Reversal of dexfenfluramine-induced anorexia and c-Fos/c-Jun expression by lesion in the lateral parabrachial nucleus

The external subdivision of the lateral parabrachial nucleus (LPBE) shows strong Fos-like immunoreactivity (FLI) following anorectic doses of the indirect serotonin agonist dexfenfluramine (DFEN). In an effort to determine the contribution of the LPBE to DFEN-induced anorexia, bilateral ibotenate lesions were made in the LPBE, and the effects of the lesion on DFEN-induced anorexia and FLI as well as c-June-like immunoreactivity (JLI) were examined. It was found that LPBE lesion significantly attenuated DFEN anorexia: in a 1-h food intake test following 24-h food deprivation, DFEN (2 mg/kg) suppressed food intake by 60% in intact rats but only 34% in rats with LPBE lesions. In addition to this behavioral change, LPBE lesion completely abolished DFEN-induced FLI and JLI in the lateral subdivision of the central nucleus of the amygdala (CeL) and laterodorsal subdivision of the bed nucleus of stria terminalis (BSTLD), both of which showed strong FLI and JLI in intact rats. DFEN-induced FLI and JLI in other brain regions were not affected by LPBE lesion, including the ventromedial and lateral hypothalamus, caudate-putamen, and the nucleus of the solitary tract (NST). The parallel loss of DFEN-induced anorexia and FLI/JLI following LPBE lesion raises the novel possibility that LPBE-CeL/BSTLD pathway may be involved in DFEN anorexia.     

Induction of Fos-like immunoreactivity (Fos-li) and stimulation of feeding by 2, 5-anhydro-d-mannitol (2, 5-AM) require the vagus nerve

The antimetabolic fructose analogue, 2, 5-anhydro-d-mannitol (2, 5-AM), stimulates feeding. Selective hepatic branch vagotomy has been shown to block feeding induced by low 2, 5-AM doses. However, hepatic vagal fibers are not the sole mediators of 2, 5-AM-induced feeding, since hepatic branch vagotomy does not impair feeding induced by higher doses of 2, 5-AM. To further evaluate the role of the vagus in the response to 2, 5-AM, we examined the effect of total subdiaphragmatic vagotomy on feeding induced by a high 2, 5-AM dose (500 mg/kg). In addition, we assessed the ability of 2, 5-AM (300 and 500 mg/kg) to induce Fos-like immunoreactivity (Fos-li) in the brain in sham-operated (SHAM), hepatic branch vagotomized (HBV) and total subdiaphragmatic vagotomized (TSDV) rats. Both doses of 2, 5-AM, but not control solutions, induced Fos-li in the area postrema (AP), nucleus of the solitary tract (NTS) and lateral parabrachial nucleus (IPBN). Very weak immunoreactivity was present in the central nucleus of the amygdala and none was observed in the locus coeruleus or paraventricular nucleus of the hypothalamus. The effect of the lower 2, 5-AM dose on Fos-li was blocked by HBV. The high dose effect was blocked by TSDV but not by HBV. Feeding induced by the high dose of 2, 5-AM was also blocked by TSDV. Results are consistent with the hypothesis that stimulation of feeding by 2, 5-AM is dependent on the vagus nerve. Hepatic branch fibers may have the lowest threshold for activation, but fibers in other vagal branches independently mediate induction ofc-fos and stimulate food intake at higher doses of the analogue.     

c-fos expression in the rat brain following central administration of neuropeptide Y and effects of food consumption

Administration of neuropeptide Y (NPY) intracerebroventricularly (i.c.v.) results in the release of a number of hypothalamic and pituitary hormones and stimulation of feeding and suppression of sexual behavior. In this study, we sought to identify cellular sites of NPY action by evaluating perikaryal Fos-like immunoreactivity (FLI), a marker of cellular activation, in those hypothalamic and extrahypothalamic sites previously implicated in the control of neuroendocrine function and feeding behavior. Additionally, we compared the topography of FLI in these brain sites when food was either available ad libitum or withheld after NPY injection (1 nmol/3 μl, i.c.v.). The results showed that one hour after NPY injection a large number of cells in the parvocellular region of the paraventricular nucleus (PVN) were FLI-positive in the absence of food consumption. However, in association with food intake, a significant number of cells were intensely stained in the magnocellular region of the PVN. An analogous increase in FLI in association with feeding was apparent in the supraotic nucleus (SON), the dorsomedial nucleus and the bed nucleus of the stria terminalis in the hypothalamus. Anong the extrahypothalamic sites, feeding facilitated FLI in a large number of cells located in the lateral subdivision of the central amygdaloid nucleus and the lateral subdivision of the solitary tract. FLI was observed in a moderate number of cells in the hypothalamic arcuate nucleus (ARC) and ventromedial nucleus, and this response was not changed by feeding. Cumulatively, these results show that neurons in a number of discrete hypothalamic and extrahypothalamic sites, previously implicated in the control of neuroendocrine function and feeding behavior, are activated by NPY and further, a divergent pattern of c-fos expression emerged in some of these sites if feeding occurs after NPY injection. Stimulation of FLI in cells of the PVN, SON and ARC by NPY imply the presence of NPY target cells that play a role in the neuroendocrine control of pituitary function. The finding that NPY induced FLI in cells located in the parvocellular subdivision of the PVN even in the absence of feeding, imply that cells involved in initiation of food intake by NPY may reside in this subdivision of the PVN. On the other hand, the appearance of Fos-cells in the magnocellular subdivision of the PVN in response to feeding, suggests neural mechanisms that operate during the post-ingestion period, including those associated with termination of NPY-induced feeding, may impinge upon this subdivision of the PVN.     

Medial versus lateral parabrachial nucleus lesions in the rat: effects on cholecystokinin- and D-fenfluramine-induced anorexia

The two major components of the pontine parabrachial nucleus (PBN), the medial (gustatory) and lateral (visceral) subdivisions, have been implicated in a variety of ingestive behaviors. The present study examined the influence of bilateral ibotenic acid lesions of the medial or lateral PBN on the anorectic effects of two systemically administered drug treatments. In Experiment 1, 24-h food-deprived rats where injected with sulfated cholecystokinin (26-33) (CCK; 0, 4.0, or 8.0 microg/kg) and then given 60 min access to food. In Experiment 2, the influence of D-fenfluramine (DFEN; 0, 0.5, 1.0, or 2.0 mg/kg) on deprivation-induced feeding was examined in the same rats using the same behavioral procedure as in Experiment 1. Lesions of the lateral PBN abolished CCK-, but not DFEN-induced anorexia whereas lesions of the medial PBN augmented DFEN-, but had no influence on CCK-induced anorexia. The results suggest that the satiating effects of CCK and DFEN are mediated through different mechanisms involving, respectively, visceral and orosensory processing.     

Medial versus lateral parabrachial nucleus lesions in the rat: effects on cholecystokinin- and -fenfluramine-induced anorexia

The two major components of the pontine parabrachial nucleus (PBN), the medial (gustatory) and lateral (visceral) subdivisions, have been implicated in a variety of ingestive behaviors. The present study examined the influence of bilateral ibotenic acid lesions of the medial or lateral PBN on the anorectic effects of two systemically administered drug treatments. In Experiment 1, 24-h food-deprived rats where injected with sulfated cholecystokinin_26-33 (CCK; 0, 4.0, or 8.0 μg/kg) and then given 60 min access to food. In Experiment 2, the influence of -fenfluramine (DFEN; 0, 0.5, 1.0, or 2.0 mg/kg) on deprivation-induced feeding was examined in the same rats using the same behavioral procedure as in Experiment 1. Lesions of the lateral PBN abolished CCK-, but not DFEN-induced anorexia whereas lesions of the medial PBN augmented DFEN-, but had no influence on CCK-induced anorexia. The results suggest that the satiating effects of CCK and DFEN are mediated through different mechanisms involving, respectively, visceral and orosensory processing.     

Effects of acute and chronic fluoxetine treatments on restraint stress-induced Fos expression

Chronic treatment with antidepressants has been shown to attenuate behavioral changes induced by uncontrollable stress. The mechanisms and brain sites of this effect, however, remain controversial. The objective of the present work was to investigate the effects of chronic and acute treatment with fluoxetine (FLX), a selective serotonin reuptake blocker, on Fos expression in animals submitted to restraint stress. Male Wistar rats (n = 3-9/group) received, during 1 or 21 days, intraperitoneal. Injections of vehicle (saline + 0.2% Tween-80, 1 ml/kg) or FLX (10 mg/kg). One hour after the last injection they were forced restrained for 2 h and sacrificed immediately after. Non-stressed animals were sacrificed 2 h after the last injection. The brains were removed and processed for immunohistochemistry. Fos-like immunoreactivity (FLI) was quantified by a computer system. In acutely treated animals FLX decreased stress-induced FLI in the medial amygdala (MeA), bed nucleus of the stria terminalis (BNST), ventrolateral part, and dorsolateral periaqueductal gray (PAG). After chronic treatment, however, the drug induced a significant increase in FLI in the BNST (ventrolateral and medial parts), lateral septal nucleus (LSN, dorsal part), dorsal raphe nucleus (DRN), and locus coeruleus in restrained group. In non-restrained animals chronic treatment with FLX increased FLI in the MeA, BNST (ventrolateral and dorsolateral parts), LSN (dorsal and intermediate parts), dorsolateral and dorsomedial PAG and in the DRN. The results suggest that chronic fluoxetine treatment induce plastic changes that result in a different regional pattern of Fos expression.     

Cholecystokinin-induced excitation in the substantia nigra: evidence for peripheral and central components

Cholecystokinin (CCK), one of the most common brain peptides, coexists with dopamine (DA) in neurons of the medial substantia nigra (SN). CCK has been shown to excite these neurons following either direct iontophoretic or systemic administration suggesting that peripherally administered CCK may cross the blood brain barrier to act directly on nigral DA cells. However, biochemical evidence suggests that CCK does not cross the blood brain barrier, and several studies have shown that the behavioral and the satiety-inducing effects of peripherally administered CCK are abolished by vagotomy. In order to test for vagal mediation of the nigral response to systemically administered CCK, we examined the effects of a series of lesions to the vagal pathways on CCK-induced excitation in the SN. Neither acute thoracic nor chronic subdiaphragmatic vagotomies had any effect on the excitatory response of nigral DA neurons to systemically administered CCK. High cervical spinal cord transections were similarly without effect. In contrast, lesions of either vagal fibers in the medulla or of the efferent pathways from the nucleus tractus solitarii, the primary sensory nucleus of the vagus, produced significant attenuations of the nigral effects of systemically administered CCK. However, neither lesion blocked effects of CCK completely. We suggest that peripherally administered CCK has two components to its excitatory action in the SN; a component probably mediated through CCK receptors in the nucleus tractus solitarii and a direct action on DA neurons.     

Central and peripheral vagal transport of cholecystokinin binding sites occurs in afferent fibers

The effects of various vagal lesions on cholecystokinin (CCK) binding sites in the nucleus tractus solitarii (NTS) and area postrema (AP) and the peripheral transport of CCK binding sites in the cervical vagus were examined in rats by in vitro autoradiography with [125I]CCK-8. Unilateral supraganglionic, but not subdiaphragmatic vagotomy significantly reduced CCK binding in the ipsilateral NTS. Specific unilateral afferent, but not efferent, vagal rootlet transections also significantly reduced NTS CCK binding ipsilateral to the transections. None of the vagal lesions altered CCK binding in the AP. Infraganglionic but not supraganglionic vagotomy eliminated the peripheral transport of vagal CCK binding sites. Together these results demonstrate that CCK receptors in the NTS are located on vagal afferent terminals, that CCK receptors in the AP are likely postsynaptic to a vagal afferent input and that the peripheral and central transport of vagal CCK binding sites occurs in afferent fibers.     

Effects of albumin‐conjugated PYY on food intake: the respective roles of the circumventricular organs and vagus nerve

The mechanism and routes through which peptide tyrosine‐tyrosine (PYY) exerts its anorectic effects are still largely unknown. In the present study, we investigated the roles of the area postrema (AP), subfornical organ (SFO) and vagus nerve in mediating the anorectic effect of PYY using PYY_3‐36 conjugated to human serum albumin (PYY_3‐36‐HSA) in rats. PYY_3‐36‐HSA is a large molecule that does not penetrate the blood–brain barrier, and thus provides a useful tool to discriminate between the central (brain) and peripheral actions of this peptide. PYY_3‐36‐HSA induced significant reductions in food and body weight gain up to 24 h after administration. The anorectic effect of PYY_3‐36‐HSA was delayed for 2 h in rats in which both AP and SFO were ablated, while lesion of either of these circumventricular organs in isolation did not influence the feeding responses to PYY_3‐36‐HSA. The PYY_3‐36‐HSA‐induced anorectic effect was also reduced during the 3‐ to 6‐h period following subdiaphragmatic vagotomy. Lesions of AP, SFO and AP/SFO as well as subdiaphragmatic vagotomy blunted PYY_3‐36‐HSA‐induced expression of c‐fos mRNA in specific brain structures including the bed nucleus of stria terminalis, central amygdala, lateral–external parabrachial nucleus and medial nucleus of the solitary tract. In addition, subdiaphragmatic vagotomy inhibited the neuronal activation induced by PYY_3‐36‐HSA in AP and SFO. These findings suggest that the anorectic effect and brain neuronal activation induced by PYY_3‐36‐HSA are dependent on integrity of AP, SFO and subdiaphragmatic vagus nerve.     

Distribution of cholecystokinin-immunoreactive cell bodies in the male and female rat: II. Bed nucleus of the stria terminalis and amygdala

The distribution of cholecystokinin-immunoreactive (CCK-I) cell bodies was studied in the bed nucleus of the stria terminalis (BST) and amygdaloid complex of colchicine-treated male and female rats. Immunoreactive cells were visualized in the BST medial amygdaloid (MeA), central lateral, basolateral, basolateral ventral, medial, intercalated, anterior cortical, and posterior cortical nuclei and the amygdalohippocampal zone. Several significant sex differences were observed. In the male, a dense aggregation of CCK-I cell bodies was visualized in the MeA, especially in the dorsocaudal part and in the encapsulated part of the BST. In comparison, female rats had relatively fewer immunoreactive cells in both of these regions. In the lateral and basolateral amygdaloid nuclei, however, more CCK-I cells were visualized in the female than in the male, but the difference was not statistically significant. These data provide characterization of a sexually differentiated CCK system. In addition, we observed that the number of CCK-I cells in the BST and posterodorsal part of the MeA was substantially reduced after castration. The number of CCK-I cells in female rats, however, was not significantly reduced after ovariectomy in any of the regions studied. These findings imply that the steroid regulation of CCK is sexually differentiated. The sexually dimorphic distribution of CCK-I cells in areas that are targets of steroid hormones and regulate reproductive processes is consistent with the possibility that CCK participates in central integration of sensory and steroidal input that modulates reproductive behavior.     

Neurons of the bed nucleus of the stria terminalis: A golgi study in the rat

Neuronal morphology in the bed nucleus of the stria terminalis (BST) was studied using Golgi techniques. The principal neurons of the lateral subdivision of BST have ovoid perikarya and 4–5 dendrites that branch several times and exhibit a dense covering of spines. Adjacent to the internal capsule is a small region, termed the “juxtacapsular subdivision” of BST, that consists of small, spiny cells. Neurons of the medial subdivision of BST have ovoid perikarya and 2–3 dendrites that branch sparingly. Dendritic spine density varies from sparse to moderate. Dendrites in the dorsocaudal portion of the medial subdivision extend into a cell-sparse zone adjacent to the lateral ventricle. Cells in the lateral portion of the preoptic continuation of BST have dendrites oriented perpendicular to fibers of the stria terminalis which traverse this area while medially located cells are oriented parallel to fibers of the stria. Axons of BST neurons emit collaterals that arborize modestly near the cell of origin. Neurons in the lateral and medial subdivisions of BST resemble, respectively, cells in the lateral and medial subdivisions of the central amygdaloid nucleus. Neurons in the juxtacapsular subdivision of BST are similar to neurons of the intercalated masses of the amygdala.     

Coexpression of prodynorphin and corticotrophin-releasing hormone in the rat central amygdala: evidence of two distinct endogenous opioid systems in the lateral division

The lateral subdivision of the central nucleus of the amygdala (CeA) comprises two groups of gamma-aminobutyric acid (GABA) neurons that express corticotrophin-releasing hormone (CRH) and enkephalin. Regulation of the expression and release of these neuropeptides by glucocorticoids and other factors has been suggested to have a regulatory function on the diverse somatic, autonomic, and neuroendocrine responses that are coordinated by the CeA. Because another opioid peptide, dynorphin, has been reported to be also expressed by neurons in the lateral CeA, this study examined the neuronal expression of this kappa-opioid (KOP) receptor-preferring ligand by using immunohistochemistry for the precursor peptide prodynorphin. Prodynorphin neurons in the extended amygdala were observed mostly in the medial and central regions of the lateral CeA and the oval of the bed nucleus of the stria terminalis (BST). About one-third of the prodynorphin neurons in the CeA coexpressed CRH, whereas no coexpression with CRH was detected in the BST. Prodynorphin was not expressed by calbindin neurons in the medial part of the lateral CeA, and indirect evidence suggested that it was not expressed by enkephalin neurons. Coexpression of prodynorphin in extrahypothalamic CRH neurons in the CeA could provide an anatomical basis for regulation of the stress responses and other CRH-related functions by the brain dynorphin/KOP receptor system.     

Area postrema and the anorectic actions of dexfenfluramine and amylin

The present study examined whether the area postrema and adjacent nucleus of the solitary tract (AP/NTS) is necessary for the expression of anorexia to two classes of anorectic agent. The first agent is the serotonergic agonist, dexfenfluramine (DFEN) and the second is the pancreatic peptide, amylin. Rats were prepared with either aspiration lesions of the AP/NTS or a sham operation. Rats with such lesions (APX) displayed normal anorexia following administration of DFEN, but the anorectic effect of amylin was completely eliminated. The magnitude of a conditioned flavor aversion to DEN was similar in APX and sham operated controls but, unlike controls, APX rats did not reduce total intake in the two-bottle preference test. Finally, the induction of Fos-like immunoreactivity (Fos-ir) following either DFEN or amylin was examined in both APX and sham operated groups. Both agents induced Fos-ir in the AP and/or NTS of sham operated rats, and this region was entirely absent in the APX rats. DFEN-induced Fos-ir was reduced greatly in the PVN of APX rats, but appeared normal in several other regions surveyed, including the central nucleus of the amygdala and the dorsal striatum. In contrast, amylin-induced Fos-ir was reduced in many rostral brain regions of APX rats. These data indicate that neither the anorexia nor the flavor aversion that are produced by DFEN are dependent upon the AP, and in particular that Fos-ir induced by DFEN in the LPBE is not due to afferents from the AP/NTS. In contrast, the anorectic effect of amylin seems to be due principally to its direct action at the AP/NTS.     

Distribution of Fos-like immunoreactivity within the rat brain following intraventricular injection of the selective NK(3) receptor agonist senktide

Neurokinin B (NKB) is one member of an evolutionarily conserved family of neuropeptides, the tachykinins. Preferential binding of NKB to endogenous NK(3) receptors affects a variety of biological and physiological processes, including endocrine secretions, sensory transmission, and fluid and electrolyte homeostasis. In light of its widespread biological actions, immunohistochemical detection of the c-Fos protein product was used to study the distribution of neuronal activation in the rat brain caused by intraventricular (icv) injections of the selective NK(3) receptor agonist (succinyl-[Asp(6), N-Me-Phe(8)] substance P [6-11]), senktide. Quantitative analysis revealed that treatment with isotonic saline or 200 ng senktide resulted in the differential expression of Fos-like immunoreactivity (FLI) throughout the brain. Senktide induced the highest number of FLI neurons in the lateral septum, bed nucleus of the stria terminalis, amygdala, paraventricular nucleus of the hypothalamus, median preoptic nucleus, organum vasculosum of the lamina terminalis, supraoptic nucleus, periaqueductal gray, and medial nucleus of the solitary tract compared to isotonic saline controls. Additional regions that contained elevated FLI following icv injection of senktide, relative to saline injection, included the cerebral cortex, lateral hypothalamic nucleus, suprachiasmatic nucleus, ventral tegmental area, substantia nigra, inferior colliculus, locus coeruleus, zona incerta, and arcuate nucleus. Our data indicate that activation of NK(3) receptors induces the expression of FLI within circumscribed regions of the rat brain. This pattern of neuronal activation overlaps with nuclei known to regulate homeostatic processes, such as endocrine secretion, cardiovascular function, salt intake, and nociception.     

Organization of immune-responsive medullary projections to the bed nucleus of the stria terminalis, central amygdala, and paraventricular nucleus of the hypothalamus: evidence for parallel viscerosensory pathways in the rat brain

Immune-responsive neurons in the brainstem, primarily in the nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM), contribute to a significant drive on forebrain nuclei responsible for brain-mediated host defense responses. The current study investigated the relative contribution of brainstem-derived ascending pathways to forebrain immune-responsive nuclei in the rat by means of retrograde tract tracing and c-Fos immunohistochemistry. Fluorogold was iontophoresed into the bed nucleus of stria terminalis (BST), central nucleus of the amygdala (CEA), paraventricular nucleus of the hypothalamus (PVN), and the pontine lateral parabrachial nucleus (PBL; an important component of ascending viscerosensensory pathways) followed 2 weeks later by intraperitoneal injection of lipopolysaccharide (LPS, 0.1 mg/kg) or saline. The NTS and VLM provide immune-responsive input to all four regions, via direct, predominantly catecholaminergic, projections to the PVN, the lateral BST, and the CEA, and mostly non-catecholaminergic projections to the PBL. The PBL provides a major LPS-activated input to the BST and CEA. The pattern of LPS-activated catecholaminergic projections from the VLM and NTS to the forebrain is characterized by a strong predominance of VLM input to the PVN, whereas the NTS provides a greater contribution to the BST. These findings indicate that direct and indirect pathways originate in the caudal brainstem that propagate immune-related information from the periphery with multiple levels of processing en route to the forebrain nuclei, which may allow for integration of brain responses to infection.     

Haloperidol induces Fos expression in the globus pallidus and substantia nigra of cynomolgus monkeys

Systemic injections of the dopamine antagonist haloperidol (0.1-2.5 mg/kg) induced a dose dependent increase in Fos-like immunoreactivity (FLI) in the internal segment of the globus pallidus (GPi) and in the substantia nigra (SN) of cynomolgus monkeys. These findings are consistent with models of basal ganglia organization which predict that blockade of dopamine receptors should result in a disinhibition of cells in these structures. In the GPi, labeling was most pronounced along the ventral, lateral and medial borders of the nucleus and none of the pallidal cells expressing FLI were immunopositive for choline acetyltransferase. In the SN, immunoreactive nuclei were concentrated in the pars reticulata and the majority of labeled nigral neurons did not display tyrosine hydroxylase-like immunoreactivity. A small number of cells displaying FLI were also observed in the external pallidal segment, but no labeling was seen in the subthalamic nucleus. These findings indicate that blockade of dopamine receptors induces a characteristic pattern of Fos expression in the primate brain which strongly resembles that previously reported in rodents.     

Seizures and Proto-Oncogene Expression offosin the Brain of Adult Genetically Epilepsy-Prone Rats

The mechanisms and brain circuitry that render genetically epilepsy-prone rats (GEPRs) susceptible to acoustically induced seizures are not completely known. The present study explores the neuroanatomy of acoustically induced seizures by immunohistochemical analysis of the proto-oncoproteinfosafter intense acoustic stimulation (AS) with and without seizures. Acoustic stimulation induced tonic convulsions in GEPR-9s, but not in control rats. Locations of brain nuclei showingfos-like immunoreactive (FLI) neurons following AS with and without seizures were mapped. Semiquantitative methods were used to compare FLI neuron numerical densities in AS control rats and GEPRs. Many brain areas exhibited profound FLI in AS control rats and GEPRs. Unexpectedly, the cochlear nuclei and the central nucleus of the inferior colliculi (ICc), both of which are requisite for AGS initiation, exhibited a diminishedfosexpression in animals having seizures compared to AS controls. In contrast, GEPRs displayed a significant increase in FLI neurons within the dorsal cortex of the IC (ICd) compared to AS controls. This finding may suggest a seizure-related amplification of the auditory signal between the ICc and the ICd. Other nuclei, known to be involved in auditory transmission (i.e., superior olivary complex; trapezoid nucleus; dorsal nucleus of the lateral lemniscus, DNLL), did not show differential FLI densities between seizure and AS control animals. In contrast, seizure-induced FLI was observed in many nonauditory brain nuclei. Of particular interest was the identification of an intensely labeled nucleus in the GEPR. This nucleus resides in the most posterior and dorsal–lateral part of the pedunculopontine tegmental nucleus–pars compacta (PPTn-pc) immediately adjacent to the DNLL and extends posteriorly into the superior lateral subnucleus of the lateral parabrachial area (SLPBn). Therefore, we have tentatively termed this nucleus the PPSLPBn. The PPSLPBn lies in a region previously described as a mesencephalic locomotor region and a suspected functional involvement of this nucleus in display of seizure activity is under investigation. Other brain stem nuclei showing differentialfosexpression between GEPRs and AS control rats are also described.     

Coexistence of somatostatin with neuropeptide Y, but not with cholecystokinin or vasoactive intestinal peptide, in neurons of the rat amygdala

A two-color immunoperoxidase procedure was used to determine whether somatostatin (SOM) containing neurons in the amygdala also contain neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), or cholecystokinin (CCK). There was no evidence that SOM-containing neurons in any of the amygdaloid nuclei contain VIP or CCK. In contrast, there was extensive colocalization of SOM and NPY in all of the amygdaloid nuclei with the exception of the intercalated masses and the lateral subdivision of the central nucleus. The greatest number of SOM-NPY double-labeled cells was observed in the medial nucleus, lateral nucleus, and intra-amygdaloid portion of the bed nucleus of the stria terminalis. The morphology of these SOM-NPY neurons was similar in all nuclei. Most exhibited fusiform or avoid cell bodies with one or two sparsely branched dendrites emerging from each pole of the cell. The extensive coexistence of SOM and NPY in non-pyramidal neurons of the basolateral amygdala is similar to that seen in the cerebral cortex and supports the concept that these brain regions share many important characteristics. The extensive colocalization of SOM and NPY in the medial amygdala, in conjuction with the results of previous studies, suggests that some of these cells may project to the bed nucleus of the stria terminalis and hypothalamus.     

cFos induction during conditioned taste aversion expression varies with aversion strength

Fos-like immunoreactivity (FLI) can indicate the location of neurons activated following expression of conditioned taste aversion (CTA). After one conditioning trial FLI has been identified in the intermediate nucleus of the solitary tract (iNTS) with little expression in other brain regions. The present study assessed the effect of increasing aversion strength on the magnitude and anatomical distribution of FLI during CTA expression. When animals received three rather than one conditioning trial, significant FLI was seen not only in the iNTS but also in the parabrachial nucleus (PBN), and the central nucleus of the amygdala (CNA), regions thought to be important in taste aversion learning.