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T Imaki

Publications and source records attributed to T Imaki.

At least 55 records · Page 3Linked to original sources
PubMed1995

Stress-induced activation of neuronal activity and corticotropin-releasing factor gene expression in the paraventricular nucleus is modulated by glucocorticoids in rats.

Intronic in situ hybridization methodology provides a means of determining the rate of gene transcription under basal and stimulated conditions. In the present study, we have used intronic in situ hybridization to the corticotropin-releasing factor (CRF) gene to measure hypothalamic CRF gene transcription after stress as well as its modulation by glucocorticoids. Using this and conventional exonic in situ hybridization we examined the time course of changes in c-fos mRNA, and CRF heteronuclear RNA (hnRNA) and mRNA concentrations in the paraventricular nucleus (PVN) of male Wistar rats after restraint stress. In addition, we determined the effects of adrenalectomy and dexamethasone administration on c-fos and CRF gene expression in the PVN. Restraint stress induced a rapid induction (within 5 min) of c-fos mRNA and CRF hnRNA expression in the PVN. Both RNA concentrations peaked at 30 min then decreased and were undetectable 2 h after stress onset. In contrast, the concentration of CRF mRNA increased gradually and a significant elevation was first detected 60 min after the beginning of stress. Adrenalectomy augmented and dexamethasone pretreatment inhibited c-fos mRNA, CRF hnRNA, and mRNA induction after stress. The data suggest that stress-induced activation of neurons, CRF gene transcription, and CRF synthesis in the PVN are modulated by glucocorticoids.

Adrenalectomy↗
PubMed1995

Dopaminergic regulation of aldosterone secretion: its pathophysiologic significance in subsets of primary aldosteronism.

Although aldosterone (Aldo.) secretion is regulated by various humoral factors, evidence has accumulated to support an involvement of dopaminergic system in its regulation. The pathophysiological significance of the dopaminergic system in primary aldosteronism (PA) however remains unknown. In the present study, we examined the effects of metoclopramide (MCP) on Aldo. secretion in normal subjects (n = 11) and patients with essential hypertension (EH, n = 8), aldosterone-producing adenoma (APA, n = 10), and idiopathic hyperaldosteronism (IHA, n = 6). Plasma Aldo., prolactin (PRL), renin, cortisol, serum sodium, and serum potassium levels were determined before and 30 min after i.v. bolus injection of 10 mg MCP at 9 a.m. Plasma Aldo. showed a significant increase after MCP in normal subjects, EH, and APA, but not in IHA. The incremental response of plasma Aldo. was largest in APA and smallest in IHA. The percentage increase in plasma Aldo. from the basal level was significantly attenuated in IHA, while no significant difference was seen among other groups. Although plasma PRL showed a significant increase in response to MCP, no difference of the change was seen among the groups. There was no significant change in plasma cortisol, renin, serum sodium, and serum potassium levels in response to MCP. In addition, the response of Aldo. to MCP was normalized in APA after unilateral adrenalectomy, while that of PRL did not change. These results indicate that the adrenal dopaminergic activity is enhanced in APA and attenuated in IHA and suggest an involvement of the dopaminergic system in the pathogenesis of IHA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1994

Beta 1-adrenergic mechanism is involved in stress-induced increase in arousal.

It has been shown that 1 h restraint shortens pentobarbital (PbNa)-induced sleeping time and that brain corticotropin-releasing hormone (CRH) is involved in the mechanism by which restraint shortens. PbNa-induced sleeping time. The present study was designed to further examine the mechanism of the antagonistic effect of 1 h restraint on PbNa in rats. Intracerebroventricular (i.c.v.) administration of propranolol and metoprolol, but not butoxamine reversed the shortening of PbNa-induced sleeping time by 1 h restraint. The i.c.v. administration of phentolamine blocked the shortening of PbNa-induced sleeping time by restraint, while the same dose of phentolamine prolonged the sleeping time in unrestrained rats. Atropine did not affect the PbNa-induced sleeping time in restrained rats. These results suggest that in addition to CRH, the brain beta 1-adrenergic system is involved in the restraint stress-induced increase in arousal.

Animals↗
PubMed1994

Restraint changes pentobarbital-induced sleeping time in rats: evidence that arousal is modulated by brain corticotropin-releasing hormone and opioid in stress.

The effect of restraint of different duration on sodium pentobarbital (PbNa)-induced sleeping time was examined in rats. 1 h-restraint significantly shortened PbNa (50 mg/kg b.wt., administered i.p. immediately after restraint)-induced sleeping time as reported previously, whereas 2 h-restraint significantly prolonged the sleeping time. Naloxone (1 mg/kg b.wt.) administered i.p. 15 min before the start of restraint further exaggerated the 1 h-restraint-caused shortening of PbNa-induced sleeping time, and it blocked the 2 h-restraint-caused prolongation of the sleeping time. SDZ202-250 (0.1 pmol and 0.5 pmol), a selective mu agonist, but not [D-Pen2-D-Pen5]enkephalin (0.1 pmol-1.0 nmol), a selective delta agonist, or U50488H (0.1 pmol-1.0 nmol), a selective kappa agonist, administered i.c.v. 15 min before the i.p. injection of PbNa significantly prolonged PbNa-induced sleeping time; its prolongation was blocked by naloxone. These results suggest that a mu receptor-binding opioid prolongs PbNa-induced sleeping time in stress. The 2 h-restraint-caused prolongation of PbNa-induced sleeping time was also blocked by alpha-helical CRH(9-41) (26 nmol), a corticotropin-releasing hormone (CRH) receptor antagonist, administered i.c.v. 15 min before the start of restraint. In conjunction with our previous findings that the i.c.v. administration of CRH shortens PbNa-induced sleeping time and the 1 h restraint-caused shortening of PbNa-induced sleeping time is blocked by the CRH receptor antagonist, the present results suggest that CRH may stimulate an opioid-specific sedative mechanism, thus causing the prolongation of PbNa-induced sleeping time in 2 h-restraint.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1993

Chlordiazepoxide attenuates stress-induced accumulation of corticotropin-releasing factor mRNA in the paraventricular nucleus.

Corticotropin-releasing factor (CRF) plays a role in coordinating endocrine, autonomic and behavioral responses to stressful stimuli. Benzodiazepines exert many effects which are antithetical to those of CRF, including anxiolysis and suppression of the pituitary-adrenal axis. Although there is evidence that benzodiazepines can modulate several electrophysiological and behavioral responses to exogenous CRF, we questioned whether this class of drug might also affect CRF biosynthesis as well. We have shown previously that footshock stress increases CRF mRNA levels as monitored by in situ hybridization histochemical techniques in the paraventricular nucleus (PVN) and Barrington's nucleus (the pontine micturition center). We report here the effects of the potent benzodiazepine, chlordiazepoxide (CDP), on stress-induced CRF mRNA accumulation in these two regions. Male albino rats were exposed to electrical footshock (1.5 mA, 1-s duration, 60 times/30 min) twice daily for 4 days and sacrificed 24 h after the last shock session. Either CDP (1, 2.5, 5 or 10 mg/kg) or saline was given i.p. 30 min before each stress. Sections were hybridized with an 35S-labeled prepro-CRF cRNA probe. Relative levels of CRF mRNA were quantified by densitometry of the autoradiography with X-ray film. CRF mRNA concentrations were significantly increased in both the PVN and Barrington's nucleus after stress, and CDP attenuated these increases in the PVN. By contrast, CDP did not affect CRF mRNA accumulation in Barrington's nucleus after stress. The results suggest that the benzodiazepine, CDP, suppresses stress-induced pituitary adrenal activation at least in part through inhibition of CRF production in the PVN.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Psychological stress increases arousal through brain corticotropin-releasing hormone without significant increase in adrenocorticotropin and catecholamine secretion.

The effect of psychological and psychophysical stress on pentobarbital (PbNa)-induced sleeping time was examined in rats to clarify the influence of psychological stress on arousal. Psychological stress and electric footshock of 5-60 min duration significantly shortened PbNa-induced sleeping time, and the shortening was reversed by intracerebroventricular administration of a corticotropin-releasing hormone (CRH)-receptor antagonist. Electrical footshock and restraint significantly raised plasma adrenocorticotropin (ACTH) and catecholamine levels, whereas psychological stress did not significantly affect the plasma hormones levels. These results suggest that both psychological and psychophysical stress increase arousal through brain CRH. It is also concluded that expression of the central nervous system action of CRH, such as increasing arousal, is not necessarily accompanied by a significant increase in the secretion of ACTH and catecholamine in psychological stress.

Adrenocorticotropic Hormone↗
PubMed1993

Intracerebroventricular administration of corticotropin-releasing factor induces c-fos mRNA expression in brain regions related to stress responses: comparison with pattern of c-fos mRNA induction after stress.

Centrally administered corticotropin-releasing factor (CRF) produces a number of physiological and behavioral changes akin to those elicited by exposure to acute stress. However, the specific brain site of action responsible for the centrally activating property of CRF has not been precisely determined. In this study, we used in situ hybridization histochemistry for c-fos mRNA to map potential neuronal structures activated after intracerebroventricular (i.c.v.) injection of CRF and compared the distribution of c-fos mRNA with that after stress. Wistar male rats were sacrificed 30, 60, 120 and 180 min after the i.c.v. injection of 1 microgram ovine CRF or vehicle alone. Another group of rats was exposed to immobilization stress for 60 min or electrical foot-shock stress (1.5 mA, 1-s duration, 30 x) for 15 min and sacrificed before and 30, 60, 120 and 180 min after the beginning of stress. Centrally administered CRF rapidly (30-60 min) induced c-fos mRNA expression in most of the areas that showed hybridization signals for c-fos after stress: the limbic structures, including the piriform cortex, cingulate cortex, the lateral septal nucleus, the hippocampus, the anterior corticomedial and the medial amygdaloid nuclei, the hypothalamic nuclei, such as the paraventricular nucleus, the supraoptic nucleus (SO) and the dorsomedial nucleus (DMD), and some brainstem nuclei like the pontine nucleus, the locus ceruleus (LC) and Barrington's nucleus. The granular layer of the cerebellum, some thalamic nuclei and the habenula also showed hybridization signals after i.c.v. injection of CRF and stress. However, c-fos induction in the bed nucleus of the stria terminalis, the central nucleus of the amygdala (CeA) and the nucleus tractus solitarius (SOL) was seen only after i.c.v. administration of CRF; in the septo-hypothalamic nucleus and the superior olive, however, c-fos mRNA expression was observed only after stress. There were no differences in the pattern of c-fos mRNA expression between the two stress paradigms. In contrast, i.c.v. injection of saline-induced expression of c-fos mRNA in the piriform cortex, neocortex, cingulate cortex and the amygdala was much less than that seen after i.c.v.-administered CRF as evident in the intensity of the signals. These results suggest that CRF produces c-fos mRNA expression in the brain areas related to stress response, and that CRF may induce behavioral and neuroendocrine responses through activating these brain structures, such as the limbic system and the hypothalamic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗
PubMed1993

Injection of anti-neuropeptide Y gamma-globulin into the hypothalamic paraventricular nucleus decreases food intake in rats.

The effect of immunoneutralization of hypothalamic neuropeptide Y (NPY) on food intake was examined to clarify the involvement of NPY in the control mechanism of feeding behavior. Injection of anti-NPY gamma-globulin into the bilateral hypothalamic paraventricular nuclei of 24-h food-deprived rats significantly inhibited food intake for 1 h after the injection compared with rats that received normal rabbit gamma-globulin. This result suggests that NPY in the paraventricular nucleus plays a role in stimulating feeding behavior.

Animals↗
PubMed1993

The functional neuroanatomy of corticotropin-releasing factor.

Descriptions of the central distribution of corticotropin-releasing factor (CRF) have been taken as generally supporting the proposition that this neuropeptide is involved in the mediation of complementary neuroendocrine, autonomic and behavioural responses to stress. The hypothalamic paraventricular nucleus (PVN) is recognized as the principal source of CRF in hypophysial portal plasma; CRF mRNA and peptide expression in parvocellular neurosecretory neurons are regulated negatively by adrenal steroids and positively by many stressors. Consistent with the latter, the hypophysiotropic zone of the PVN receives a rich, and biochemically differentiated, afferent supply that provides visceral, somatic and special sensory systems with access to the 'CRF neuron'. Within the PVN, CRF is also expressed, and differentially regulated, in oxytocinergic magnocellular neurosecretory neurons and in autonomic-related projection neurons. CRF expression in at least some extrahypothalamic cell groups (olfactory bulb, Barrington's nucleus) is responsive to certain stressful stimuli, but not to perturbations of the steroid environment. Refinement of our understanding of the central distribution of CRF has been provided by the recognition that most CRF antisera cross-react with an amidated dipeptide encoded by the melanin-concentrating hormone precursor, and by the likelihood that some central sites of CRF peptide expression may be muted or masked by the presence of a CRF-binding protein (CRF-BP). The CRF-BP is expressed prominently in the telencephalon, where it is co-localized with CRF in some neurons, and in anterior pituitary corticotrophs.

Afferent Pathways↗
PubMed1993

A patient with primary hyperparathyroidism associated with osteomalacia: markedly increased serum levels of intact PTH and 1,25-dihydroxyvitamin D with normo- and hypercalcemia.

A 65-year-old female patient was admitted with complaining chiefly of lower back pains and arthralgia in the bilateral knee joints of 10-years duration. The serum calcium concentration was normal or only slightly increased, whereas the serum intact PTH and 1,25-dihydroxyvitamin D concentrations were substantially increased. Serum phosphate and 25-hydroxyvitamin D concentrations were decreased. Renal function was normal. Serum alkaline phosphatase activity, the osteocalcin concentration and urinary hydroxyproline excretion were markedly increased. Bone X-ray examination showed severe osteopenia and bone biopsy revealed hyperosteoidosis without tetracycline deposition, consistent with osteomalacia. A parathyroid adenoma was demonstrated by echography and CT-scan. Surgical exploration of the neck revealed a chief cell adenoma behind the right upper pole of the thyroid gland. After parathyroidectomy, all the abnormal biochemical data gradually normalized and the patient has been doing well without any symptoms for the last 13 months. These clinical data suggest that osteomalacia of the patient was probably induced by hypophosphatemia of prolonged duration. When hypercalcemia is not evident in a patient with primary hyperparathyroidism, in whom serum alkaline phosphatase and intact PTH levels are inappropriately increased, osteomalacia should be taken into consideration.

Adenoma↗
PubMed1993

Increased 1,25-(OH)2D2 concentration in a patient with malignancy-associated hypercalcemia receiving intravenous hyperalimentation inadvertently supplemented with vitamin D2.

A 55-year-old patient with hypercalcemic crisis due to gastric carcinoma with bone marrow metastasis was treated with bisphosphonate (pamidronate) and calcitonin. Urinary excretion of parathyroid hormone-related protein (PTHrP) was increased. When normocalcemia had been attained, intravenous hyperalimentation was started, in which 1,000 U vitamin D2 was inadvertently supplemented on days 5-18, On days 15-18, hypercalcemia rapidly recurred, accompanied by markedly increased serum levels of 25-OHD2 (9.1 ng/dl) and 1,25-(OH)2D2 (161 pg/ml). This clinical course suggests that PTHrP, like PTH, stimulated 1 alpha-hydroxylase activity and produced excessive 1,25-(OH)2D2. Vitamin D should not be administered to patients with malignancy-associated hypercalcemia, particularly that due to PTHrP-producing tumors.

Calcitriol↗
PubMed1992

Co-localization of neuroactive substances in the endocrine hypothalamus.

In addition to their characterizing secretory products, both magnocellular and parvocellular neurosecretory neurons are now known to express other neuroactive substances. Parvocellular neurons that make corticotropin-releasing factor (CRF) for example are capable of synthesizing at least seven neuropeptides. Some of these, like arginine vasopressin (AVP), interact with CRF at the level of the anterior pituitary to promote corticotropin secretion, and, like CRF, are regulated negatively by glucocorticoids and positively by at least some stressors. others are inert in these two contexts but are responsive to various challenges. Magnocellular neurosecretory oxytocin- and AVP-containing neurons are capable of producing similarly broad and distinctive complements of neuroactive principles. These are typically expressed at levels far lower than those of the nonapeptides, suggesting local modulatory effects on oxytocin and/or AVP secretion at the level of the posterior lobe. Differential regulation of coexisting molecules within magnocellular neurons by systemic challenges and steroid hormones has also been described. Secretory products of magnocellular neurons may gain access to the anterior pituitary via exocytotic release at the level of the median eminence or through vascular links between the posterior and anterior lobes, suggesting another form of 'co-localization' by which the two neurosecretory cell types may interact in the control of stress and perhaps other pituitary-mediated responses.

Animals↗
PubMed1992

Regulation of corticotropin-releasing factor mRNA in neuroendocrine and autonomic neurons by osmotic stimulation and volume loading.

Corticotropin-releasing factor (CRF) has been reported to be expressed in oxytocin-containing magnocellular neurosecretory neurons of the paraventricular (PVN) and supraoptic (SON) nuclei, and in Barrington's nucleus, a pontine micturition center. Each of these cell groups is known to play a role in fluid and electrolyte homeostasis. To gain a better understanding of the role of CRF in this context, the effects of osmotic stimulation and volume loading on CRF mRNA levels in the PVN, SON and Barrington's nucleus were examined using in situ hybridization histochemistry with an 35S-labeled cRNA probe. Adult male rats received either normal tap water (control), or hypertonic (2%) saline (HS) for up to 3 days. In a second experiment, normal saline was infused through a jugular vein cannula at 6 ml/h for 3 days; control rats were cannulated but received no infusion. Relative levels of CRF mRNA were compared by estimating both the number of positively hybridized cells and the density of silver grains in emulsion-dipped autoradiograms. HS treatment resulted in marked increases in CRF mRNA in the magnocellular neurosecretory system. All recognized oxytocinergic cell clusters, i.e., the anterior, medial and posterior magnocellural subdivisions of the PVN, the dorsal aspect of the SON, and components of the accessory magnocellular system, displayed this effect. By contrast, HS treatment resulted in significant decreases in CRF mRNA levels in the parvocellular (hypophysiotropic) division of the PVN and in Barrington's nucleus. By contrast, volume loading, which failed to affect plasma osmolality, significantly increased CRF mRNA levels in Barrington's nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Early induction of c-fos precedes increased expression of corticotropin-releasing factor messenger ribonucleic acid in the paraventricular nucleus after immobilization stress.

CRF plays a role in coordinating endocrine, physiological, and behavioral responses to stressful stimuli. Several kinds of stressors have been reported to induce an increase in CRF mRNA expression in the paraventricular nucleus of the hypothalamus (PVN). Recently, the expression of c-fos mRNA has shown promise as a useful tool for metabolic mapping at the cellular level, because various types of stimulation induce c-fos mRNA expression in specific neuron populations in various brain regions. The aim of the present study is to clarify a possible anatomical-temporal correlation between the early induction of c-fos and the enhanced expression of CRF mRNA after stress. Wistar male rats were exposed to immobilization stress for 60 min and killed before and 15, 30, 60, 90, 120, and 180 min after the beginning of immobilization. In situ hybridization was performed by hybridizing sections with 35S-labeled prepro-CRF and c-fos cRNA probes. Relative levels of CRF and c-fos mRNA were compared by estimating the number of grains over the PVN in emulsion-dipped autoradiograms. Rapid induction (within 15 min) of c-fos mRNA was noted in the parvocellular division of the PVN after immobilization stress. The level of c-fos mRNA peaked at 30 min, then gradually declined to the control level within 90 min after the beginning of stress [the number of grains over the PVN: control, 326 +/- 180; 15 min, 2091 +/- 680 (P less than 0.05 vs. control); 30 min, 3385 +/- 239 (P less than 0.05 vs. control)]. The distribution of c-fos mRNA was almost identical to that of CRF mRNA in the PVN. On the other hand, the time course of CRF mRNA induction was delayed to the c-fos mRNA expression. A significant increase in CRF mRNA levels was noted only 120 and 180 min after stress [the number of grains over PVN: control, 3868 +/- 221; 120 min, 5957 +/- 677 (P less than 0.05 vs. control); 180 min, 6600 +/- 450 (P less than 0.05 vs. control)]. The results demonstrate that increased expression of CRF mRNA is preceded by c-fos mRNA induction in the PVN after stress suggesting a role of c-fos in the activation of CRF gene expression.

Animals↗
PubMed1992

Rat melanin-concentrating hormone messenger ribonucleic acid expression: marked changes during development and after stress and glucocorticoid stimuli.

Melanin-concentrating hormone (MCH) is a cyclic neuropeptide first isolated from fish and rats. MCH may be involved in the control of the hypothalamic-pituitary-adrenocortical axis and, more generally, of specific goal-oriented behaviors and homeostatic functions in mammals. In this paper we examine 1) the cellular distribution of MCH gene transcripts in the rat central nervous system, 2) the changes in neuronal expression of MCH mRNA during rat development, and 3) the effects of stress and hormonal stimuli on rat MCH (rMCH) gene activity. Northern blot analysis and in situ hybridization histochemistry show that mature rMCH mRNA (1.0 kilobase) is very abundant in the zona incerta and the dorsolateral hypothalamus. While this is in agreement with previous peptide mapping by immunohistochemical techniques, a surprising new result is that a few clusters of rMCH mRNA-containing cells are found outside the hypothalamus, in the olfactory tubercle and the pontine tegmentum. Developmentally, rMCH mRNA is detected on embryonic day 18; its level increases gradually during early postnatal life and rises abruptly at weaning to reach a constant value in adult rats. In addition, striking variations in rMCH mRNA length occur during postnatal development and are found to be variations in the polyadenylate tail. Interestingly, this structural modification appears to be independent of the increase in rMCH mRNA levels. The regulation of rMCH mRNA expression by glucocorticoids and chronic stress is examined by Northern blot analysis. Chronic intermittent footshock stress causes a 58% or 29% decrease in rMCH mRNA content in the whole hypothalamus after a 1- or 3-day regimen, respectively. In contrast, the rMCH mRNA level returns to normal after a 7-day regimen. Two weeks after adrenalectomy (ADX) the whole hypothalamus rMCH mRNA content decreases 2.5-fold, but rises close to the control value 3 weeks after ADX. Dexamethasone administration 2 weeks after ADX not only reverses the fall in rMCH mRNA, it even provokes a slight increase (123% of control). No change in rMCH mRNA length is observed after chronic stress or ADX and dexamethasone injection. These results provide evidence for a negative regulation of rMCH gene expression by stress and suggest a major role for glucocorticoids in a positive feedback control of rMCH gene activity.

Adrenalectomy↗
PubMed1991

Brain corticotropin-releasing hormone increases arousal in stress.

The effect of restraint stress on pentobarbital-induced sleeping time was examined in rats. Restraint for 60 and 75 min significantly shortened pentobarbital-induced sleeping time. The shortening of sleeping time by restraint was completely reversed by intracerebroventricular (i.c.v.) administration of alpha-helical CRH(9-41), a corticotropin-releasing hormone (CRH) receptor antagonist. In conjunction with our previous finding that i.c.v. administration of CRH shortens pentobarbital-induced sleeping time, the results suggest that restraint stress increases arousal through brain CRH.

Animals↗
PubMed1991

Distribution of corticotropin-releasing factor mRNA and immunoreactivity in the central auditory system of the rat.

Hybridization histochemical and immunohistochemical methods were used to characterize the distribution of corticotropin-releasing factor (CRF) messenger RNA (mRNA) and peptide, respectively, in the central auditory system of the rat. Cell bodies expressing CRF mRNA and/or immunoreactivity (IR) were detected at each level of the system, including sparse or equivocal localizations in the dorsal cochlear nucleus, the medial nucleus of the trapezoid body, and the lateral superior olive. More prominent groups of cells expressing CRF mRNA and CRF-IR were found in the nuclei of the lateral lemniscus, the shell of the inferior colliculus, the medial division of the medial geniculate body and in primary auditory cortices. The latter showed the greatest density of CRF-expressing interneurons, distributed primarily in layers II, III and V, of any neocortical area. Results obtained using the two staining methods were in good agreement, except in the cochlear and superior olivary nuclei, where cells displaying CRF-IR were apparent in far greater abundance than those expressing CRF mRNA. CRF-IR fibers and terminals were detected in regions generally consistent with the cellular localizations described above. These results provide evidence for a surprisingly widespread expression of CRF in the auditory system of the rat. This includes generally low levels of expression in components of the primary auditory path (cochlear nucleus, trapezoid body, superior olive, lemniscal nuclei). CRF appears to be more prominently expressed in so-called non-primary components of the auditory system, including aspects of the medial geniculate body that constitute an interface between the auditory system and stress-related limbic system circuitry.

Animals↗