preparations. The vast majority of cells studied were identified as pyramidal cells on the basis of their accommodation response and by a prominent afterhyperpolarization that followed a current-evoked burst of action potentials. The second class of cells consisted of late-firing neurons that were distinguished electrophysiologically by their very negative resting membrane potential (-82 mV) and conspicuous delay in the onset of spike firing in response to depolarizing current injection. The third class of cells, termed fast-firing neurons, possessed many of the features of intrinsic inhibitory interneurons found elsewhere in the brain. These included very brief action potentials (0.7 msec), a relatively depolarized resting membrane potential (-62 mV), and spontaneous firing at a high rate and the absence of spike frequency accommodation. Intracellular labeling with Lucifer yellow of electrophysiologically identified pyramidal and late-firing cells showed them to have pyramidal to stellate cells bodies and spine-covered dendrites. Although having an overall pyramidal-like morphology, late-firing neurons possessed cells bodies and dendritic fields that were smaller than those of pyramidal cells. Lucifer yellow-labeled fast-firing neurons had a nonpyramidal morphology, with somata that were spherical to multipolar in shape and spine-sparse or aspiny dendrites. The morphological features of these cells corresponded closely to those of GABA-containing interneurons that have been described previously in the rat BLA using immunohistochemical techniques (McDonald, 1985b). Thus, it seems likely that activation of fast-firing neurons underlies inhibitory synaptic events that are recorded in the rat BLA. Our data support the conclusion derived from previous anatomical studies that pyramidal neurons constitute the predominant cell type in the BLA and function as projection neurons in this region of the amygdala. The determination of whether late-firing cells constitute a unique class of projection neurons distinct from pyramidal cells must await the outcome of studies in which the anatomical terminations of this cell type are specified.

Action Potentials↗

Chronic social stress during puberty enhances tyrosine hydroxylase immunoreactivity within the limbic system in golden hamsters.

The present study was carried out to determine the effects of chronic exposure to social stress during puberty on the dopamine system in male golden hamsters. Experimental animals were socially subjugated between postnatal days 28 (P28) and 42. All animals were sacrificed on P46 and their brains processed for immunocytochemistry to tyrosine hydroxylase (TH). A large increase in the number of TH-immunoreactive (TH-ir) neurons was noted within the posterior portion of the medial amygdaloid nucleus and the posterior portion of the medial division of the bed nucleus of the stria terminalis in subjugated animals as compared to controls. This effect appeared to be site-specific as no difference was seen between groups in the periventricular nucleus, another steroid receptor-rich area. The data suggest that these dopamine neurons may play an important role in the behavioral changes associated with chronic social stress during puberty.

Aging↗

Distribution of thyrotropin-releasing hormone receptor messenger RNA in the rat brain: an in situ hybridization study.

Based on the recent cloning of the mouse thyrotropin-releasing hormone receptor, oligonucleotide probes complementary to the DNA sequence were constructed and used for in situ hybridization studies on the rat brain. Thyrotropin-releasing hormone receptor messenger RNA was found in many areas of the brain, mostly showing high degree of overlap with the distribution thyrotropin-releasing hormone binding sites as previously revealed in autoradiographic studies. Thus, a strong signal was observed in the accessory olfactory bulb, the perirhinal sulcus, the ventral aspects of the hippocampal formation, some amygdaloid nuclei, the diagonal band nucleus, parts of nucleus accumbens, the bed nucleus of the stria terminalis, dorsomedial, lateral and perifornical hypothalamic regions, the septohippocampal nucleus, parts of the vestibular complex, as well as many bulbar motoneurons including the facial, dorsal vagal, ambiguus and hypoglossal nuclei, the superficial layer of the spinal trigeminal nucleus, and motoneurons and dorsal horn neurons in the spinal cord. Cells within one and the same nucleus expressed varying levels of thyrotropin releasing hormone receptor messenger RNA suggesting marked differences in rate of receptor synthesis. Most of these areas receive an input by thyrotropin-releasing hormone-positive nerve endings. Taken together these results suggest that thyrotropin-releasing hormone receptors are mostly localized in the vicinity of the cell bodies which express thyrotropin-releasing hormone receptor messenger RNA and mediate the wide range of actions that have been recorded after administration of exogenous thyrotropin-releasing hormone.

Animals↗

Norepinephrine-gamma-aminobutyric acid (GABA) interaction in limbic stress circuits: effects of reboxetine on GABAergic neurons.

BACKGROUND: Reboxetine is a selective norepinephrine (NE) reuptake inhibitor that exerts significant antidepressant action. The current study assessed norepinephrine-gamma-aminobutyric acid (GABA)-ergic mechanisms in reboxetine action, examining glutamic acid decarboxylase (GAD) mRNA expression in limbic neurocircuits following reboxetine within the context of chronic stress. METHODS: Male rats received 25 mg/kg reboxetine/day, p.o. Reboxetine and vehicle animals were exposed to 1 week of variable stress exposure or handling. Behavioral responses to stress (open field) were tested on day 7, and animals were killed on day 8 to assess neuroendocrine stress responses and limbic GAD65/67 mRNA regulation (in situ hybridization). RESULTS: Reboxetine significantly decreased behavioral reactivity in the open field. Reboxetine administration did not affect expression of GAD65/67 mRNA in handled rats; however, administration to stressed animals reduced GAD67 (but not GAD65) mRNA in the medial amygdaloid nucleus, posteromedial bed nucleus of the stria terminalis, and dentate gyrus. In contrast, GAD65 mRNA expression was increased by reboxetine in the lateral septum of stressed animals. CONCLUSIONS: Norepinephrine pathways appear to modulate synthesis of GABA in central limbic stress circuits. Decreases in GABA synthetic capacity suggest reduced activation of stress-excitatory pathways and enhanced activation of stress-inhibitory circuits, and is consistent with a role for GABA in the antidepressant efficacy of NE reuptake inhibitors.

Analysis of Variance↗

Fos-like immunoreactivity in the brain associated with freezing or escape induced by inhibition of either glutamic acid decarboxylase or GABAA receptors in the dorsal periaqueductal gray.

GABAergic neurons exert tonic control over the neural substrates of aversion in the dorsal periaqueductal gray (dPAG). It has been shown that electrical stimulation of this region at freezing or escape thresholds activates different neural circuits in the brain. Since electrical stimulation activates cell bodies and fibers of passage, it is necessary to use chemical stimulation that activates only post-synaptic receptors. To investigate this issue further, reduction of GABA transmission was performed with local injections of either the GABA-A receptor antagonist bicuculline or the glutamic acid decarboxylase (GAD) inhibitor semicarbazide into the dorsolateral periaqueductal gray (dlPAG). Local infusions of semicarbazide (5.0 microg/0.2 microl) or bicuculline (40 ng/0.2 microl) into this region caused freezing and escape, respectively. The results obtained showed that freezing behavior induced by semicarbazide was associated with an increase in Fos expression in the laterodorsal nucleus of the thalamus (LD) and ventrolateral periaqueductal gray (vlPAG), while bicuculline-induced escape was related to widespread increase in Fos labeling, notably in the columns of the periaqueductal gray, hypothalamus nuclei, the central amygdaloid nucleus (Ce), the LD, the cuneiform nucleus (CnF) and the locus coeruleus (LC). Thus, the present data support the notion that freezing and escape behaviors induced by GABA blockade in the dlPAG are neurally segregated: freezing activates only structures that are mainly involved in sensory processing, and bicuculline-induced escape activates structures involved in both sensory processing and motor output of defensive behavior. Therefore, the freezing elicited by activation of dlPAG appears to be related to the acquisition of aversive information, whereas most brain structures involved in the defense reaction are recruited during escape.

Analysis of Variance↗

Calcitonin gene-related peptide-containing pathways in the rat forebrain.

The present study focuses on the topographical distribution of calcitonin gene-related peptide (CGRP)-containing cell bodies and fibers and their connections and pathways in the rat forebrain. We confirm previously reported CGRP projections from the perifornical area of the hypothalamus to the lateral septum, from the posterior thalamus to the caudate putamen and cerebral cortex, and from the parabrachial nuclei to the central extended amygdala, lateral hypothalamus, and ventromedial thalamus. Despite previous descriptions of CGRP in the central nervous system, important neuroanatomical aspects of the forebrain CGRP system remained obscure, which we addressed by using brain lesion techniques combined with modern immunohistology. We first report CGRP terminal fields in the olfactory-anterior septal region and also CGRP projections from the parabrachial nuclei to the olfactory-anterior septal region, the medial prefrontal cortex, the interstitial nucleus of the anterior commissure, the nucleus of the lateral olfactory tract, the anterior amygdaloid area, the posterolateral cortical amygdaloid nucleus, and the dorsolateral part of the lateral amygdaloid nucleus. In addition, we identified a CGRP cell group in the premamillary nuclei and showed that it projects to the medial CGRP layer of the lateral septum. CGRP fibers usually join other pathways rather than forming bundles. They run along the fornix from the hypothalamus, along the supraoptic decussations or the inferior thalamic peduncle-stria terminalis pathway from the posterior thalamus, and along the superior cerebellar peduncle, thalamic fasciculus, and ansa peduncularis from the parabrachial nuclei. This description of the forebrain CGRP system will facilitate investigation of its role in higher brain functions.

Animals↗

Theophylline attenuates microwave-induced impairment of memory acquisition.

Numerous studies have shown that acute microwave exposure causes cognitive deficits in animals, possibly via hyperthermia, but the biological effect of microwave exposure on memory processing is still unknown. The release of adenosine is demonstrated to be a general way for the cells to respond to metabolically stressful conditions such as hypoxia and ischemia. The present study aimed to examine whether adenosine mediates biological effects of microwave exposure on memory processing using a continuous multiple-trial inhibitory avoidance task. Results demonstrated that microwave exposure for 20 min before training impaired memory acquisition and retention performance in mice, assessed by the number of training trials and by latency to enter the dark compartment. The mice exposed to microwave radiation showed a dose-dependent hyperthermia. Moreover, the cell numbers of hippocampus were decreased in the mice receiving microwave exposure at an average power density of 50 mW/cm(2), indicating the anatomical correlation to hippocampal-amygdaloid structures corresponding with the memory disrupt of the mice. Administration of theophylline, a nonspecific adenosine receptor antagonist, 30 min before microwave exposure, completely antagonized the impairment of inhibitory avoidance acquisition but not retention. These results suggest that the adenosine regulation pathway was partially involved in microwave-induced impairment of inhibitory avoidance memory.

Adenosine↗

A comparative study of the mammalian amygdala: a Golgi study of the basolateral amygdala.

The lateral (LA), basolateral (BL) and basomedial (BM) amygdaloid nuclei were compared in the guinea pig (Cavia porcellus), rabbit (Oryctolagus cuniculus) fox (Vulpes vulpes) and pig (Sus scrofa) by using the Golgi techniques. The interspecific comparisons of the individual basolateral nuclei have shown that the neuronal structure in each of them is extremely stable and remains almost unchanged in the series of animals studied. The only difference is the size of the basolateral neurons, which increases with the increasing size of the brain. Moreover, the intraspecific comparisons revealed that in all the animals studied LA, BL and BM form a fairly homogenous mass of cells in which similar cell types are present. The most numerous neurons in all basolateral nuclei are the spiny cells that often show a pyramidal or semi-pyramidal appearance (the Type I cells). Many of these have conical cell bodies and easily recognisable "apical" and "basal" dendrites. The Type II neurons are the most common variety of non-pyramidal cell and have round cell bodies and smooth or sparsely spined dendrites. The axons of these cells often form a dense terminal field that remains in the vicinity of the parent soma. The Type III cells, which are only occasionally seen, are small spine-sparse neurogliaform neurons with a few extremely delicate beaded dendrites and a poorly branching local axon. These neurons were only located in LA and BL.

Amygdala↗

Some observations on hypothalamo-amygdaloid connections in the monkey.

The projections of the hypothalamus to the amygdala have been studied autoradiographically in a series of eleven cynomolgus monkeys (Macaca fascicularis) in which injections of [3H]amino acids had been made in different regions of the caudal two-thirds of the hypothalamus. The most prominent projection arises from the ventromedial nucleus of the hypothalamus and terminates most heavily in the medial, magnocellular division of the central nucleus. Injections confined to the ventromedial nucleus also result in labeling of the piriform cortex, the periamygdaloid cortex, the anterior amygdaloid area, the medial amygdaloid nucleus and the parvocellular divisions of both the basal and basal accessory nuclei. All these projections are bilateral (although the contralateral component is much smaller) and show evidence of a rostro-caudal topographic organization. Isotope injections that involve the caudal part of the lateral hypothalamic area label projections to the medial division of the central amygdaloid nucleus, to the medial and cortical nuclei and to the anterior amygdaloid area. When such caudally placed injections also involved the lateral mamillary nucleus, the lateral division of the central amygdaloid nucleus was additionally labeled. Although the medial mamillary nucleus does not project to the amygdala, there is evidence for a minor projection from the supramamillary region to the medial amygdaloid nucleus. The ventral tegmental area appears to project to the lateral division of the central nucleus and the medial portion of the substantia nigra has a small projection to both divisions of the central nucleus. All of these projections reach the amygdala by way of the so-called ventral amygdalofugal pathway, but at least some of the fibers that arise in the ventromedial nucleus run in the stria terminalis.

Afferent Pathways↗

Long-lasting enhancement of rapid eye movement sleep and pontogeniculooccipital waves by vasoactive intestinal peptide microinjection into the amygdala temporal lobe.

STUDY OBJECTIVES: The effect of a vasoactive intestinal peptide (VIP) microinjection into the amygdaloid central (CN) and basal nuclei (BN) on sleep organization and on the number and pattern of occurrence of pontogeniculooccipital (PGO) waves was analyzed. DESIGN: One group of 8 cats was studied in baseline conditions and after the microinjection of two doses of VIP applied into the CN and BN. SETTING: Sleep research laboratory. PARTCIPANTS AND INTERVENTIONS: Eight cats were prepared with sleep-recording electrodes and with guide tubes in both amygdalae for saline and VIP microinjections. Neuropeptide doses of 0.10 microg/1 microl (30 microM) and 0.33 microg/1 microl (99.24 microM) were employed. MEASUREMENTS AND RESULTS: Once the microinjection was applied, 23-hour polygraphic sleep recordings were performed for 5 consecutive days. Concomitantly the PGO waves were tape-recorded on each day and computationally analyzed. Results show that the 0.10 microg/1 microl microinjection produced no change. Unilateral VIP 0.33 microg/1 microl injection into the CN provoked a significant and lasting increase in the percentage of slow-wave sleep with PGO waves. Bilateral application of VIP increased the percentage of slow-wave sleep with PGO waves and rapid eye movement sleep for 5 days. Bilateral microinjection of the neuropeptide into the BN only enhanced the percentage of slow wave sleep with PGO waves. For both amygdaloid nuclei, we observed that VIP increased the number and modified the PGO wave pattern of occurrence during slow-wave sleep with PGO waves and during rapid eye movement sleep. CONCLUSIONS: The VIP microinjection into both the CN and BN induces increased amounts of rapid eye movement sleep, PGO waves, and slow-wave sleep with PGO waves, having a more robust effect on all of these three variables when applied into the CN.

Amygdala↗

The role of the temporal lobe amygdala in ponto-geniculo-occipital activity and sleep organization in cats.

Ponto-geniculo-occipital (PGO) spikes propagate to different structures of the limbic system, including the temporal lobe amygdala. There is direct connection between the amygdala and the pontine nuclei involved in the generation of PGO spikes. It has also been shown that both the amount and the pattern of PGO spike discharges are under the influence of several brainstem and forebrain structures. In the present work, PGO activity was analyzed in unrestrained cats submitted to low-intensity amygdaloid electrical stimulation during paradoxical sleep (PS) episodes. General sleep organization as well as number, mean duration and percentage of PS episodes, were assessed in 8-h sleep recordings during amygdaloid stimulation. Amygdaloid stimulation significantly increased PGO number, spike density and, specially, PGO burst density. No significant changes were found in PS episodes or in the slow-wave sleep. It is concluded that the amygdala plays a role in the modulation of PGO activity by means of a facilitatory influence. It is proposed that this influence is probably exerted through a positive feedback mechanism. The independence between PGO generation and PS maintenance mechanisms is emphasized.

Action Potentials↗

Visual pathways involved in fear conditioning measured with fear-potentiated startle: behavioral and anatomic studies.

Visual pathways to the amygdala, a brain structure critical for classical fear conditioning, were investigated. Conditioned fear was measured in rats as increased acoustic startle amplitude in the presence versus absence of a light or an odor paired previously with foot shock (fear-potentiated startle). Post-training lesions of both the lateral geniculate body (LG) and lateral posterior nucleus (LP) of the thalamus together, but not lesions of LG or LP alone, completely blocked the expression of fear-potentiated startle to a visual conditioned stimulus (CS) but not to an olfactory CS. These lesions also did not block contextual fear conditioning using startle or freezing as measures. Local infusion of 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f] quinoxaline-7-sulfonamide disodium, an AMPA antagonist, into the visual thalamus immediately before testing also blocked fear-potentiated startle to a visual CS, suggesting that the lesion effects were not attributable to damage of fibers of passage. Iontophoretic injections into the LP of the anterograde tracer biotinylated dextran amine resulted in heavy anterograde labeling in two amygdala-fugal cortical areas: area TE2 and dorsal perirhinal cortex (PR), and moderate labeling in the lateral amygdaloid nucleus (L). These results suggest that, during classical fear conditioning, a visual stimulus can be transmitted to the amygdala via either lemniscal (i.e., LG --> V1, V2 --> TE2/PR) or non-lemniscal (i.e., LP --> V2, TE2/PR) thalamo-cortico-amygdala pathways, or direct thalamo-amygdala (i.e., LP --> L) projections.

Amygdala↗

Forebrain projections of the rostral nucleus raphe magnus shown by iontophoretic application of choleratoxin b in rats.

The nucleus raphe magnus belongs to the thermoafferent system. Following iontophoretic choleratoxin b injections in its rostral part, a substantial to large number of anterogradely labeled varicose fibres were observed in the medial and lateral preoptic areas, the bed nucleus, the substantia innominata, the ventral pallidum, the median preoptic nucleus, the paraventricular hypothalamic nucleus, the central amygdaloid nucleus and the lateral and dorsal hypothalamic areas. A small to moderate number were seen in the septal nuclei, the diagonal band, the magnocellular preoptic nucleus, the anterior hypothalamic area and the paraventricular and intralaminar thalamic nuclei. After choleratoxin b injections in the preoptic, dorsal and lateral hypothalamic areas, a substantial number of retrogradely labeled serotonin immunonegative neurones were specifically found in the rostral nucleus raphe magnus. Thus, non-serotonergic rostral nucleus raphe magnus cells might directly modulate hypothalamic thermointegrative neurones.

Afferent Pathways↗

The human amygdaloid complex: a cytologic and histochemical atlas using Nissl, myelin, acetylcholinesterase and nicotinamide adenine dinucleotide phosphate diaphorase staining.

We examined the distribution of acetylcholinesterase and nicotinamide adenine dinucleotide phosphate diaphorase enzyme activity in the human amygdala using histochemical techniques. Both methods revealed compartments of higher or lower enzyme activity, in cells or neuropil, which corresponded to the nuclear subdivisions of the amygdala as defined with classical Nissl and myelin methods. The boundaries between the histochemical compartments were usually so sharp that the identification of these nuclear subdivisions was enhanced. There was also variation of staining intensity within many of the nuclear subdivisions, such as the lateral and central nuclei, anterior amygdaloid area and the intercalated groups. This histochemical difference corresponded to more subtle differences in Nissl and myelin staining patterns, and suggests further structural subdivisions of potential functional significance. We present a revised scheme of anatomical parcellation of the human amygdala based upon serial analysis with all four techniques. Our expectation is that this will allow the delineation of a clearer homology between the cytoarchitectonic subdivisions of the human amygdala and those of experimental animals.

Acetylcholinesterase↗

Distribution of Fos immunoreactivity in the rat brain after freezing or escape elicited by inhibition of glutamic acid decarboxylase or antagonism of GABA-A receptors in the inferior colliculus.

It has been shown that electrical stimulation of the central nucleus of the inferior colliculus (IC) at freezing or escape thresholds activates different neural circuits in the brain. Since electrical stimulation activates cell bodies and fibers of passage it is necessary to use chemical stimulation that activates only post-synaptic receptors. To examine this issue in more detail, we took advantage of the fact that GABAergic neurons exert tonic control over the neural substrates of aversion in the IC. Reduction of GABA transmission in this structure was performed with the use of semicarbazide - an inhibitor of the GABA synthesizing enzyme glutamic acid decarboxylase (GAD) - and the GABA-A receptor antagonist bicuculline. Depending on the dose employed local infusions of semicarbazide (6.0 microg/0.2 microl) or bicuculline (40 ng/0.2 microl) into this region caused freezing and escape, respectively. The results obtained showed that freezing behavior induced by semicarbazide was associated with an increase in Fos expression in the dorsomedial column of the PAG (dmPAG) only, while bicuculline-induced escape was related to widespread increase in Fos labeling, notably in the periaqueductal gray, hypothalamus nuclei, amygdaloid nuclei, the laterodorsal nucleus of thalamus (LD), the cuneiform nucleus (CnF) and the locus coeruleus (LC). Thus, the present data support the notion that freezing and escape behaviors induced by GABA blockade in the IC are neurally segregated: acquisition of aversive information of acoustic nature from the IC probably uses the dmPAG column as a relay station to higher brain centers whereas bicuculline-induced escape activates structures involved in both sensory processing and motor output of defensive behavior. These results support the existence of distinct neural circuits mediating the sensory and motor responses of the defense reaction. The extent of the brain activation during freezing appears to be limited to the anatomical connections of the dmPAG, whereas an overall activation of the limbic system predominates during escape behavior induced by IC stimulation.

Animals↗

CNS innervation of vagal preganglionic neurons controlling peripheral airways: a transneuronal labeling study using pseudorabies virus.

The CNS cell groups that project to vagal preganglionic neurons which innervate the most distal part of the airways were identified by the viral retrograde transneuronal labeling method. Pseudorabies virus (PRV) was injected into the lung parenchyma of C8 spinal rats and after 5 days survival, brain tissue sections from these animals were processed for immunohistochemical detection of PRV. Retrogradely labeled parasympathetic preganglionic cells (first-order neurons) were seen mainly in the ventral medulla oblongata: the compact portion of the nucleus ambiguus and the area ventral to it. Occasionally, a few labeled cells were seen within the rostral part of the dorsal vagal nucleus. This labeling pattern correlated well with the retrograde cell body labeling seen following cholera toxin beta-subunit (CT-b) injections in the lung parenchyma. PRV transneuronally labeled neurons (second-order and/or presumed third-order neurons) were found throughout the CNS with the characteristic labeling in the brainstem. Labeled neurons were identified along and just beneath the ventral medullary surface, and in nearby areas: the parapyramidal, retrotrapezoid, gigantocellular and lateral paragigantocellular reticular nuclei, as well as the caudal raphe nuclei (raphe pallidus, obscurus, and magnus). Several nucleus tractus solitarius (nTS) regions contained labeled cells including the commissural, medial, and ventrolateral nTS subnuclei. The A5 cell group and a small number of locus coeruleus neurons were also labeled. PRV-infected neurons were present in the Kölliker-Fuse and Barrington's nuclei. In the mesencephalon, neurons within the ventral periventricular gray matter were labeled. Labeling was present in the dorsal, lateral and paraventricular hypothalamic nuclei, and within the amygdaloid complex. In summary, the parasympathetic preganglionic neurons that innervate the peripheral airways are controlled by networks of lower brainstem and suprapontine neurons that lie in the same regions known to be involved in central regulation of autonomic functions.

Amygdala↗

Medial forebrain bundle of the rat: III. Cytoarchitecture of the rostral (telencephalic) part of the medial forebrain bundle bed nucleus.

The boundaries of the medial forebrain bundle (MFB) of the rat have been presented in previous work on the structure of this fiber system (Nieuwenhuys et al.: J. Comp. Neurol. 206:49-81, '82). Neuronal cell bodies within these outlines constitute the bed nucleus of the MFB. Many fiber components of the MFB appeared to be spatially arranged within the bundle and featured an orderly topography (Veening et al.: J. Comp. Neurol. 206:82-108, '82). As the fibers of the MFB are thought to be a major source of afferents to the bed nucleus (Millhouse: In P.J. Morgane and J. Panksepp (eds): Anatomy of the Hypothalamus, Vol. 1. New York: Marcel Dekker, pp. 221-265, '79), the latter has been subjected in this and the companion study (Geeraedts et al.: J. Comp. Neurol. 294:537-568, '90) to a detailed cytoarchitectonic analysis. This analysis is based on continuous series sectioned in the three conventional planes. On the basis of cytoarchitectonic characteristics, including size and shape, staining intensity, packing density, and spatial orientation of the cell bodies, it was found that the bed nucleus of the MFB as described in the literature is by no means a cytoarchitectonic unit per se. Rather, the neuronal cell population located within the telencephalic stream of the MFB can be parcellated into a number of cellular groups, which partly or entirely belong to more-or-less known basal telencephalic structures. These structures are designated here as the MFB-related areas. They correspond largely to the subcommissural substantia innominata (SIC), the sublenticular substantia innominata (SIL), the nucleus of the diagonal band of Broca, the olfactory tubercle, the magnocellular preoptic nucleus (POMA), the lateral preoptic area (LPOA), and the interstitial nucleus of the stria medullaris (ISM). The complex of the MFB-related areas is surrounded by the following cellular entities: the nucleus accumbens (ACB), the caudatus-putamen region (CPU), the globus pallidus (GP), the bed nucleus of the stria terminalis (BST), the anterior amygdaloid area (AAA), the amygdaloid nuclear complex (A), the medial preoptic area (MPOA) and the anterior hypothalamic area (AHA). Both MFB-related areas and their surroundings have been identified and delimited in this study. This resulted in a new cytoarchitectonic atlas of the rat's basal telencephalon. Our atlas does not only show the relative positions of the above mentioned cellular groups, but also those of their subdivisions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗