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PubMed1994

Catecholamine release in the rat hypothalamic paraventricular nucleus in response to haemorrhage, desipramine and potassium.

In vivo microdialysis and HPLC were used to measure catecholamine release in the rat hypothalamic paraventricular nucleus (PVN) during haemorrhage. The effects of noradrenaline uptake blockade with 1 microM desipramine (DMI) and a depolarising concentration of potassium (100 mM) through the probe were also examined. Dialysis probes implanted in the PVN of urethane anesthetised rats were perfused with modified Ringer solution at 1.1 microliter/min. Thirty minute collections were analysed for DOPA, noradrenaline, DOPAC, HVA and 5-HIAA. Basal concentrations, in the absence of DMI, were: DOPA 203.6 +/- 44.0 pg/ml, noradrenaline 128.0 +/- 20.4 pg/ml; DOPAC 5.6 +/- 0.7, HVA 5.1 +/- 2.2 and 5-HIAA 87.2 +/- 17.8 ng/ml. Basal noradrenaline was doubled in the presence of DMI while basal and stimulated DOPA, DOPAC, HVA and 5-HIAA were not affected by DMI. Haemorrhage resulted in a significant noradrenaline release (48% over resting levels) in the presence of DMI (n = 10, P < 0.05); in the absence of DMI, a smaller and non-significant increase (30% over basal levels) was observed. Potassium-induced depolarisation caused a significant two- and four-fold increase in noradrenaline release (P < 0.001), with decreases in the dopamine metabolites DOPAC (31%, 44%) and HVA (35%, 28%), and the serotonin metabolite, 5-HIAA (41%, 33%), in the presence and absence of DMI, respectively. The catecholamine precursor DOPA did not vary throughout either experiment. The results indicate that haemorrhage induces a 48% increase in noradrenaline release in the rat PVN which provides evidence for a role of noradrenergic projections to the PVN in cardiovascular control.

Animals↗

PubMed2006

Different signaling molecules responsible for IL-1beta-induced oxytocinergic and vasopressinergic neuron activation in the hypothalamic paraventricular nucleus of the rat.

It has been well known that oxytocin (OT)-ergic and arginine vasopressin (AVP)-ergic neurons located in the hypothalamic paraventricular nucleus (PVN) and super optic nucleus (SON) are two kinds of neuroendocrine cells with diverse functions. It has also been demonstrated that immune stimuli can activate these neurons to secret OT and AVP. However, the intracellular signal transduction molecules responsible for the activation of these OT-ergic and AVP-ergic neurons in PVN by immune stimuli are still unclear. In this experiment, the roles of Fos, a protein product of immediate early gene c-fos, and extracellular signal-regulated protein kinase (ERK) 1/2, a signal transduction molecule of mitogen-activated protein kinase (MAPK) family, in these processes were studied in the PVN of the rat following IL-1beta stimulation. The Sprague-Dawley rats were received either 750 ng/kg IL-1beta or equal volume normal saline (NS) injection intravenously (i.v.), and perfused transcardially by 4% paraformaldehyde 3h later. Fos and phosphorylated ERK1/2 (pERK1/2)-immunoreactivity (-ir) was observed in PVN by ABC immunohistochemical staining. Meanwhile, the double staining for OT/Fos, AVP/Fos, OT/pERK1/2 and AVP/pERK1/2 were also processed. The ABC immunohistochemical staining results showed that after an i.v. injection of IL-1beta, the expressions of Fos and pERK1/2 increased evidently in the PVN. Double-staining results showed that a large number of OT-ir cells contained strong Fos-ir products in their nuclei, while only a few of OT cells were double labeled with pERK1/2. As to AVP neurons, great quantities of AVP cells were strongly double labeled with pERK1/2 while there were nearly no Fos-ir nuclei in AVP-ir cells. We conclude from these results that the intracellular IL-1beta-induced events in OT and AVP neurons in PVN are quite different. The OT neurons are mainly activated via Fos without involvement of ERK1/2 pathway, while the latter, but not Fos, involves the intracellular event in AVP neurons activated by IL-1beta.

Animals↗

PubMed1992

Met-enkephalin-Arg6-Gly7-Leu8- and substance P-containing projections from the nucleus preopticus medianus to the paraventricular hypothalamic nucleus.

The nucleus preopticus medianus (POMe) is known to be important for the regulation of fluid balance and cardiovascular control. Direct projections from the POMe to the paraventricular hypothalamic nucleus (PVN), where vasopressin-containing neurons exist, were examined in the rat using immunohistochemistry combined with a retrograde tract tracing method. After injection of WGA-HRP-colloidal gold into the PVN, many neurons were retrogradely labeled in the POMe; some of them were immunoreactive to Met-enkephalin-Arg6-Gly7-Leu8 (mE8) or substance P (SP). The results indicate that mE8- and SP-immunoreactive neurons in the POMe send their axons to the PVN.

Animals↗

PubMed1996

Regulation of galanin gene expression in the hypothalamic paraventricular nucleus of the obese Zucker rat by manipulation of dietary macronutrients.

Lean and obese male Zucker rats were fed high fat (72% of energy as fat), high carbohydrate (66% of energy as carbohydrate) or intermediate diets for 4 weeks commencing 1 week after weaning. We examined the effects of these diets on growth rates, plasma insulin and corticosterone titres, and hypothalamic gene expression of 3 appetite-related neuropeptides. Messenger RNA levels for neuropeptide Y (NPY), galanin (GAL) and corticotropin-releasing factor (CRF) in critical hypothalamic locations were measured by in situ hybridization in each brain. Obese rats grew more rapidly and had elevated plasma insulin and corticosterone concentrations relative to their lean littermates. The obese phenotype was also associated with elevated NPY gene expression in the arcuate nucleus of the hypothalamus and increased GAL gene expression in the hypothalamic paraventricular nucleus. There was no effect of diet on NPY or CRF gene expression in either lean or obese rats. However, maintenance on the high fat diet had a significant effect on GAL gene expression in obese but not lean rats: high fat diet significantly reduced mRNA levels in the obese rats. This reduction in GAL mRNA was accompanied by attenuation of the hyperinsulinemia that is characteristic of this genetic obesity.

Animals↗

PubMed2004

Central administration of cocaine- and amphetamine-regulated transcript increases phosphorylation of cAMP response element binding protein in corticotropin-releasing hormone-producing neurons but not in prothyrotropin-releasing hormone-producing neurons in the hypothalamic paraventricular nucleus.

Cocaine- and amphetamine-regulated transcript (CART) has an important action on hypophysiotropic thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) neurons to regulate the hypothalamic-pituitary-thyroid and adrenal axis, respectively. To elucidate the mechanisms by which CART mediates its effect on TRH and CRH neurons, we determined whether the exogenous administration of CART into the cerebrospinal fluid (CSF) phosphorylates the transcription factor, cyclic adenosine 5'-monophosphate response element binding protein (CREB), in the nucleus of TRH and CRH neurons. CART dramatically increased the percentage of phosphoCREB (PCREB) immunolabeled cell nuclei in the hypothalamic paraventricular nucleus (PVN) in fasted as well as fed rats at 10-min postinjection, particularly in the medial parvocellular subdivision of the PVN. Double immunolabelling with CRH antiserum revealed that CART increased the number of CRH neurons containing PCREB from 10.5+/-1.2 % to 87+/-1.2% (P<0.001) in fasting animals and from 3.7+/-0.8% to 74+/-5.3% (P<0.001) in fed animals. In contrast, no significant change was observed in the percentage of proTRH neurons colocalizing with PCREB either in the fasted (11.7+/-1.85%) or fed animals (4.2+/-2.2%) as compared to their respective vehicle controls (2.5+/-1.4% and 4.6+/-1%). Ultrastructural analysis revealed that CART establishes axosomatic and axodendritic contacts with CRH neurons in the PVN. These data demonstrate a selective effect of CART to phosphorylate CREB in CRH, but not TRH neurons in the PVN. Since CART is capable of increasing the gene expression of both CRH and TRH in hypophysiotropic neurons, and CART-containing axon terminals establish synaptic relationships with hypophysiotropic CRH and TRH neurons, we propose that CART may signal to the nucleus by more than one pathway.

Animals↗

PubMed2006

Non-NMDA glutamate receptor antagonist injected into the hypothalamic paraventricular nucleus inhibits the prolactin response to formalin stress of male rats.

The aim of the present investigations was to test the involvement of the glutamatergic innervation of the hypothalamic paraventricular nucleus in the prolactin response to stress. A non-NMDA (6-cyano-7-nitroquinoxaline-2,3-dione disodium, CNQX) or an NMDA glutamate receptor antagonist (dizocilpine hydrogen malate, MK-801) was injected bilaterally into the paraventricular nucleus of freely moving male rats and 15 min later the animals were exposed to formalin stress. Blood samples for prolactin and corticosterone were taken at different time points before and after administration of formalin. CNQX, when injected into the paraventricular nucleus, inhibited the formalin-induced rise in plasma prolactin and not significantly the increase in corticosterone. A similar effect was not observed if MK-801 was administered into the paraventricular nuclei or CNQX was injected outside the cell group. The findings indicate that the glutamatergic innervation of the paraventricular nucleus is involved in the mediation of the formalin-induced prolactin release.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1989

Bombesin microinfusion into the rat hypothalamic paraventricular nucleus increases blood glucose, free fatty acids and corticosterone.

Bombesin is a particularly potent hyperglycemic agent when administered intraventricularly or intracisternally in the rat. Because bombesin-like immunoreactivity is found in several forebrain regions implicated in glucoregulation, the ability of direct hypothalamic microinfusions of this peptide to affect serum metabolic fuel levels was tested. Three experiments, using anesthetized, acutely infused rats, or unanesthetized rats with chronic intracranial implants, showed that microinfusion of bombesin into the hypothalamic paraventricular nucleus caused significant, dose-related increases in serum glucose; infusions into the lateral hypothalamus or the caudate nucleus were ineffective. Infusions into the ventromedial nucleus significantly elevated glucose only in acutely anesthetized rats. In unanesthetized rats with chronic intracranial cannulae, bombesin infusions into all 3 hypothalamic sites, but not the caudate-putamen, significantly elevated blood free fatty acids, while only infusions into the paraventricular nucleus caused significant dose-related increases in blood corticosterone. The results demonstrate that the paraventricular nucleus is a sensitive site for bombesin-induced elevation of blood glucose, free fatty acids, and corticosterone. They also imply that the bombesin binding sites and immunoreactive terminals previously identified in these regions may be involved in the central regulation of circulating metabolic fuel levels and the pituitary-adrenal axis, and that the effects of acute surgery may augment the hyperglycemic response to intrahypothalamic bombesin administration.

Animals↗

PubMed2004

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↗

PubMed1984

Role of the hypothalamic paraventricular nucleus in neuroendocrine responses to daylength in the golden hamster.

Daylength regulates reproduction in golden hamsters through a mechanism which involves the pineal indoleamine, melatonin. Retinal input to the suprachiasmatic nucleus of the hypothalamus (SCN) and sympathetic innervation of the pineal are critical to the inhibition of reproduction by short photoperiods. Since the hypothalamic paraventricular nucleus (PVN) receives extensive input from the SCN in the rat, and may influence autonomic function via its brainstem and spinal cord projections, we studied the role of this nucleus in photoperiodically induced gonadal regression in the hamster. Bilateral electrolytic destruction of either the paraventricular nucleus (PVN) or suprachiasmatic nucleus (SCN) of the hypothalamus completely blocked testicular regression induced by either blinding or exposure to short days (10L:14D). Lesions in the retrochiasmatic hypothalamus (RCA) which may have interrupted the pathway of previously identified efferents from the SCN to the PVN were also effective in preventing short day-induced gonadal regression. Pineal melatonin content was measured in intact and lesioned hamsters sacrificed 3-5 h before lights on, at the time of the expected nocturnal peak. While SCN and RCA lesions significantly reduced pineal melatonin content, PVN lesions were still more effective in this regard. We conclude that the hamster's neuroendocrine response to photoperiod is mediated by neural pathways which include retinohypothalamic input to the SCN and efferents from this nucleus to the PVN which travel dorsocaudally through the retrochiasmatic area of the hypothalamus. Effectiveness of lesions restricted to the PVN suggests that direct projections from the PVN to spinal autonomic centers convey photoperiodic information which regulates pineal, and hence gonadal, function.

Animals↗

PubMed1995

Responses of median preoptic neurons projecting to the hypothalamic paraventricular nucleus to osmotic stimulation in Wistar-Kyoto and spontaneously hypertensive rats.

Twenty-one median preoptic nucleus (MnPO) neurons in normotensive Wistar-Kyoto rats (WKY) and 18 MnPO neurons in spontaneously hypertensive rats (SHR) were antidromically activated by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) under urethane anesthesia. No significant differences in the latency, conduction velocity, or threshold of antidromic activation were observed between WKY and SHR. The spontaneous discharge rate was significantly higher in SHR than in WKY. The activity of these identified MnPO units was examined for response to intracarotid injections of isotonic (0.15 M NaCl solution, 0.05 ml) or hypertonic (0.3 M NaCl solution, 0.05 ml) saline. All the units did not change their activity to the injections of isotonic saline. Of these units, 14 units in WKY and 12 units in SHR displayed and 3 units in WKY and 4 units in SHR exhibited a reduction in neuronal activity following the injections of hypertonic saline, while the remaining 4 units in WKY and 2 units in SHR were unresponsive. The duration and frequency of excitatory response, but not the inhibitory response, caused by the osmotic stimulation was much greater in SHR than in WKY. These results show that MnPO neurons projecting to the PVN may carry the information from osmosensitive elements and that there is a difference between WKY and SHR in the responsivity of these MnPO neurons to the osmotic stimulation.

Animals↗

PubMed1986

Horizontal knife cuts either ventral or dorsal to the hypothalamic paraventricular nucleus block testicular regression in golden hamsters maintained in short days.

The possible involvement of efferent pathways from the suprachiasmatic nucleus (SCN) in the photoperiodic regulation of reproduction was studied by measuring the testis size of hamsters bearing a horizontal knife cut either ventral or dorsal to the hypothalamic paraventricular nucleus (PVN) that were transferred from photostimulatory long days (light:dark (L:D) 14:10 h) to non-stimulatory short days (L:D 6:18 h). Knife cuts placed either ventral or dorsal to the PVN blocked testicular regression induced by exposure to short days. These results indicate that efferent fibers running dorsally from the SCN to the PVN are involved in relaying photoperiodic information from the SCN to the PVN. Furthermore, recently-defined efferents that leave the PVN dorsally and terminate in the spinal cord appear to be responsible for relaying seasonal information about day-length to the pineal-reproductive axis of hamsters.

Animals↗

PubMed1990

Electron microscopic studies of medullary synaptic inputs to vasopressin-containing neurons in the hypothalamic paraventricular nucleus.

We have observed the ascending projections from the lower brain stem to the magnocellular vasopressin-like immunoreactive (VP-LI) neurosecretory neurons in the paraventricular nucleus (PVN) using electron microscopy. The tissues were prepared by a double labeling technique combining anterograde tracing after iontophoretic injection of wheat germ agglutinin-coupled horseradish peroxidase (WGA-HRP) in the A1 group (lateral reticular nucleus in the medulla oblongata) with VP immunocytochemistry. Both the WGA-HRP-labeled and the unlabeled axon terminals made synaptic contacts with VP-LI cell bodies and processes in the PVN. This indicates a direct synaptic influence of medullary A1 group on the secretory activity of the VP-containing neurons in the hypothalamic paraventricular nucleus.

Animals↗

PubMed1996

Muscimol acts in dorsomedial but not paraventricular hypothalamic nucleus to suppress cardiovascular effects of stress.

Both the dorsomedial hypothalamic nucleus (DMH) and the paraventricular hypothalamic nucleus (PVN) have been implicated in the neural control of the cardiovascular response to stress. We used the GABAA agonist muscimol to inhibit neuronal activation and attempted to identify hypothalamic nuclei required for the cardiovascular response to air stress. Chronically instrumented rats received bilateral injections of either 80 pmol of muscimol or 100 nl of saline vehicle into the DMH, the PVN, or an intermediate area (including the rostral edge of the DMH and the region between the two nuclei) and were placed immediately in a restraining tube and subjected to 20 min of air stress. In all rats, air stress after vehicle injections caused marked increases in heart rate (137 +/- 6 beats/min) and blood pressure (26 +/- 2 mmHg). Microinjection of muscimol into the DMH suppressed the heart rate and blood pressure response by 85 and 68%, respectively. Identical microinjection of muscimol into the intermediate area between the DMH and the PVN attenuated the increases in heart rate by only 46% and in blood pressure by 52%. In contrast, similar injections into the vicinity of the PVN failed to alter the cardiovascular response to air stress. These findings demonstrate that muscimol-induced inhibition of neuronal activity in the region of the DMH blocks air stress-induced increases in heart rate and arterial pressure, whereas similar treatment in the area of the PVN has no effect.

Air↗

PubMed1998

Corticotropin releasing factor mRNA expression in the hypothalamic paraventricular nucleus and the central nucleus of the amygdala is modulated by repeated acute stress in the immature rat.

Age-appropriate acute stress, such as cold exposure, provokes the secretion of corticotropin releasing factor (CRF) from the hypothalamus, leading to a robust increase of plasma corticosterone in the immature rat. This activation of the hypothalamic-pituitary-adrenal system is accompanied by a stress-induced increase of steady-state CRF-mRNA expression in the hypothalamic paraventricular nucleus (PVN). In the current study, we analysed changes in CRF-mRNA expression in the PVN and the central nucleus of the amygdala (ACe) in the immature rat in response to a single episode of cold stress and three repeated exposures to this same stressor. CRF-mRNA expression in the PVN increased after a single, but not repeated exposures to cold stress, while repeated acute stress increased the content of the CRF peptide in the anterior hypothalamus. In the ACe, repeated episodes of cold stress resulted in increased expression of CRF-mRNA. These findings indicate a differential regulation of CRF gene expression in the PVN and ACe of the immature rat by single and repeated acute stress.

Acute Disease↗

PubMed1993

Ventral subicular interaction with the hypothalamic paraventricular nucleus: evidence for a relay in the bed nucleus of the stria terminalis.

The axonal projections of the ventral subiculum to the bed nucleus of the stria terminalis (BST) were examined in the rat with the anterograde neuronal tracer Phaseolus vulgaris-leucoagglutinin (PHA-L). Axons originating in the ventral subiculum coursed to the BST through either the fimbria-fornix, or a pathway involving the stria terminalis via the amygdala. Ventral subicular axons gave rise to dense terminal networks that were preferentially distributed in medial and ventral subregions of the BST. The distribution of subicular fibers and terminals was examined in relation to BST neurons that project to the hypothalamic paraventricular nucleus (PVN). In these cases, discrete iontophoretic injections of the retrograde tracer Fluoro-gold were made in the PVN, with PHA-L delivered to the ipsilateral ventral subiculum. An immunocytochemical double-labeling protocol was then employed for the simultaneous detection of PHA-L and Fluoro-gold, and provided light microscopic evidence for subicular input to PVN-projecting cells located within the BST. In a second series of experiments, the gamma-amino butyric acid (GABA)ergic nature of the BST was examined by in situ hybridization histochemistry for detection of transcripts encoding GAD67 mRNA. The studies revealed that a high proportion of BST neurons express GAD67 transcripts. Also, experiments combining Fluoro-gold tracing with GAD67 in situ hybridization suggested that a proportion of PVN-projecting neurons in the BST are GABAergic. Taken together, the results of these sets of studies suggest that the inhibitory influences of the hippocampus on the PVN might be relayed through specific portions of the BST. These findings may have important implications for our understanding of the neural regulation of the hypothalamic-pituitary-adrenal axis.

Amygdala↗

PubMed1990

Increased density of glutamic acid decarboxylase-containing terminals in the medial preoptic nucleus and the area surrounding the paraventricular hypothalamic nucleus is associated with deoxycorticosterone acetate (DOCA)-salt hypertension.

gamma-Aminobutyric acid (GABA) is a major inhibitory neurotransmitter and has been shown to exert considerable influence on the neural control of the cardiovascular function. It is not clear, however, which GABAergic systems are involved in salt-induced hypertension. This study was designed to investigate the GABAergic neurons in specific regions of the brain possibly linked to salt-induced hypertension. After 4 weeks of deoxycorticosterone acetate (DOCA) and salt treatments, the rats developed cardiac hypertrophy. All of the animals were sacrificed for immunocytochemical localization of GABAergic terminals using specific antibodies to glutamic acid decarboxylase (GAD). GAD-positive GABAergic terminal densities in discrete regions of the brain were determined by using morphometric quantitation. Results showed that GABAergic terminal densities in the medial preoptic nucleus and the area lateral to the paraventricular hypothalamic nucleus were significantly increased in DOCA-salt-treated rats 4 weeks after the experiment as compared with 4 week controls. This study provides new evidence to support further the idea that central GABAergic neurons are closely associated with pathogenesis of salt-induced hypertension. Different hypertensive mechanisms between salt-induced hypertension and genetic hypertension are also discussed.

Animals↗

PubMed2004

Hypothalamic paraventricular nucleus neurons regulate medullary catecholamine cell responses to restraint stress.

Both physical and psychological stressors recruit catecholamine cells (CA) located in the ventrolateral medulla (VLM) and the nucleus of the solitary tract (NTS). In the case of physical stressors, this effect is initiated by signals that first access the central nervous system at or below the level of the medulla. For psychological stressors, however, CA cell recruitment depends on higher structures within the neuraxis. Indeed, we have recently provided evidence of a pivotal role for the medial amygdala (MeA) in this regard, although such a role must involve a relay, as MeA neurons do not project directly to the medulla. However, some of the MeA neurons that respond to psychological stress have been found to project to the hypothalamic paraventricular nucleus (PVN), a structure that provides significant input to the medulla. To determine whether the PVN might regulate medullary CA cell responses to psychological stress, animals were prepared with unilateral injections of the neurotoxin ibotenic acid into the PVN (Experiment 1), or with unilateral injections of the retrograde tracer wheat germ agglutinin-gold (WGA-Au) into the CA cell columns of the VLM or NTS (Experiment 2). Seven days later, animals were subjected to a psychological stressor (restraint; 15 minutes), and their brains were subsequently processed for Fos plus appropriate cytoplasmic markers (Experiment 1), or Fos plus WGA-Au (Experiment 2). PVN lesions significantly suppressed the stress-related induction of Fos in both VLM and NTS CA cells, whereas tracer deposits in the VLM or NTS retrogradely labeled substantial numbers of PVN cells that were also Fos-positive after stress. Considered in concert with previous results, these data suggest that the activation of medullary CA cells in response to psychological stress may involve a critical input from the PVN.

Animals↗

PubMed1998

Contribution of dopamine neurons in the medial zona incerta to the innervation of the central nucleus of the amygdala, horizontal diagonal band of Broca and hypothalamic paraventricular nucleus.

Results of previous studies suggested that incertohypothalamic dopamine (IHDA) neurons located in the medial zona incerta (MZI) project to the central nucleus of the amygdala (cAMY), horizontal diagonal band of Broca (HDB), and paraventricular nucleus (PVN). The overall goal of the present study was to determine the relative contribution of IHDA neurons to the DA innervation of these brain regions. A combined fluorescent and in situ hybridization histochemical procedure was employed to localize the retrograde tracer fluoro-gold (FG) in cells expressing tyrosine hydroxylase (TH) mRNA in the MZI following its iontophoretic injection into either the cAMY, HDB or PVN. For comparison, the numbers of dual labeled FG/TH mRNA neurons in the midbrain were also determined. One week after unilateral injection of FG into the cAMY, cells containing FG+TH mRNA were found in the ipsilateral MZI, substantia nigra zona compacta (SNC) and ventral tegmental area (VTA). The total numbers of cells labeled with FG varied with the size of the injection site, but the ratio of dual labeling in the MZI to that of the SNC-VTA remained constant across animals at approximately 1:6. FG injections into the HDB resulted in a ratio of dual labeled cells in the ipsilateral MZI and VTA of approximately 1:2, but no dual labeled cells were found in the SNC. Dual labeled cells were only found in the ipsilateral MZI in animals receiving FG injections in the PVN. Thus, DA terminals in the PVN originate exclusively from IHDA neurons in the MZI, whereas these neurons provide only a portion of the DA innervation of the cAMY and HDB. The similar distribution of dual labeled cells in the MZI following FG injections into the cAMY, HDB and PVN suggests that perikarya of IHDA neurons projecting to these regions are not organized into distinct groups.

Amygdala↗