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PubMed1996

Effect of fasting and immobilization stress on estrogen receptor immunoreactivity in the brain in ovariectomized female rats.

The present study examined the effect of 48-h fasting and 1-h immobilization on estrogen receptor immunoreactivity in selected hypothalamic areas and the nucleus of the solitary tract (NTS) in ovariectomized rats. Fasting induced an increase in ER-immunoreactive cells in the paraventricular nucleus (PVN), periventricular nucleus (PeVN) and NTS compared with the unfasted control group. Similarly, immobilization caused an increase in ER-positive cells in the same areas, PVN, PeVN and NTS, versus the non-immobilized group. There was no significant increase in the number of ER-immunoreactive cells in the preoptic area (POA), arcuate nucleus (ARC) or ventromedial hypothalamic nucleus (VMH) following fasting and immobilization. Our previous work in ovariectomized rats with estrogen microimplants in the brain revealed that the PVN and A2 region of the NTS are the feedback sites of estrogen in activating the neural pathway to suppress pulsatile LH secretion during 48-h fasting. The result in the food-deprived rats suggests that estrogen modulation of the suppression of LH secretion during fasting is partly due to the increase in estrogen receptors in the PVN and A2 region. The physiological significance of the increase in neural ER following immobilization remains to be elucidated.

Animals↗

PubMed1985

Gastrointestinal somatostatin: distribution, secretion and physiological significance.

Somatostatin-like immunoreactivity (SLI) has been found throughout the gastrointestinal tract in all species examined. In the stomach it is mainly present in endocrine-type D-cells whereas in the intestine there is also an extensive distribution in enteric neurones. In all regions of the gastrointestinal tract multiple forms of somatostatin exist. A precursor (prosomatostatin) has been partially sequenced, three forms with 20 (SS-20), 25 (SS-25) and 28 (SS-28) amino acids completely sequenced, and somatostatin-14 (SS-14) demonstrated by radioimmunoassay. Both SS-14 and SS-28 exert a wide range of actions on the gastrointestinal tract and there is strong supportive evidence for a role in the regulation of gastric acid and gastrin secretion, gastrointestinal motility and intestinal transport. Both in vivo and in vitro studies on the secretion of gastric SLI into the vasculature have shown that nutrients initiate the process but that subsequent events are regulated by a complex interplay between hormonal and neuronal pathways. GIP is one of the most potent hormonal secretagogues. In the stomach, acetylcholine, opioid peptides and substance P are probably involved in parasympathetic inhibitory pathways and gastrin releasing peptide in stimulatory pathways. The sympathetic nerves are also stimulatory. Regulation of secretion of intestinal SLI has not been so extensively studied. Although SLI is also found in the gastrointestinal lumen the significance is unclear. Despite these advances the exact route of delivery of somatostatin to its target organs is uncertain and paracrine, endocrine and neural pathways may all be involved.

Animals↗

PubMed2000

Fos expression in the rat brain after exposure to gravito-inertial force changes.

The immediate-early genes constitute useful neurobiological tools for mapping brain functional activity after sensory stimulation. We immunohistochemically investigated Fos protein expression in the brain of rats exposed to gravito-inertial force changes. Experiments were performed in hypergravity rats born and housed for 60 days in terrestrian gravity (1xg) and thereafter exposed for 90 min to 2xg or 4xg in a centrifuge, and in hypogravity rats born and housed for 60 days at 2xg and submitted for 90 min to 1xg. Data from these two experimental groups were quantified by light microscopy and compared to those from two groups of control rats born and permanently housed in either 1xg or 2xg environments that never had to adapt to novel gravito-inertial environments. Results showed a low basal Fos expression in the controls and a strong Fos staining in the experimental rats. Only the hypergravity rats displayed Fos-positive cells in vestibular-related brainstem regions (medial, inferior, and superior vestibular nuclei (VN); group y; dorsomedial cell column (DMCC) of the inferior olive (IO)). By contrast, many suprabulbar areas were strongly labeled in both the hyper- and hypogravity rats, as shown by the numerous Fos-positive cells in mesencephalic (colliculus, laterodorsal periaqueductal gray, autonomic nuclei), diencephalic (hypothalamic and thalamic nuclei), and telencephalic (parietal, temporal, entorhinal and visual cortices) structures. These spatial patterns of Fos expression suggest that an increase in gravito-inertial force activates otolith-vestibulo-olivar pathways and various suprabulbar structures underlying the corticovestibular interactions, which govern the multiple representations of vestibular information in the cortex. A decrease in gravito-inertial force has the opposite effects on the vestibulo-olivar structures as a result of otolith system disfacilitation which, in turn, modifies the activity of complex neural pathways. Exposure to both hyper- and hypogravity environments likely induces neurovegetative and/or stress effects that could account for Fos labeling in autonomic nuclei and in nervous structures involved in the hypothalamo-pituitary-adrenal axis.

Animals↗

PubMed1987

Central inhibitory control of sodium appetite in rats: correlation with pituitary oxytocin secretion.

In the present experiments we examined neurohypophyseal hormone secretion in various models of sodium appetite in rats. Basal plasma levels of oxytocin were found to be low in sodium-deficient adrenalectomized rats and in intact animals treated daily with desoxycorticosterone acetate, both of which groups drank large amounts of NaCl solution, whereas basal plasma levels of arginine vasopressin were neither stimulated nor suppressed. Conversely, sodium appetite consistently was inhibited by treatments that stimulated pituitary oxytocin secretion. However, sodium appetite was not inhibited by administration of exogenous oxytocin, nor was it stimulated by administration of an oxytocin receptor antagonist. These and other results suggest that sodium appetite may be inhibited by activity in the supraoptic and/or paraventricular nuclei, the location of the neurons responsible for the synthesis of oxytocin, and can be stimulated only when activity in those neurons is reduced. Whatever the final neural pathway, our data support the hypothesis that the control of sodium appetite is governed by inhibitory as well as excitatory central mechanisms.

Adrenal Glands↗

PubMed1981

Connections of medial preoptic neurons with the median eminence and amygdala. An electrophysiological study in the rat.

An electrophysiological investigation was conducted on the connection of medial preoptic neurons with the median eminence and the basal and corticomedial amygdala in pentobarbital anesthesized male Sprague-Dawley rats. Of 411 medial preoptic neurons tested with median eminence stimuli, antidromic responses (mean latency 11.4 +/- SEM 0.4 ms) identified 177 cells as tuberoinfundibular neurons. Most were located in the periventricular area; 21 cells were in the area of the suprachiasmatic nucleus. Axon conduction velocities ranged between 0.01 and 0.9 m/s. 16 neurons displayed two distinct antidromic latencies when the median eminence stimulus was increased above threshold, indicating that their axons may branch in the region of the median eminence. Following suprathreshold stimulation, only 10% of spontaneously active neurons displayed features to suggest activation of a recurrent inhibitory pathway. In response to amygdala stimulation, 23% of tuberoinfundibular neurons displayed an orthodromic response; most (80%) responded with an increase in excitability after a latency of 21.6 +/- 2.4 ms; the remainder displayed a decrease in excitability at latencies of 20-28 ms lasting in excess of 100 ms. These data suggest an additional neural pathway whereby the amygdala can influence neuroendocrine regulation, i.e. through its actions on the excitability of medial preoptic tuberoinfundibular neurons.

Action Potentials↗

PubMed2007

Postural context alters the stability of bimanual coordination by modulating the crossed excitability of corticospinal pathways.

The tendency for movements of the upper limbs to be drawn systematically toward one another and to follow similar spatiotemporal trajectories is well known. Although suppression of this tendency is integral to tasks of daily living, its exploitation may prove to be critical in the rehabilitation of acquired hemiplegias. In general, however, the task-related factors that determine the degree of coupling between the upper limbs and the mechanisms that mediate bilateral interactions between neural pathways projecting to the muscles of the arm and hand are not yet well understood. We present evidence that the postural context in which human participants perform upper limb movements determines the relative stability of patterns of bimanual coordination. Manipulation of the axes of rotation of forearm movements reversed the relative stability of simultaneous and alternating patterns of bimanual coordination. Transcranial magnetic stimulation of motor cortex revealed that these manipulations of postural context altered the crossed modulation of excitability in corticospinal pathways that arises from movement of the opposite limb. Furthermore, modulation of responses to electrical stimulation of the cervicomedullary junction indicated that crossed modulation was also expressed at the level of the spinal motoneurons. Our data support the view that crossed modulation of excitability in corticospinal pathways mediates the stability of bimanual coordination. Furthermore, task-related factors that are sufficient to give rise to changes in the stability of bimanual coordination are accompanied by crossed modulation of excitability at multiple levels of the neuraxis, indicative of a failure of inhibitory control.

Adult↗

PubMed2006

Neurological complications in beta-thalassemia.

Over the years, several reports have demonstrated involvement of the nervous system in beta-thalassemia patients. Neurological complications have been attributed to various factors such as chronic hypoxia, bone marrow expansion, iron overload, and desferrioxamine neurotoxicity. In most cases, neurological involvement does not initially present with relevant signs or symptoms (i.e., is subclinical) and can only be detected during neurophysiological or neuroimaging evaluation. Abnormal findings in the visual, auditory, and somatosensory evoked potential recordings are mainly attributed to DFO neurotoxicity. On the other hand, nerve conduction velocity abnormalities are associated either to chronic hypoxia and older age or to hemosiderosis, whether by means of pancreas involvement or not. Neuropsychological studies available reveal a considerably high prevalence of abnormal IQ, not correlating, however, to factors such as hypoxia or iron overload. It is proposed that factors associated to severe chronic illness, rather than the disease per se, could be responsible for these findings. Such factors include regular school absence due to transfusions and frequent hospitalizations, physical and social restrictions resulting from the disease and its treatment, abnormal mental state due to the awareness of being chronically ill, and, last, the overly protective family attitude that leads to restricted initiative and psychosocial development. As life expectancy for beta-thalassemia patients extends, the use of neurophysiologic and neuropsychologic monitoring becomes imperative, enabling early detection of neural pathway impairment and allowing for appropriate management, in order to achieve a better life quality for this patient group.

Evoked Potentials↗

PubMed1990

Facilitation and inhibition of the human startle blink reflexes by stimulus anticipation.

The cutaneous eyeblink has 2 electromyographic components, 1 unilateral and early (R1) and 1 bilateral and late (R2), which are served by different neural pathways. These 2 reactions were measured when the eliciting stimulus was expected or relatively surprising. Forewarning was varied in 3 ways: Subjects received notice that the stimulus was about to occur on some trials (Experiment 1); delivered the stimulus to themselves on some trials (Experiments 2 & 3); or experienced a series of trials in which a tone was paired with the eliciting stimulus, followed by tone-alone trials interspersed with test trials (Experiment 4). In each case, forewarning enhanced R1 amplitudes while depressing R2 but reduced the latency of both components. This mixed pattern of effects reveals that the preparatory state provoked by forewarning focuses excitatory and inhibitory processes simultaneously on different reflex pathways: inhibition central and excitation peripheral.

Adult↗

PubMed1984

Involvement of central nervous system in diabetes mellitus.

Brainstem auditory evoked responses were recorded in 22 diabetic patients with a variable duration of illness (mean 5.8 years) and 14 normal healthy controls of comparable age. The initial 10 millisecond components, found to be most consistent and reproducible, were analysed. Variations in the form of individual wave latency, interpeak latencies and V wave amplitude were compared in both the groups. No difference was found in any of the parameters. It was concluded that central neural pathways are not involved at least initially in diabetes mellitus.

Adolescent↗

PubMedDate not supplied

The endocannabinoid-CB receptor system: Importance for development and in pediatric disease.

Endogenous cannabinoids (endocannabinoids) and their cannabinoid CB1 and CB2 receptors, are present from the early stages of gestation and play a number of vital roles for the developing organism. Although most of these data are collected from animal studies, a role for cannabinoid receptors in the developing human brain has been suggested, based on the detection of "atypically" distributed CB1 receptors in several neural pathways of the fetal brain. In addition, a role for the endocannabinoid system for the human infant is likely, since the endocannabinoid 2-arachidonoyl glycerol has been detected in human milk. Animal research indicates that the Endocannabinoid-CB1 Receptor ('ECBR') system fulfills a number of roles in the developing organism: 1. embryonal implantation (requires a temporary and localized reduction in anandamide); 2. in neural development (by the transient presence of CB1 receptors in white matter areas of the nervous system); 3. as a neuroprotectant (anandamide protects the developing brain from trauma-induced neuronal loss); 4. in the initiation of suckling in the newborn (where activation of the CB1 receptors in the neonatal brain is critical for survival). 5. In addition, subtle but definite deficiencies have been described in memory, motor and addictive behaviors and in higher cognitive ('executive') function in the human offspring as result of prenatal exposure to marihuana. Therefore, the endocanabinoid-CB1 receptor system may play a role in the development of structures which control these functions, including the nigrostriatal pathway and the prefrontal cortex. From the multitude of roles of the endocannabinoids and their receptors in the developing organism, there are two distinct stages of development, during which proper functioning of the endocannabinoid system seems to be critical for survival: embryonal implantation and neonatal milk sucking. We propose that a dysfunctional Endocannabinoid-CB1 Receptor system in infants with growth failure resulting from an inability to ingest food, may resolve the enigma of "non-organic failure-to-thrive" (NOFTT). Developmental observations suggest further that CB1 receptors develop only gradually during the postnatal period, which correlates with an insensitivity to the psychoactive effects of cannabinoid treatment in the young organism. Therefore, it is suggested that children may respond positively to medicinal applications of cannabinoids without undesirable central effects. Excellent clinical results have previously been reported in pediatric oncology and in case studies of children with severe neurological disease or brain trauma. We suggest cannabinoid treatment for children or young adults with cystic fibrosis in order to achieve an improvement of their health condition including improved food intake and reduced inflammatory exacerbations.

Adolescent↗

PubMed1987

Forebrain and brainstem afferents to the arcuate nucleus in the rat: potential pathways for the modulation of hypophyseal secretions.

Doxorubicin, an anti-oncogenic agent, was used as a retrograde marker to identify arcuate nucleus afferent projections. Injections of this tracer into the arcuate nucleus indicated that the subfornical organ, the organum vasculosum of the lamina terminalis, the nucleus raphe dorsalis and median raphe send projections to the arcuate nucleus. Immunocytochemical procedures were used to demonstrate that the raphe projections to the arcuate nucleus are serotoninergic. This anatomical investigation provides evidence that neural pathways exist between forebrain body fluid and mineral nuclei, mesencephalic serotonin nuclei and the arcuate nuclei.

Afferent Pathways↗

PubMed1999

Peripheral and central actions of orphanin FQ (nociceptin) on murine colon.

Orphanin FQ (OFQ), also known as nociceptin, is a recently isolated endogenous peptide with a structure similar to the endogenous opioid peptides. The present study examines the actions of centrally administered OFQ on in vivo murine gastrointestinal and colonic transit as well as the actions of OFQ on the isolated colon. Intracerebroventricular injections of OFQ dose dependently inhibited colonic propulsive activity. OFQ inhibition of colonic propulsion was unaffected by coadministration of the competitive opioid receptor antagonist naltrexone. A subadditive response was observed when approximately equipotent doses of either morphine sulfate or the delta-agonist DPDPE were coadministered with OFQ. No subadditivity was observed with coadministration of the micro-agonist DAMGO, suggesting a functional interaction between OFQ and delta-opioid central pathways regulating colonic transit. High, but not low, doses of OFQ also inhibited the transit of a nonabsorbable charcoal marker through the stomach and/or small intestine. OFQ potently contracted isolated colon preparations; contractile activity was abolished by TTX or chlorpromazine. Our results suggest that OFQ may be an important peptide ligand acting on a novel inhibitory neural pathway that modulates gastrointestinal transit.

Animals↗

PubMed1986

Growth hormone and prolactin secretion after hypothalamic deafferentation in pigs.

Control of growth hormone (GH) and prolactin (PRL) secretion was investigated in ovariectomized, prepuberal Yorkshire gilts by comparing the effects of anterior (AHD), complete (CHD), and posterior (PHD) hypothalamic deafferentation with sham-operated controls (SOC). Blood samples were collected sequentially via an indwelling jugular catheter at 20-min intervals during surgery and recovery from anesthesia (Day 0) and Days 1 and 2 after cranial surgery. Mean serum concentrations of GH after AHD, CHD, and PHD were reduced (P less than 0.01) when compared with SOC gilts. Furthermore, episodic GH release evident in SOC animals was obliterated after hypothalamic deafferentation. PRL concentrations in peripheral serum of hypothalamic deafferentated gilts remained similar (P greater than 0.05) to those of SOC animals. These results indicate that anterior and posterior hypothalamic neural pathways play a minor role in the control of PRL secretion in the pig in as much as PRL levels remained unchanged after hypothalamic deafferentation. These findings may be interpreted to suggest that the hypothalamus by itself seems able to maintain tonic inhibition of PRL release. In contrast, the maintenance of episodic GH secretion depends upon its neural connections traversing the anterior and posterior aspects of the hypothalamus in the pig.

Animals↗

PubMed2000

Modulation of exteroceptive suppression periods in human jaw-closing muscles induced by summation of nociceptive and non-nociceptive inputs.

Convergence of various afferent inputs onto brain-stem neurons may play an important role in the regulation of trigeminal motor function. The present study examined the efficacy of nociceptive and non-nociceptive perioral stimulation for the modulation of the two exteroceptive suppression periods (ES1 and ES2) in human jaw-closing muscles. The inhibitory jaw-reflexes, ES1 (10-15 ms onset) and ES2 (40-50 ms onset), were recorded as the surface electromyogram of masseter and temporalis muscles in 14 healthy subjects. Non-painful electrical stimuli were applied to the right mental nerve while the subject was biting at 50% of the maximal voluntary force. Five conditions were compared: baseline, repetitive tactile stimulation (1 Hz) on the right cheek, topical application of capsaicin (5%) on the right cheek, repetitive tactile stimulation plus capsaicin, and postbaseline. The perceived intensity of the electrical stimuli was evaluated by the subjects on a 0-10 rating scale. Capsaicin alone failed to induce significant changes of ES1 and ES2; tactile stimulation alone induced a significant delay in the onset of ES2 (P < 0.001). During repetitive tactile stimulation plus capsaicin, the duration of ES1 and ES2 was shortened (ES1 and ES2: P < 0.001) and the degree of suppression was reduced (ES1: P < 0.05; ES2: P < 0.005). Perceived intensity of the electrical stimuli was unchanged during the different experimental conditions. The present results suggest that summation of simultaneous nociceptive and non-nociceptive inputs plays an important role in the modulation of the neural pathways involved in the short-latency ES1 and long-latency ES2.

Adult↗

PubMed1987

The relationship between gastrointestinal motility and secretion.

Few studies have addressed specifically or systematically the question of whether motility and secretion within the gastrointestinal tract are linked and if so by what mechanisms. The evidence for such a relationship is discussed in this review and we conclude that increased motor activity of the stomach is frequently associated with increased acid and pepsin secretion. Similarly, an increase in small intestinal motility is accompanied by elevated fluid and electrolyte secretion. Two possible mechanisms linking motility to secretion are considered. These could coexist. The first consists of parallel but separate neural pathways to smooth muscle and epithelium that might be activated synchronously and, therefore, produce simultaneous activation of motility and secretion. The existence of such parallel pathways in the stomach and small intestine are described, but their physiological significance is unresolved. The second mechanism we discuss is a sequential process in which increased motility provides a sensory stimulus for reflexly activated secretion. In the stomach the evidence for such a mechanism is largely deductive. In the intestine, however, we provide experimental evidence for an intrinsic neural mechanism activated by motor activity, which then stimulates fluid and electrolyte secretion. We conclude that such a sequential relationship exists and probably operates under physiological conditions but that further study is required.

Animals↗

PubMedDate not supplied

Treatment of spasticity with botulinum toxin.

Spasticity is an abnormal increase in muscle contraction often caused by damage to central motor pathways that control voluntary movement. During clinical examination, spasticity manifests as an increase in stretch reflexes, producing tendon jerks and resistance appearing as muscle tone. There are many causes of spasticity, including demyelination from multiple sclerosis, congenital damage from diseases such as cerebral palsy, trauma to the brain or spinal cord, hemorrhage or infarction, and other pathologic conditions that interrupt neural pathways. Effects of spasticity range from mild muscle stiffness to severe, painful muscle contractures and repetitive spasms that reduce mobility and substantially impede normal activities of daily living. Botulinum toxin therapy reduces spasticity and pain associated with several disorders. Local treatment with botulinum toxins can be used as adjunctive therapy, along with oral antispasticity medications, or alone to provide localized decrease in symptoms of spasticity and pain. Botulinum toxin therapy may be particularly useful for patients with spasticity due to stroke, whose treatment can be tailored based on recovery of function over time. In addition, botulinum toxin therapy is safe for pediatric patients, including children with cerebral palsy, who may not be able to tolerate the cognitive side effects of oral medications. Results of studies evaluating botulinum toxin for the treatment of spasticity due to various causes are presented here.

Botulinum Toxins↗

PubMed2000

Adrenergic influences on coeliac ganglion affect the release of progesterone from cycling ovaries: characterisation of an in vitro system.

The superior ovarian nerve (SON) arrives at the ovary through the suspensory ligament and innervates mainly the ovarian stroma. Most neurones from which the SON fibres originate are located in the complex coeliac and mesenteric ganglia. Taking into account that other ganglia have been shown to have alpha- and beta-adrenergic receptors, and that the coeliac ganglion receives adrenergic fibres from other sympathetic paravertebral and preaortic ganglia, we utilised adrenergic agonists and antagonists specific to the ganglion, to analyse the role of the alpha and beta receptors in ovarian physiology. To that end, it was necessary to develop and standardise an in vitro coeliac ganglion-SON-ovary (coeliac ganglion-SON-O) experimental system that would enable study of the release of steroids in the ovary in the absence of humoral factors. We investigated the effect of adrenergic agents on the liberation of progesterone in the different stages of the oestrous cycle. To this end we placed the coeliac ganglion and the ovary in different compartments, connected through the SON, to produce a system being studied as a whole. Combined neural and hormonal (luteinising hormone (LH)) effects were also examined. Non-specific stimulation with KCl in the ganglion compartment evoked different responses in terms of release of progesterone, depending on the physiological conditions of the cycle; this demonstrated the sensitivity and viability of the system. During pro-oestrus, stimulation of the ganglion compartment with adrenergic agents such as the agonist noradrenaline or the beta-adrenergic antagonist propranolol, did not modify the release of progesterone. In contrast, the alpha-adrenergic antagonist, phentolamine, induced a strong inhibitory response. During the oestrous stage, noradrenaline was inactive, but phentolamine and propranolol exerted a strong stimulus throughout the experiment. On dioestrus day 1 (D1), both noradrenaline and propranolol increased the release of ovarian progesterone, whereas phentolamine had the opposite effect. Finally, on dioestrus day 2 (D2), what was noteworthy was the pronounced inhibitory effect of noradrenaline, whereas phentolamine was inactive and propranolol showed its greatest stimulatory effect. In order to compare the combined neural and endocrine effects on the ovarian release of progesterone, the experiment was carried out during stages D1 and D2, when the corpora lutea are at their peak of activity. Adrenergic agents were added to the ganglion and LH in a final concentration of 50 ng/ml was added to the ovarian comparment. Different effects were observed indicating a differential response to these agents in stimulated and basal conditions. We conclude that the in vitro coeliac ganglion-SON-ovary system is a functional entity because it possesses its own autonomic tone. This is verified because different basal values of progesterone appear in the different stages of the oestrous cycle. In similar fashion, variations of progesterone induced via the neural pathway were observed under different experimental conditions. In contrast, on D2, noradrenaline added to the ganglion compartment had an inhibitory effect on the liberation of ovarian progesterone. This would indicate that, during this phase, noradrenaline may not be the neurotransmitter released in the ovarian compartment, but that other inhibitory molecules might participate in the observed effects. Finally, during D2, the neural input would condition the ovarian response to LH, facilitating the decrease in progesterone necessary to start a new cycle. The experimental scheme is, in our opinion, a valuable tool for the study of peripheral neural participation in ovarian physiology.

Adrenergic Agents↗

PubMed1991

Food deprivation and hypothalamic neuropeptide gene expression: effects of strain background and the diabetes mutation.

We have used a novel method to identify genes expressed in the hypothalamus which may be potentially involved in controlling food intake and energy metabolism. We assumed that food deprivation, a powerful stimulus of food intake, would stimulate the activity of neural pathways involved in feeding behavior which should be reflected in an increase in the synthesis of any relevant neuropeptide and its messenger RNA. A study of 5 neuropeptides in 5 strains of mice has identified neuropeptide Y (NPY) as a gene whose expression in the hypothalamus is controlled by nutritional status, suggesting that hypothalamic NPY neurons are a link in the neural network regulating feeding behavior and energy metabolism. In addition, we have studied the effect of the diabetes mutation on neuropeptide gene expression during fasting and refeeding. Our findings suggest that abnormal NPY and enkephalin gene expression in the hypothalamus may be two important determinants of the expression of the diabetes mutation.

Animals↗