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A Szafarczyk

Publications and source records attributed to A Szafarczyk.

At least 19 recordsLinked to original sources
PubMed2001

An endogenous adrenoceptor ligand potentiates excitatory synaptic transmission in cultured hippocampal neurons.

Noradrenergic inputs modulate hippocampal function via distinct receptors. In hippocampal neuronal cultures, mRNA expression of adrenoceptor subtypes is maintained from 1 day in vitro (DIV) to 22 DIV. Noradrenaline dose-dependently stimulates phosphoinositide (PI) breakdown in both immature and mature cultures through the activation of alpha1 receptors. At 22 DIV, basal PI breakdown depends on excitatory synaptic activity since it is decreased by tetrodotoxin or glutamate receptor antagonists. At 22 DIV, a similar decrease of basal PI breakdown is also observed with alpha1, alpha2 or beta adrenoceptor antagonists. These effects are not additive with that produced by tetrodotoxin. Adrenergic antagonists also strongly reduce spontaneous excitatory post-synaptic currents (sEPSC) as evidenced by whole cell recording. Therefore, in hippocampal cultures, excitatory transmission is modulated by a tonic activation of adrenoceptors probably produced by an endogenous ligand. Indeed, (i) the depletion of catecholamine pools by reserpine also decreases both basal PI metabolism and sEPSC; (ii) hippocampal neurons possess both tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase mRNAs, encoding enzymes required for catecholamine synthesis; and (iii) some hippocampal neurons show TH-immunoreactivity. TH-positive cells are also detected in E18 hippocampal sections. Thus, cultured hippocampal neurons synthesize and release an adrenergic-like ligand, which tonically potentiates excitatory synaptic transmission in mature cultures.

Adrenergic Uptake Inhibitors↗
PubMed1999

Opposite regulation by glucocorticoids of the alpha 1B- and alpha 2A-adrenoreceptor mRNA levels in rat cultured anterior hypothalamic slices.

In this study we investigated whether the expression of alpha1B- and alpha2A-adrenoreceptor mRNAs is differently modulated by glucocorticoids in rat cultured anterior hypothalamus slices. Using a semi-quantitative reverse transcription-polymerase chain reaction assay, the level of the alpha1B-adrenoreceptor mRNA was significantly reduced in slices cultured in steroid free-medium when compared with that measured in standard medium (i.e. containing basal adrenosteroid plasma concentrations). In contrast, the expression of the alpha2A-adrenoreceptor mRNA was markedly increased. Finally, the ratio of alpha1B- versus alpha2A-mRNA levels was about 1.7 and 0.7 in standard and steroid-free medium, respectively. These responses were completely reversed by supplementation with corticosterone. These findings provide the first evidence that in vitro glucocorticoids may regulate, in an opposite manner, the expression of the alpha1B-and alpha2A-adrenoreceptor mRNAs in the hypothalamus. This kind of regulation could be related to steroid-dependent changes in the noradrenergic control of neuroendocrine secretions.

Animals↗
PubMed1998

Glucocorticoids provoke a shift from alpha2- to alpha1-adrenoreceptor activities in cultured hypothalamic slices leading to opposite noradrenaline effect on corticotropin-releasing hormone release.

We have shown previously that noradrenaline (NA) stimulated or inhibited the release of corticotropin-releasing hormone (CRH) according to the availability of adrenal steroids. The aim of the present work was to examine whether the changes in the NA modulation of CRH release from hypothalamic neurons result from a steroid-induced plasticity of the adrenergic transduction pathways. From anterior hypothalamic slices cultured in standard medium (i.e., containing adrenal steroids at a final dilution of 61 +/- 9 ng/ml), (a) the stimulatory effect of NA on CRH release was reversed in a dose-dependent manner by increasing concentrations of the alpha1-adrenoreceptor antagonist prazosin, (b) activation of protein kinase C by acute treatment with phorbol 12-myristate 13-acetate (0.5 microM, 1 h) mimicked NA stimulation of CRH secretion, and (c) the activation of L-type Ca2+ channels by Bay K 8644 also produce an increased CRH secretion. In contrast, the inhibitory effect of NA on CRH secretion from slices cultured in steroid-free medium was markedly reversed by the alpha2-adrenoreceptor antagonist yohimbine, by pretreatment with pertussin toxin, or by the addition of 4-aminopyridine, a K+-channel blocker. Acute treatment with phorbol 12-myristate 13-acetate did not change the inhibitory NA effect. Moreover, all these effects were reversed by daily corticosterone supplementation, for as long as they were tested. These results are consistent with a steroid-dependent change in the nature of adrenergic receptors and its associated transduction pathways involved in the regulation of CRH secretion in the hypothalamus.

4-Aminopyridine↗
PubMed1995

Removal of adrenal steroids from the medium reverses the stimulating effect of catecholamines on corticotropin-releasing hormone neurons in organotypic cultures.

An organotypic culture system of anterior hypothalamic slices was developed for studying the secretory responses of corticotropin-releasing hormone (CRH) neurons to corticosteroid-catecholamine interactions. The standard culture medium included 5% horse serum containing 50 micrograms/l cortisol. In 1- to 3-day cultures, the tissue viability was demonstrated by the presence of arginine vasopressin immunolabeled perikarya and axons in the paraventricular nucleus and by sustained tissue concentrations of CRH (around 50 pg/mg protein). However, immunoreactive CRH neurons were not detectable in cultures in the standard medium. Exposure of cultures to high K+ (56 mM) in the medium induced a ten-fold increase in basal CRH release which was completely abolished in a Ca(2+)-free medium containing 2 mM EGTA. Noradrenaline (NA) triggered CRH release in a dose-dependent (1-20 microM) and time-dependent (0.5-6 h) manner. Removal of corticosteroids from the media by charcoal treatment led to (1) the visualization of immunolabelled CRH perikarya and fibers and a 55% rise in CRH content of the paraventricular nucleus tissue and (2) to a five-fold increase in CRH release. Both effects were reversed by supplementation of the culture medium with corticosterone (50 micrograms/l). Under steroid-free conditions, NA (1-10 microM) not only failed to induce CRH release, but strongly inhibited the consistent baseline in CRH release. This was reminiscent of a similar corticosteroid-dependent inversion of the NA effect on the hypothalamic-pituitary-adrenal axis described in vivo. Overall, these results are direct evidence of complex corticosteroid-catecholamine interrelationships as major regulatory factors of the hypothalamic-pituitary-adrenal axis.

Adrenal Cortex Hormones↗
PubMed1995

Lesions of the afferent catecholaminergic pathways inhibit the temporal activation of the CRH and POMC gene expression and ACTH release induced by human interleukin-1beta in the male rat.

A number of recent studies have suggested that interleukin-1beta (IL-1beta) is a major mediator contributing to the recruitment of the hypothalamo-pituitary-adrenal (HPA) axis following infectious aggressions. Central catecholamines modulate the response of the HPA axis. To investigate the importance of the afferent catecholaminergic pathways in a pathophysiological situation, we used the intraperitoneal (i.p.) IL-1beta injection (mimicking peripheral infections) and we investigated the effects on the HPA responses to IL-1beta of bilateral neurotoxic (6-OHDA) deletion of the ventral noradrenergic ascending bundle (VNAB-X). The VNAB is an essential stimulating pathway linking the brainstem and the paraventricular nucleus (PVN). We determined the time courses of a number of HPA variables up to 240 min after i.p. injection of IL-1beta. We followed: plasma ACTH and corticosterone (CORT) concentrations, AP POMC nuclear primary RNA transcripts, AP POMC nuclear intermediate transcript RNA, AP POMC cytoplasmic mRNA, and hypothalamus (HT) CRH cytoplasmic mRNA. Compared to sham-lesioned male rats, VNAB-X animals displayed: (1) a reduced increase in plasma ACTH, and to a lesser extent in CORT throughout the experimental period with a 85% inhibition at the peak (90 min); (2) an increase in AP POMC primary nuclear transcript and in AP POMC nuclear intermediate transcript RNAs which last 60 min, instead of sustained significantly higher levels up to 240 min; (3) a similar, although reduced inhibition in the corresponding POMC cytoplasmic mRNA; (4) an almost complete abolishment of the marked biphasic rise in HT CRH mRNA. In conclusion, activation of the HPA axis by peritoneal IL-1beta challenge involves CRH-producing neurons, and afferent catecholaminergic innervation of the PVN plays a crucial role in the signaling machinery linking the peritoneal aggression to the HPA axis.

Adrenocorticotropic Hormone↗
PubMed1995

[The corticotropic axis response after subcutaneous endotoxin injection is not associated with the increase of plasma interleukin-1 beta].

When injected through an intra-arterial (i. a.) cannula, LPS induced a rapid (15-30 min) and long-lasting (> 300 min) increase in plasma ACTH and corticosterone (CORT) levels. The duration of these responses depended on the LPS dose, and except for very small LPS doses, their amplitudes appeared independent of the dose of endotoxin. ACTH peaks (2,200 pg.ml-1) occurred between 30 and 120 min, whereas CORT always reached maximal levels at 120 min. Plasma Interleukin-1 beta (IL-1 beta) levels were always undetectable during the early phase of corticotropic stimulation, but increased strikingly 120 min after LPS injection. Increasing LPS doses, resulted in enhanced and prolonged IL-1 beta plasma circulating levels (up to 3.0 +/- 0.2 ng.ml-1). By contrast, no sub-cutaneous LPS dose used induced early increases in ACTH and CORT levels, whereas time-course of the hormonal response was evocative of the sustained phase of the corticotropic response to i. a. LPS, with both peaks occurring 120 min post-LPS. Increasing the s. c. LPS bolus 50-fold vs the i. a. dose did not affect the maximal amplitude of the ACTH response, whereas the amplitude of the CORT response, instead, appeared dependent on the LPS dose. On the other hand, even for the largest LPS doses, plasma IL-1 beta levels remained undetectable. Sub-cutaneous injection of LPS therefore appears as a new model for the study of the mechanisms of corticotropic responses to endotoxin without a direct involvement of bloodborne IL-1 beta.

Adrenocorticotropic Hormone↗
PubMed1993

Complex catecholaminergic modulation of the stimulatory effect of interleukin-1 beta on the corticotropic axis.

We recently showed that bilateral neurotoxic microlesions (6-OH-DA) of the ventral noradrenergic ascending bundle (VNAB-X) at stereotaxic coordinates that blocked corticotropic stress responses did not affect the ACTH surge after bilateral intra-paraventricular (i.PVN) injections of interleukin-1 beta (IL-1 beta), and that lesioning at these stereotaxic coordinates obliterated the dorsal axonal populations of the VNAB (dVNAB-X), but spared the bundle's most ventral axons (vVNAB). The present study compares the effects of IL-1 beta given i.PVN (2 x 5 ng) of intra-arterially (i.a.) (100 ng) on plasma ACTH in rats with bilateral 6-OH-DA microlesions placed in the dVNAB or the vVNAB, or in an intermediary central position (cVNAB-X). Unlike our previous results, in which dVNAB-X did not alter the biphasic ACTH response to i.PVN IL-1 beta, both vVNAB-X and cVNAB-X reduced by 50-75% the early and delayed ACTH surges which are typical of the i.PVN route. On the other hand the swift monophasic ACTH surge usually occurring after an i.a. injection of IL-1 beta was 65% smaller after dVNAB-X, but was doubled after vVNAB-X or cVNAB-X. Hence, the release of ACTH after both i.PVN or i.a. IL-1 beta requires brainstem afferences conveyed to the hypothalamus by the VNAB. However, the VNAB appears to include at least two functionally different subsets of axons, the roles of which in the ACTH response to IL-1 beta depend on the route by which the cytokine is given.

Adrenocorticotropic Hormone↗
PubMed1993

Effects of discrete lesions in the ventral noradrenergic ascending bundle on the corticotropic stress response depend on the site of the lesion and on the plasma levels of adrenal steroids.

Stereotaxic deletion of selected areas of the ventral noradrenergic ascending bundle (VNAB-X) by discrete bilateral injections of 6-hydroxydopamine (6-OHDA; 4 micrograms in 0.2 microliter saline) was used to explore the role of brain catecholamines (CA) and their interaction with corticosteroid feedback in stress responses of the ACTH-corticosterone (CORT) axis. The stereotaxic coordinates used for 6-OHDA lesions and the optimization of postlesion delays were determined by (a) radioautographic labeling of the VNAB axons after tracer injections into the dorsal A2/C2, or the ventral A1/C1 medullary areas, (b) histofluorescence and immunocytochemical location of interrupted CA pathways versus the postlesional scar, and (c) postlesional noradrenaline and adrenaline concentrations in whole hypothalami and paraventricular nuclei (PVN) punch samples. Two sites of 6-OHDA lesions were selected; both led to striking falls in PVN concentrations of both CA. The more dorsal lesion (dVNAB-X) was the same as that of our earlier studies and interrupted pathways originating predominantly in the A2/C2 area; the second more ventral lesion (vVNAB-X) interrupted axons stemming preferentially from the A1/C1 area. Both VNAB lesions inhibited the ether stress-induced ACTH and CORT surges in rats with intact adrenals. But the blockade (overall poststress release, amplitude and swiftness of hormonal responses) by dVNAB-X was greater than by vVNAB-X. The basal ACTH level in adrenalectomized rats (ADX) was elevated 20-fold and ether stress induced a 4-fold ACTH surge. As in sham-ADX rats, vVNAB-X in ADX rats induced only moderate inhibition of the ACTH response versus ADX + sham-vVNAB-X controls. On the other hand ADX + dVNAB-X rats showed a greatly amplified ACTH stress response over the ADX-sham dVNAB-X controls. This amplification was reversed by oral CORT supplementation. The data suggest that the CA pathways of the VNAB participating, directly or indirectly, in the poststress corticotropic activation may include subsets of CA axons of different origins, whose functional roles in stress are modulated in opposite directions by the plasma corticosteroid level.

Adrenal Cortex Hormones↗
PubMed1993

[Stress. Neurophysiologic studies].

The hypothalamic-pituitary-adrenocortical (HPA) axis knowingly plays a key role in the physiological response to various stressing situations, owing to its gluconeogenetic function, and also, possibly, to its large range of modulating effects on a series of more specific defense mechanisms including the immune system, the latter effect serving to protect the organism against overactive defense reactions. It has long been accepted that under most aggressive conditions the CNS is an essential part of the mechanism controlling the subsequent acute stimulation of the HPA axis. In this line of research, the HPA axis reacts within a few minutes after a standard ether-stress, with a 6 fold increase over the baseline of CRH41 secretion, and at the periphery with 20-fold and 14-fold increases, respectively, in plasma concentrations of ACTH and corticosterone in unanesthetized free-moving rats. From a series of additional experiments a few selected brain structures emerged as basic components of the CNS control involved in the HPA axis stress responses: 1) The catecholamine (CA) producing neurons of the medulla oblongata (A1/C1 and A2/C2 nuclei) which directly innervate the CRH41-secreting neurons in the paraventricular nuclei (PVN) via the ventral noradrenergic bundle (VNAB), yield the major stimulatory pathway to the stress-induced CRH-ACTH surge. Not only was this surge dramatically obliterated by a neurotoxic deletion of the VNAB, with a local microinfusion of 6-hydroxydopamine (6-OHDA) but it was restored by intra-cerebroventricular (icv) microinfusions of adrenaline (AD) or noradrenaline (NA).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Glucocorticoids, transmitters and stress.

Many kinds of stress stimulate the neuroendocrine systems controlling catecholamine and glucocorticoid secretion. Stress-induced stimulation of CRF-containing neurons appears to be mediated by serotonergic, noradrenergic, and possibly other neuronal pathways. Stress can alter various neurobiological and endocrine functions, two essential components of the neuroendocrine responses being release of adrenalin from chromaffin cells of the adrenal medulla and secretion of glucocorticoids from adrenocortical cells. Activation of adrenal steroid secretion is mainly by a reflex activation of hypothalamic neurons, which stimulate ACTH secretion from the anterior pituitary. While the neuropeptide CRF plays a major role in the neuroendocrine response to stress, the neuronal signals which are responsible for the regulation of CRF neurons have not been completely elucidated. A number of other regulatory substances may also participate, alone or with CRF, in the control of ACTH secretion by pituitary corticotrophs, and there is increasing evidence that classical neurotransmitters or neuropeptides may act directly on adrenocortical cells to modulate corticosteroid secretion. We review the neuronal, neuroendocrine, and humoral pathways which participate in the regulation of stress-induced corticosteroid secretion, and present preliminary data on the effect of the tricyclic antidepressant, tianeptine in the response of the HPA axis to stress.

Animals↗
PubMed1991

Inhibitory interactions between alpha 2-adrenergic and opoid but not NPY mechanisms controlling the CRF-ACTH axis in the rat.

Following a series of investigations supporting the concept that the brain stem catecholaminergic (CA) system played a major stimulatory role on both basal and stress-triggered states of the hypothalamic-pituitary-adrenocortical (HPA) axis, across alpha 1 and beta receptors and also via alpha 2 receptors, the present study was designed to gain a deeper insight into the fine mechanism of functional interactions between the alpha 2 receptors mediated CA system and two peptidergic mechanisms, both shown to take part in the stimulatory control of the HPA axis: beta-endorphin and NPY. All experiments were conducted on rats whose noradrenergic bundles, which directly innervate the CRF neurons and are strongly implicated in the ether stress-induced corticotropic response, had been bilaterally obliterated by an intracerebral (i.c.) injection of 6-OHDA (NAB-X). Results showed that: (1) the blockade of the ether-stress induced ACTH response resulting from NAB-X was entirely reversed by an intraventricular (i.c.v.) infusion of the alpha 2 antagonist idazoxan (10 nmol), which appeared ineffective under basal conditions; (2) the restoration of a normal post-stress ACTH surge by i.c.v. idazoxan was itself blunted by an i.c.v. pretreatment with naloxone (10 nmol), whereas an i.c. pretreatment with an anti-NPY serum appeared ineffective. These data suggest that, in addition to a stimulatory control exerted by postsynaptic alpha 2 receptors directly on CRF neurons, other alpha 2 receptors participate, exclusively under the stress conditions above, in a tonic inhibitory control, indirectly mediated to the HPA axis across a stimulatory opioid, but not NPY regulatory component.

Adrenal Cortex↗
PubMed1991

The involvement of noradrenergic ascending pathways in the stress-induced activation of ACTH and corticosterone secretions is dependent on the nature of stressors.

The aim of the present study was to explore in male rats the role of the catecholaminergic innervation of the hypothalamus in corticotropic and adrenal responses to different kinds of stress conditions. For this purpose, 6-hydroxydopamine (3 micrograms in 0.2 microliter saline) was stereotaxically and bilaterally infused at two levels of the main noradrenergic ascending brain stem bundle (NAB-X). The efficiency of catecholaminergic denervation of the hypothalamus was checked by measuring noradrenaline concentrations in paraventricular nuclei punches by HPLC and was confirmed by a 86% fall in noradrenaline levels of NAB-X rats killed after the stress experiments. Seven days after lesioning the NAB, sham operated controls and NAB-X lesioned animals were divided into 4 groups and submitted to 4 different stressors, i.e.: 2 min ether vapors (n = 5), 1 h immobilization (n = 7), i.v. histamine (2 mg/kg; n = 7) or i.v. insuline (10 I.U./kg; n = 8) injections. ACTH and corticosterone were measured in blood samples sequentially taken from a chronic carotid cannula, before stress and at short intervals over the 2 following hours. In comparison to the respective control groups, NAB-X dramatically reduced the ACTH response to ether (-78%) and to restraint (-53%) stress whereas the corticosterone response was affected to a lesser extent. In contrast, NAB-X slightly altered these responses in the histamine-treated group, although, surprisingly, the ACTH response tended to decrease and that of corticosterone to increase. Finally, NAB-X provoked a biphasic response to insuline-induced hypoglycemia, with a very early (5 min) rise in ACTH and corticosterone in comparison to the control group, followed by a trend to low hormonal levels up to 120 min. These results strongly suggest a differential involvement of the hypothalamic noradrenergic innervation upon the hypothalamic-pituitary-adrenal axis according to the nature of stress conditions.

Adrenocorticotropic Hormone↗
PubMed1990

Intrahypothalamic infusion of interleukin-1 beta increases the release of corticotropin-releasing hormone (CRH 41) and adrenocorticotropic hormone (ACTH) in free-moving rats bearing a push-pull cannula in the median eminence.

In two simultaneous studies on unanesthetized rats implanted 1 week earlier with either an intracerebral (i.c.) cannula adjacent to the paraventricular nucleus of the hypothalamus and an intracarotid cannula, or the same i.c. cannula together with a push-pull cannula in the median eminence (ME), we explored the effect of i.c. infused interleukin-1 beta (IL 1 beta, 5 ng in 0.25 microliter of vehicle within 2 min) on the release of corticotropin-releasing hormone (CRH) 41 and adrenocorticotropic hormone (ACTH). Intracerebral infusion of the vehicle alone had no significant effect on either the pulsatility or the level of CRH 41 release and only a short-lived minor effect on plasma ACTH, whereas i.c. IL 1 beta injection led to a significant and long lasting (1-2 h) rise in CRH 41 release peaking 3 times higher than the mean peaks of basal pulsatility (26.1 +/- 3.5 pg/5 min vs 9.5 +/- 0.7 pg/5 min), and in plasma ACTH culminating 15-20 times higher than basal levels. Simultaneously, body temperature was increased by 2.3 +/- 0.3 degrees C. In another experiment, i.c.v. infusion of IL 1 beta produced a similar increase in plasma ACTH in rats whose catecholaminergic innervation to the hypothalamus had been obliterated by a bilateral injection of 6-hydroxydopamine into the ventral noradrenergic bundle, which appears to rule out modulation of this innervation in the stimulatory effect of IL 1 beta. The precise cellular site of action of IL 1 beta on CRH 41 secreting neurons and the physiological relevance of the study are discussed within the framework of functional interactions between the neuroendocrine and immune systems.

Adrenocorticotropic Hormone↗
PubMed1990

[Implication of alpha-2 adrenergic post-synaptic receptors in the central catecholaminergic stimulation of the corticotropic axis in rats].

We have recently assigned a major stimulatory role to the brain catecholamines (CA) via alpha 1 and beta receptors on CRH-ACTH secretion, e.g. in the physiological response to stress. In the present study, we explored the possible participation in this regulation of post-synaptic alpha 2 receptors in free moving rats, one week after CA denervation of the hypothalamus by bilateral neurotoxic lesions of the noradrenergic ascending brain stem bundles (NAB). Intracerebroventricular (i.c.v.) injection of clonidine (alpha 2 agonist; 1 nmol) induced a 3 fold rise of ACTH release (measured by RIA) above vehicle (PBS) injected controls (p less than 0.001). This stimulatory effect was completely reversed by an i.c.v. pretreatment with the alpha 2 antagonist idazoxan (10 nmol; without action by itself), whereas it was only slightly affected by an i.c.v. pretreatment with a combination of an alpha 1 and beta blocker (prazosin + propranolol; 5/5 nmol; p greater than 0.1). The results strongly suggest the participation of alpha 2 post-synaptic receptors in the central catecholaminergic activation of ACTH secretion.

Adrenergic alpha-Antagonists↗
PubMed1988

Central catecholaminergic system stimulates secretion of CRH at different sites.

To explore a possible differential role of distinct catecholamine (CA) innervation sites in corticotropin-releasing hormone (CRH) secretion, especially under stress conditions, we compared the effects in adult female rats of selective CA denervation of either the whole hypothalamus, by a discrete pharmacological lesion of the ventral noradrenergic ascending bundle [VNAB; 3 micrograms of 6-hydroxydopamine (6-OHDA) in 0.2 microliter of vehicle, bilaterally] or of the paraventricular nuclei (PVN) alone (1 microgram of 6-OHDA in 0.2 microliter of vehicle, bilaterally). Although both procedures induced a similar dramatic fall in norepinephrine and epinephrine concentrations (-55 to -65%) measured by high-performance liquid chromatography in PVN punches, the VNAB lesion, unlike PVN denervation, depleted the median eminence (ME) of both amines (-80%). Concomitantly, the VNAB lesion led to a 97% reduction of the immunoreactive (ir) CRH-41 concentration in the hypophysial portal vessels, associated with a 64% fall in plasma adrenocorticotropic hormone (ACTH), and, in another group, with an 80% inhibition of ether stress-induced ACTH surge. The deletion of CA innervation of the PVN alone reduced irCRH-41 levels in the portal vessels by only 57% and plasma ACTH by 35%. This lesion did not significantly impair stress-induced ACTH release. These results suggest that the CA innervation of the hypothalamus exerts a stimulatory control on CRH-41-secreting neurons not only directly at the perikaryal level but also at other hypothalamic sites of VNAB innervation including peripheral contacts between the terminals of CA and CRH nerves in the external ME.

Adrenocorticotropic Hormone↗
PubMed1987

Increase of thyrotropin-releasing hormone immunoreactivity in the nucleus of the solitary tract following bilateral lesions of the hypothalamic paraventricular nuclei.

The effects of bilateral electrolytic lesions of hypothalamic paraventricular nucleus on thyrotropin-releasing hormone (TRH)-immunoreactive fibers of the nucleus of the solitary tract were studied by both immunocytochemistry and radioimmunoassay. Contrasting with a near disappearance of TRH immunoreactivity in the median eminence, both morphological and biochemical approaches demonstrate that such hypothalamic lesions induced significant increase of TRH immunoreactivity in the nucleus of solitary tract. These results confirm that TRH fibers of the nucleus of the solitary tract do not originate in the hypothalamic paraventricular nucleus (PVN). They further indicate that these TRH neurons projecting to the nucleus of the solitary tract are strongly influenced by neurons located within the PVN area.

Animals↗