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At least 19 recordsLinked to original sources
PubMed1998

GABA receptor mediated suppression of defensive rage behavior elicited from the medial hypothalamus of the cat: role of the lateral hypothalamus.

Recently, our laboratory has demonstrated that predatory attack behavior in the cat, elicited by electrical stimulation of the lateral hypothalamus, is suppressed following activation of the region of the medial hypothalamus from which defensive rage behavior is elicited [Han, Y., Shaikh, M.B., Siegel, A., Medical amygdaloid suppression of predatory attack behavior in the cat: II. Role of a GABAergic pathway from the medial to the lateral hypothalamus, Brain Res., 716 (1996) 72-83.]. The mechanism for this suppression is a direct GABAergic projection from the medial to lateral hypothalamus. The present study tested the hypothesis that the inhibitory relationship between these two regions of hypothalamus is reciprocal, namely, that a GABAergic neuron, which also projects from the lateral to medial hypothalamus, serves to suppress defensive rage elicited from the medial hypothalamus. Monopolar stimulating electrodes were implanted into lateral hypothalamic sites from which predatory attack behavior was elicited. In addition, cannula-electrodes were implanted into the medial hypothalamus for elicitation of defensive rage behavior and for microinjections of GABA compounds. Initially, in the absence of drug administration, the effects of dual stimulation of the lateral and medial hypothalamus upon response latencies were compared with those following single stimulation of the medial hypothalamus alone. Dual stimulation significantly (p<0.01) suppressed defensive rage behavior elicited from the medial hypothalamus. Then, administration of the GABAA receptor antagonist, bicuculline (10-60 pmol), into medial hypothalamic sites from which defensive rage was elicited blocked the suppressive effects of lateral hypothalamic stimulation. The GABAA receptor agonist, muscimol (0.3-30 pmol), microinjected into the medial hypothalamus, suppressed defensive rage elicited by single stimulation of the medial hypothalamus in a dose dependent manner. These suppressive effects of muscimol upon defensive rage were blocked following pretreatment with bicuculline (60 pmol). Administration of muscimol into adjoining regions of the lateral hypothalamus had no effect upon defensive rage, indicating its site specificity. Bicuculline (60 pmol) delivery into the medial hypothalamus had no effect upon defensive rage, suggesting the, presence of a phasic rather than tonic mechanism. A combination of immunocytochemical and retro grade tracing procedures were then employed to determine the origin of the putative GABAergic pathway projecting to the medial hypothalamus. In this experiment, the retrograde tracer, Fluoro-Gold (8%, 0.5 microl), was microinjected through a cannula-electrode in the medial hypothalamus from which defensive rage had been elicited. Following survival periods of 5-6 days, cats were perfused with 4% paraformaldehyde and brain tissue was processed for immunocytochemical staining of GABA neurons. Retrogradely labeled, immunopositively labeled, as well as Fluoro-Gold and GABA labeled cells, were identified in the lateral hypothalamus. Each type of neuron was distributed over wide regions of the lateral hypothalamus, extending from the area immediately caudal to the optic chiasm to the level of the posterior hypothalamus. Together, the behavioral pharmacological and anatomical data provide evidence of a direct inhibitory projection from the lateral to medial hypothalamus whose functions are mediated by GABAA receptors. When coupled with our previous findings, these results reveal the presence of reciprocal GABAergic inhibitory pathways between the medial and lateral hypothalamus. The findings suggest that functions associated with either the lateral or medial hypothalamus, but not both, can be activated at a given time.

Aggression↗
PubMed1985

The role of the anterior hypothalamus in affective defense behavior elicited from the ventromedial hypothalamus of the cat.

In the preceding paper a hypothalamic circuit subserving feline affective defense behavior was described. This circuit included an ascending component from the ventromedial nucleus to the anterior hypothalamus and a descending component from the anterior hypothalamus to the midbrain central gray substance. The present study was undertaken to test the hypothesis that the anterior hypothalamus plays a central role in the organization of this functional pathway. In the first part of this study, dual stimulation methods were utilized to demonstrate that concurrent stimulation of the ventromedial hypothalamus facilitates the occurrence of affective defense responses elicited from the anterior hypothalamus. In the second part of the study, lesions placed in the anterior hypothalamus significantly increased the latency and threshold current for affective defense responses elicited from the ventromedial hypothalamus. [14C]2-deoxyglucose autoradiography confirmed the fact that anterior hypothalamic lesions effective in blocking affective defense were placed in regions where the vast majority of ventromedial hypothalamic fibers terminate. In contrast, lesions which had little or no effect upon the latency or threshold for affective defense elicited from the ventromedial hypothalamus appeared to leave intact the connections from the ventromedial to the anterior hypothalamus. These findings are consistent with the proposed intrahypothalamic anatomical substrate subserving affective defense behavior described in the preceding paper.

Aggression↗
PubMed1993

Alpha 2 and beta adrenoceptors in the mediobasal hypothalamus and alpha 2 adrenoceptors in the preoptic-anterior hypothalamus stimulate prolactin secretion in the conscious male rat.

Plasma prolactin concentrations were measured in unanaesthetized male rats before and after stereotaxic microinjection of adrenergic agents into the mediobasal and preoptic-anterior hypothalamus. In the mediobasal hypothalamus injection of the alpha 2 agonist clonidine produced a dose-dependent increase in prolactin secretion over the dose range 0.1 to 10 nmoles, the stimulation due to 1 nmole being blocked by idazoxan (alpha 2 antagonist). Stimulation of prolactin release was also caused by isoprenaline (beta agonist) and was significantly reduced by the beta antagonist propranolol. The beta 2 agonist salbutamol was also effective in stimulating prolactin secretion. However, the adrenergic agonists, noradrenaline (mixed alpha and beta), phenylephrine (alpha 1) and tyramine (sympathomimetic) failed to affect prolactin secretion. In the preoptic-anterior hypothalamus clonidine caused a dose-dependent increase in prolactin secretion over the dose range 0.001 to 10 nmoles, the stimulation due to 0.1 nmole being abolished by idazoxan. While prolactin levels were significantly elevated by noradrenaline and tyramine, phenylephrine was ineffective. We conclude that the activation of alpha 2 and beta 2 adrenoceptors in the mediobasal hypothalamus and of alpha 2 adrenoceptors in the preoptic-anterior hypothalamus, on or near prolactin-regulating neurons, results in increased prolactin secretion. An alpha 1 inhibitory action in the mediobasal hypothalamus has however not been ruled out. Adrenergic inputs in the preoptic-anterior hypothalamus appear to exert a predominant facilitatory effect on prolactin secretion.

Adrenergic alpha-Agonists↗
PubMed1998

[Effects of glutamate, glutamate receptor in limbic system and hypothalamus on hypothalamus-pituitary-adrenal axis after rats MCAO].

OBJECTIVE: To investigate the features of activity changes of glutamate(Glu), glutamate receptors(GluR) in hippocampus and hypothalamus during rats middle cerebral artery occlusion (MCAO) or reperfusion. METHODS: Using radio-legend binding assay of receptor (RBA), high-performance liquid chromatography (HPLC) and hybridization in situ and radioimmunometric assay, (RIA), we determined the dynamic changes of Glu content, GluR capacity and it's Kd in cell membrane from the hippocampus of the ischemic brain and the hypothalamus CRHmRNA expression levels in every brain areas and ACTH concentrations in plasma at different time after middle cerebral artery occlusion(MCAO) or reperfusion. RESULTS: Glu content rapidly increased in the hippocampus and the hypothalamus at 15 minutes after MCAO, and reached the peak values at I1 h, and rapidly decreased to the basic-line level after reperfusion. Glu content IR24 h to IR48 h, was elevated again moderately, and declined slowly 48 hours after reperfusion. The GluR was down-regulated and the affinity enhanced in during the ischemic period. During the reperfusion period, the GluR was typically up-regulated. The CRHmRNA expressive levels were markedly enhanced in the tempol cortex, the hippocampus and the hypothalamus at I1 h, and kept to IR96 h, the ACTH concentration in the plasma increased relatively. In the peak time of reperfusion, the Glu content of hypothalamus was positively corrected with CRHmRNA expressive positive cell amounts of the hypothalamus. CONCLUSION: CRH may aggravate ischemic neuronal damage, and Glu participates in the pathogenesis of HPA axis be excited strongly and may be an important impel factor for ACI specially condition.

Animals↗
PubMed1976

Efferents from medial basal forebrain and hypothalamus in the rat. II. An autoradiographic study of the anterior hypothalamus.

Using tritiated amino acid autoradiography, the efferent projections of the anterior hypothalamic area (AHA) were studied in albino rats. Axons from AHA neurons were not confined to local projections in the hypothalamus. Ascending AHA axons ran through the preoptic region, joined the diagonal band and distributed in the lateral septum. Descending AHA efferents within the hypothalamus coursed in a bundle ventromedial to the fornix. Projections were observed to the dorsomedial, ventromedial, arcuate and dorsal premammillary nuclei, and to the median eminence. Sweeping dorsomedially in the posterior hypothalamus, some AHA axons distributed in the central grey. AHA axons staying ventral projected to the supramammillary region, ventral tegmental area, raphe nuclei and midbrain reticular formation. Other AHA efferents distributed to the periventricular thalamus, to the medial amygdala via the stria terminalis or supraoptic commissure, and to the lateral habenula through the stria medullaris. For comparison with the AHA, efferent projections from the paraventricular nucleus (PVN) and from the ventromedial nucleus and adjacent basal hypothalamus (VMR) were studied. Projections from PVN neurons were not restricted to the median eminence and neurohypophysis. PVN efferents also distributed to many of the same regions as did those of the AHA but had somewhat different fiber trajectories and longer descending projections. VMR efferents were more widespread than those of the AHA, with projections extending into the lateral zona incerta and pontine reticular formation. Projections from the AHA were distinct from those of the medial preoptic area (mPOA). For example, while AHA axons descended in a bundle ventromedial to the fornix, mPOA axons ran in the medial forebrain bundle. Such anatomical differences may underlie experimentally demonstrated functional differences between the mPOA and AHA, for instance, in mediation of male and female sex behaviors.

Animals↗
PubMed1982

The hypothalamus of Lacerta sicula R. I. A Golgi study on the caudal hypothalamus.

The posterior (caudal) hypothalamus of the lizard, Lacerta sicula R. was investigated by means of Golgi methods. The periventricular grey is formed mainly by isodendritic bipolar and multipolar neurons, while in the lateral hypothalamus a more stellate form of neuronal elements is encountered. CSF-contacting neurons are restricted to the tuberal area and to the paraventricular organ. In the latter area they are highly differentiated and endowed with laterally branched processes. The overall pattern of the lizard hypothalamus (organization of neuropil, lateral nuclei, appearance of cell clusters, morphology of the neuronal elements) represents an intermediate stage in the phylogenetic development of the hypothalamus, being more advanced than the amphibian stage.

Animals↗
PubMed1981

Effects of neonatal exposure to monosodium glutamate on the electrical activity of neurones in the mediobasal hypothalamus, and on the plasma concentrations of thyroid-stimulating hormone and prolactin, following stimulation of the rostral hypothalamus in adult female rats.

Action potentials were recorded from 174 neurones in the mediobasal hypothalamus of ovariectomized adult female rats exposed neonatally to monosodium glutamate (MSG) and from 145 neurones in control rats. All of the animals, which were anaesthetized with urethane, had been ovariectomized for at least 3 weeks and received two injections of oestradiol benzoate (20 microgram/100 g body weight, i.m.) 72 h and immediately before the recording experiments. The response of each neurone to electrical stimulation of the median eminence and rostral hypothalamus (preoptic and anterior hypothalamus areas; PO/AH) was analysed. The most striking feature of the results obtained was the significant (P less than 0.001) loss of inhibitory responses in those neurones remaining in the adult rats after neonatal treatment with MSG. The loss of inhibitory responses applied to both stimulation sites. In each rat the response of one neurone, which was antidromically identified as projecting to the median eminence, was recorded before and during stimulation of the PO/AH at 50 Hz for 30s in every min for 15 min. Before and after this stimulation blood was collected from a jugular vein for estimation by radioimmunoassay of concentrations of prolactin and TSH. In the MSG-treated rats significantly (P less than 0.05) fewer neurones were inhibited by the 50 Hz stimulation than in control rats. In control rats the plasma concentrations of prolactin nearly quadrupled as an immediate consequence of this treatment, whereas in MSG-treated rats plasma concentrations barely doubled. However, in the MSG-treated rats plasma concentrations of prolactin continued to rise after stimulation ceased, possibly as a consequence of enhanced secretion of thyrotrophin releasing hormone.

Action Potentials↗
PubMed1975

Blood supply of the rat hypothalamus. III. Anterior region of the hypothalamus (nucleus suprachiasmatis, nucleus hypothalamicus anterior, nucleus periventricularis).

The arterial and venous blood supply of the anterior hypothalamus was studied by means of double perfusion technique. The angiotopography and cytoarchitecture of the hypothalamus were compared on serial sections by accounting for the three-dimensional coordinates. A detailed description is given of the arteries and veins contributing to the blood supply of the suprachiasmatic, the anterior hypothalamic and the periventricular nuclei. The topography of the arterial and venous trunk on the base surface of the rat diencephalon is described, as well as that of the larger branches which enter from below and pass through the anterior hypothalamus.

Animals↗
PubMed1982

Beta-endorphin concentrations in serum, hypothalamus and central gray of hypophysectomized and mediobasal hypothalamus lesioned rats.

The serum and brain concentrations of beta-endorphin immunoreactivity have been studied in intact, mediobasal hypothalamus (MBH) lesioned and hypophysectomized male rats. After hypophysectomy there is a major reduction (90%) of beta-endorphin concentration in the serum but only a partial reduction (20%) in the mediobasal hypothalamus. However, MBH lesions enhance beta-endorphin serum values in previously hypophysectomized rats. Long-term MBH lesions alone lead to an almost complete disappearance of beta-endorphin in the central gray matter with a slight decrease in the serum. These data clearly show that: (1) the pituitary is the major source of beta-endorphin in the serum; (2) the hypothalamus is the major source of beta-endorphin in the central gray matter; and (3) there is clear influence of the pituitary on hypothalamic beta-endorphin.

Animals↗
PubMed2001

Prepro-orexin mRNA levels in the rat hypothalamus, and orexin receptors mRNA levels in the rat hypothalamus and adrenal gland are not influenced by the thyroid status.

Orexins are two recently discovered neuropeptides that play an important role in the regulation of food intake and in the regulation of the sleep-wake cycle. In this work we examined the effects of thyroid hormones on prepro-OX expression in the rat hypothalamus, and OXRs expression in the rat hypothalamus and adrenal gland. Hypo- and hyperthyroidism were induced in adult male rats, and the levels of hypothalamic prepro-OX and OXRs mRNA, and adrenal OXRs mRNA were determined using semiquantitative reverse transcription-polymerase chain reaction and/or in situ hybridization. Our results indicate that thyroid status affects neither prepro-OX in the hypothalamus nor hypothalamic and adrenal gland OXRs expression.

Adrenal Glands↗
PubMed2000

The distribution of progesterone receptor immunoreactivity and mRNA in the preoptic area and hypothalamus of the ewe: upregulation of progesterone receptor mRNA in the mediobasal hypothalamus by oestrogen.

The distribution of progesterone receptors (PR) was mapped in the hypothalamus of the ewe using immunocytochemistry. These results were confirmed using in situ hybridization with a sheep-specific 35S-labelled riboprobe. In addition, the effect of oestrogen on the level of PR mRNA in the hypothalamus was examined in ovariectomized (OVX) ewes following treatment with an oestrogen implant or without treatment. PR immunoreactive (-ir) cells were readily detected in OVX animals. Labelled cells were observed in four main hypothalamic regions: the preoptic area (POA), including the organum vasculosum of the lamina terminalis, periventricular nucleus (PeVN), ventromedial nucleus (VMN) and the arcuate nucleus (ARC) (including the region ventral to the mamillary recess). In addition, lightly stained PR-ir cells were observed in the supraoptic nucleus and a few PR-ir cells were also found in the diagonal band of Broca. No PR-ir cells were found in the brainstem. PR mRNA-containing cells were found in the same hypothalamic regions as the PR-ir cells. Image analysis of emulsion-dipped slides following in situ hybridization indicated that oestrogen treatment increased (P<0.01) the mean number of silver grains/cell and the density of labelled cells in the VMN and ARC but had no effect on the level of PR mRNA expression in the POA or PeN. The distribution of PR-containing cells in the hypothalamus is similar to that described in other species and all cells were located in nuclei that contain large populations of oestrogen receptor-containing cells. These include regions implicated in the regulation of reproductive neuroendocrine function, and reproductive behaviour. Oestrogen and progesterone synergize to inhibit GnRH secretion and the present results suggest that these functions may involve cells of the VMN and ARC, with oestrogen acting to upregulate PR.

Animals↗
PubMed1977

A superfusion system technique for the study of the sites of action of glucocorticoids in the rat hypothalamus-pituitary-adrenal system in vitro. II. Hypothalamus-pituitary cell-adrenal cell superfusion.

Basal and stimulated CRF release by hypothalamic blocks was studied by coupling the effluent of superfused hypothalamus tissue to a joint pituitary cell-adrenal cell superfusion system and measuring corticosterone production. Log dose-response curves of the adrenal cells for ACTH and of the pituitary cell-adrenal cell system for CRF were linear over the ranges used. Ca++-independent basal CRF release by the hypothalamus could be blocked in vitro by 0.2 mug/ml dexamethasone in the medium, or in vivo by treating the hypothalamus donor rats with corticosterone, 1 mg/rat ip 30 min before decapitation. These treatments did not impair CRF release caused by Veratridine (5 x 10(-6)M or by electrical stimulation. Adrenalectomy increased only basal but not stimulated CRF release. These results indicate that glucocorticoids have a hypothalamic site of action.

Adrenal Glands↗
PubMed1982

Blood supply of the rat hypothalamus. VII. The lateral hypothalamus (medial forebrain bundle).

Using the double ink-filling technique the arteries and veins of the lateral hypothalamus are described in detail. This region occupied mainly by the fibres and interposed cells of the medial forebrain bundle is supplied by some own arteries and branches of the large basal vessels. Most of the arteries running to the rostral part of the lateral hypothalamus originate from the internal carotid, others belong to the anterior and middle cerebral arteries. Blood supply of the middle part comes from the middle hypothalamic and three tuberal arteries. All arteries of the caudal part originate from the posterior communicans. The abundant drainage of the lateral hypothalamus is collected by the basal and anterior interpeduncular veins from the rostral two-thirds and the caudal one-third, respectively.

Animals↗
PubMed1988

The effect of fetal hypothalamus grafts on weight gain resulting from lesions of the ventromedial hypothalamus.

Bilateral ventromedial hypothalamic lesions in female adult rats which resulted in hyperphagia and rapid weight gain were followed by placement of fetal brain tissue in the anterior third ventricle. The treatment group received fetal hypothalamus grafts, and fetal cortical tissue of identical age was grafted into the control group. A significant reduction in average daily weight gain was noted from 4 to 12 weeks following transplantation in the treatment group. At 12 weeks posttransplantation, the animals were sacrificed for histological analysis. Examination of the hypothalamus grafts revealed neurons, ependymal clusters, and axonal processes which appeared to infiltrate the surrounding hypothalamic parenchyma.

Animals↗
PubMed1977

Blood supply of the rat hypothalamus. V. The medial hypothalamus (nucleus ventromedialis, nucleus dorsomedialis, nucleus perifornicalis).

Using the India ink double-perfusion technique, the blood vessels of the rat's medial hypothalamus were reconstructed from serial sections. The area studied comprised the ventromedial, dorsomedial and perifornical nuclei. The arterial supply of this territory comes from the middle hypothalamic and the anterior, middle and posterior tuberal arteries. The drainage is strictly undirectional: ventralward by the anterior, middle and posterior ventromedial, the posteromedial and posterolateral hypothalamic veins, all ending in the basal vein. The arteries of the ventromedial and dorsomedial nuclei are distinct from those of the arcuate nucleus and median eminence, and their drainage is not connected with the portal vessels. The nuclei studied, even at the levels of their subdivisions, possess own arteries whose territories of supply can well be distinguished with a minimum of overlap. The topography of these arteries is described in detail. The medial hypothalamus has no vascular connections with other regions of the diencephalon including the thalamus.

Animals↗
PubMed1983

Ontogeny of hypothalamus-pituitary function in the fetal pig: gonadotropin release in response to electrical and electrochemical stimulation of the hypothalamus.

The ontogeny of hypothalamic control of anterior pituitary gonadotropin secretion was studied in anesthetized fetal pigs at different gestational ages (60, 80, and 105 days gestation; term, 114 days). Three or four fetuses from one mother simultaneously received either no treatment (control), sham operation, electrical stimulation (EL), or electrochemical stimulation (EC). Electrodes were implanted unilaterally into the hypothalamus. Fetuses remained in utero during surgery. A distinct difference in the development of basal LH and FSH secretion was observed. Basal plasma LH concentrations almost doubled (P less than or equal to 0.001) between days 60 and 80, with no further significant increase between 80 and 105. Plasma FSH concentrations did not change significantly between days 60 and 80, but increased more than 5-fold (P less than or equal to 0.001) between days 80 and 105. EL or EC did not affect LH secretion at 60 days. At 80 days, EL and EC significantly (P less than or equal to 0.05) elevated plasma LH concentrations 30 and 50 min after the onset of stimulation. At 105 days, EL and EC caused a rise in plasma LH levels within 10 min; the maximum level, reached 30 min after the onset of stimulation, was double that in 80-day-old fetuses. Plasma FSH values were not significantly affected by EL or EC in any age group. The results indicate that the fetal pig hypothalamus is able to influence pituitary LH secretion by day 80 (70% of gestation). Further, maturation of hypothalamic control of LH secretion becomes demonstrable between days 80 and 105. The development of hypothalamic control of FSH secretion is delayed relative to LH.

Animals↗
PubMed1995

The opposing effects of interleukin -1 beta microinjected into the preoptic hypothalamus and the ventromedial hypothalamus on nociceptive behavior in rats.

The effects of microinjections of recombinant human interleukin-1 beta (rhIL-1 beta) into the hypothalamus and neighboring basal forebrain on nociceptive behavior were studied using a hot-plate test in rats. The microinjection of rhIL-1 beta at doses between 5 pg/kg and 50 pg/kg into the medial part of the preoptic area (MPO) reduced the paw-withdrawal latency. The maximal reduction was obtained 30 min after the injection of rhIL-1 beta at 20 pg/kg. RhIL-1 beta (20 pg/kg)-induced hyperalgesia was completely blocked by the simultaneous injection of IL-1 receptor antagonist (IL-1ra, 20 ng/kg), Na salicylate (200 ng/kg) or alpha-melanocyte-stimulating hormone alpha-MSH, 20 ng/kg). The intra-MPO injection of rhIL-1 beta at doses of less than 5 pg/kg or more than 50 pg/kg (up to 2 ng/kg) into the paraventricular nucleus, the lateral hypothalamic area and the septal nucleus had no effect on nociception. The microinjection rhIL-1 beta (20 pg/kg-50 pg/kg) into the ventromedial hypothalamus produced a prolongation of the paw-withdrawal latency. A maximal prolongation was obtained 10 min after the injection of rhIL-1 beta at 50 pg/kg. This reaction was also blocked by the simultaneous injection of IL-1ra (50 ng/kg) and Na salicylate (500 ng/kg). These findings indicate that IL-1 beta in the MPO and the VMH produces hyperalgesia and analgesia, respectively, while, in addition, both effects are mediated by IL-1 receptors and the synthesis of prostaglandins.

Animals↗
PubMed1996

The hypothalamus-pituitary-ovary and hypothalamus-pituitary-thyroid axes in spinal cord-injured women.

Sixteen women with spinal cord injury (SCI) underwent studies of the hypothalamus-pituitary-ovary (HPO) and hypothalamus-pituitary-thyroid (HPT) axes with luteinizing hormone (LH) releasing hormone (LHRH) and thyrotropin (TSH) releasing hormone (TRH) stimulation tests during the early follicular phase. The mean interval from injury to participation in this study was 7.5 years (range, 1.5 to 13.1). All subjects were menstruating regularly. Five (35.7%) SCI subjects who were menstruating before injury had postinjury amenorrhea for 1 to 12 months, and the other nine (64.3%) SCI subjects had no interruption of menstruation after injury. Two SCI subjects whose injury occurred in preadolescence proceeded to menarche without any delay. The amount of menstrual flow was noted to be reduced in nine (64.3%) SCI subjects. Two and three SCI subjects had elevated follicle-stimulating hormone (FSH) and prolactin (PRL) levels, respectively. LH responses to LHRH were significantly higher in the SCI group (P < .001). Ten (62.6%) SCI subjects had enhanced LH responses to LHRH. The mean TSH, PRL, and FSH responses to TRH and LHRH of the SCI group were not significantly different from those of age-matched controls. However, five (31.2%), four (25.0%), and five (31.2%) SCI subjects had enhanced TSH, PRL, and FSH responses to TRH and LHRH, respectively. Six (37.5%) SCI subjects had a delayed FSH response to LHRH. In total, 13 (81.2%) SCI subjects had at least one axis abnormality. These findings are consistent with the hypothesis that changes of central neurotransmitters may occur after SCI.

Adolescent↗