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A microdialysis study of the noradrenergic response in rat frontal cortex and hypothalamus to a conditioned cue for aversive, naturalistic environmental stimuli.

RATIONALE: Extracellular noradrenaline concentration in the rat forebrain is increased by aversive environmental stimuli. This study investigated whether conditioned cues for such stimuli have the same effect. METHODS: After training rats to associate a tone (conditioned cue) with transfer from a neutral zone to a brightly lit zone of a light/dark shuttle-box (unconditioned stimulus), microdialysis probes were implanted into the frontal cortex and hypothalamus under halothane anaesthesia. Changes in extracellular noradrenaline concentration were then monitored on exposure to the tone alone. Parallel experiments monitored rats' behaviour in the light arena. RESULTS: A single exposure to the light arena increased extracellular noradrenaline in the frontal cortex and the hypothalamus but neither a single, nor repeated, exposure to the tone alone had any effect. After conditioning trials, the tone alone increased extracellular noradrenaline in the frontal cortex but not the hypothalamus, whilst the tone+transfer to the light arena resulted in a prolonged increase in extracellular noradrenaline in both brain regions. The time that rats spent within the light arena was also prolonged. CONCLUSIONS: Noradrenergic neurones in the frontal cortex, but not the hypothalamus, respond to conditioned cues for aversive environmental stimuli. However, prolongation of the noradrenergic response in both brain regions could contribute to the behavioural adaptation to such unconditioned stimuli.

Acoustic Stimulation↗

Post-session sulpiride infusions within the perifornical region of the lateral hypothalamus enhance consolidation of associative learning.

Whilst neurons within the lateral hypothalamus are well known to be responsive to the presentation of previously learned associative stimuli, the consolidation of a Pavlovian association is thought to depend in large part upon other brain regions, including the amygdala. The present study addressed this assumption directly, by examining the effect of post-session infusions of sulpiride within the lateral hypothalamus upon the acquisition of a conditioned approach response in an appetitive differential conditioning task. Subjects were exposed to an initially neutral stimulus (CS+), which immediately preceded the availability of a 10% sucrose reward (US). A second, control stimulus (CS ) was also presented. but never in close temporal proximity to the US. The number and duration of alcove approaches were recorded. Immediately following each training session, subjects were infused bilaterally with sulpiride (0, 0.5, 5 microg) in the vicinity of the perifornical region of the lateral hypothalamus. Sulpiride dose-dependently enhanced the rate of acquisition of a conditioned approach response to presentation of the CS+, but was without affect upon approach behaviour during CS(-) or US presentations. Thus, 0.5 microg sulpiride facilitated at an early stage (session 2 onwards) the number of alcove approaches to the CS+, while 5 microg sulpiride enhanced to a greater extent the duration of conditioned approach, particularly during later sessions. A subsequent locomotor test using 0.5 mg/kg d-amphetamine indicated that repeated infusions of the higher dose sulpiride (5 microg), but not the lower dose (0.5 microg), resulted in behavioural sensitisation to administration of the psychomotor stimulant. Acquisition of a novel conditioned instrumental response was not affected by previous exposure to sulpiride. These data suggest that dopamine-sensitive neurons within the lateral hypothalamus may play a significant role in the acquisition of appetitive Pavlovian associations.

Animals↗

Sheep 5HT2A receptors: partial cloning of the coding sequence and mRNA localization by in situ hybridization in the ewe hypothalamus.

UNLABELLED: Serotonin and serotonin receptors of class II (5HT2-R) are thought to be involved in the neural mechanisms which regulate the LH release associated with photoperiodic changes in sheep. A specific premammillary hypothalamic area displaying a significant binding of 3H-ketanserin, a potent 5HT2-R antagonist, was previously identified. The aim of the present study was to ascertain by in situ hybridization (ISH) that 5HT2-R mRNA-containing cells were also present in this specific hypothalamic area. Total RNA was prepared from sheep pars tuberalis/median eminence, and a cDNA fragment of 546 bp was amplified by reverse transcriptase polymerase chain reaction (RT-PCR) using degenerated primers deduced from the human and rat 5HT2A-R sequences. After cloning and sequencing, the sheep nucleotide sequence had the highest homology (85.1-92.3%) with the other known mammalian 5HT2-R or 5HT2A-R sequences. Homology with other 5HT-R subtypes or other monoamine receptors was much lower, 60% at maximum. After ISH using sense and antisense 35S-riboprobes, specific labelling was found in different parts of the hypothalamus, especially in the mammillary bodies where the binding was higher. Within the hypothalamus, the density of labelled cells, mainly neurons, varied considerably. It was maximal in the mammillary bodies and also in a restricted ventral region of the premammillary hypothalamus located from about 500/700 micrometer to 1200/1400 micrometer in front of the mammillary recess, where 3H-ketanserin binding was previously reported. IN CONCLUSION: (1) the structural study of the sequence indicated that the new cloned cDNA corresponds to the sheep 5HT2-R class and, probably, to the 5HT2A-R subtype and (2) the ISH studies revealed that a restricted area of the premammillary hypothalamus shows a large number of 5HT2-R mRNA-containing neurons.

Animals↗

Further evidence for a hypothalamus-parotid gland endocrine axis in the rat.

The existence of a hypothalamus-parotid gland endocrine axis that stimulates intradentinal dye penetration (IDDP) in rat teeth was suggested in earlier studies and IDDP-stimulating factors were isolated or purified from porcine parotid glands and hypothalamic tissues, respectively. In the present study, infusion of carbamyl-DL-aspartic acid (CAA) into rats was used to demonstrate the role of the endogenous hormones of the hypothalamus-parotid gland endocrine axis in stimulating IDDP, as observed by fluorescence microscopy of longitudinal sections of molar teeth. Intra-arterial infusion of CAA into intact rats stimulated IDDP in a dose-related fashion (between 49-390 nmol/100 g body weight); however, infusion of 390 nmol into parotidectomized rats was ineffective. Infusion of plasma from CAA-treated rats was equally effective in stimulating IDDP in intact and in parotidectomized animals. In contrast, plasma obtained from parotidectomized, CAA-treated rats stimulated IDDP in intact recipient animals but not in parotidectomized ones. Moreover, plasma from adult rats treated with CAA after an electrolytic lesion of the hypothalamus, and infused back into young intact rats, was ineffective in stimulating IDDP. These results indicate that: (1) CAA requires the functional integrity of the parotid gland to express its IDDP-stimulating activity, (2) a hormonal factor is secreted by the parotids in response to CAA stimulation and is directly responsible for IDDP stimulation, (3) release of the endocrine parotid IDDP-stimulating factor after infusion of CAA involves a second endocrine factor that appears to originate from the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Acriflavine↗

Beta-adrenergic receptor binding in human and rat hypothalamus.

Quantitative autoradiographic analysis of beta-adrenergic binding sites was conducted in human postmortem hypothalamus using the radioligand 125I-pindolol. The focus was on the hypothalamic nuclei most clearly involved in corticotropin-releasing hormone (CRH) release, the PVN and SON. For comparison, the distribution of hypothalamic beta-adrenergic receptors was evaluated in the rat. A high level of beta-adrenergic receptor binding was found in the human paraventricular nucleus (PVN) and supraoptic nucleus (SON), but not in the rat. The majority of the beta-adrenergic receptors found in the human hypothalamus were of the beta 2-subtype. In contrast, in the rat hypothalamus, the majority of receptors were of the beta 1-subtype. These results show that the anatomical loci exist for direct beta-adrenergic influence on hypothalamic neuroendocrine function in the human and that the topography of beta-adrenergic receptors is markedly different in the rat and human hypothalamus.

Adult↗

Histochemical and pharmacological analysis of catecholaminergic projections to the perifornical hypothalamus in relation to feeding inhibition.

Three techniques, namely, midbrain lesions, fluorescence histochemistry and brain cannulation, were used in combination to analyze catecholamine (CA) projections to the perifornical hypothalamus and their function in suppressing feeding behavior. The convergence of evidence indicates that the ventral adrenergic component of the central tegmental tract and dopaminergic projections from midbrain A8 and possibly A9 cell groups contain the crucial fibers which innervate the perifornical hypothalamus and mediate CA suppression of feeding behavior. The primary evidence for this conclusion is that ventral tegmental electrolytic or 6-OHDA lesions which damaged specifically these fibers invariably caused: (1) a marked reduction of CA varicosities in the perifornical area; (2) a strong reduction or loss of the anorectic response produced by perifornical injection of the presynaptically acting drugs amphetamine and mazindol; and (3) a potentiation of the anorectic response produced by perifornical injection of the CA receptor agonists dopamine and epinephrine. Lesions in the dorsal midbrain tegmentum, which left intact the ventral adrenergic and dopaminergic fibers but damaged the compact dorsal tegmental bundle, the dorsal fibers of the central tegmental tract and the medial and lateral tegmental CA radiations, had no apparent effect on the responsiveness of the perifornical hypothalamus to CA drug stimulation, as well as on the CA fluorescence in that region. Lesions in the area of the dopaminergic A10 cells and the midline tegmental CA radiations actually potentiated the effectiveness of the anorexigenic drugs in the perifornical hypothalamus.

Adrenergic Fibers↗

beta-Endorphin alters dopamine uptake by the dopamine neurons of the hypothalamus and striatum.

Opioid peptides have well-documented modulatory effects on the synaptic transmission of several neurotransmitters. In both hypothalamus and striatum there is dense innervation by the beta-endorphin and/or enkephalin neuronal systems, and physiologically relevant neuroregulatory interactions of these neurons occur with other important neurotransmitter neuronal systems, such as the dopaminergic tuberoinfundibular and nigroneostriatal systems. Previous reports have examined the effects of opioid peptides on release, synthesis and degradation of dopamine in these brain regions. In this report, we describe the effects of the intracerebral administration of beta-endorphin to increase dopamine (re)uptake by dopaminergic nerve terminals of the hypothalamus and striatum. The specific, high affinity uptake of [3H]dopamine by dopaminergic nerve terminals was studied in a synaptosomal preparation by pharmacological exclusion, using desmethylimipramine, of dopamine uptake into other monoaminergic nerve terminals. The augmentation of in vitro dopamine uptake in both hypothalamus and striatum following intracisternal administration of beta-endorphin is specifically mediated by opiate receptors, since it could be prevented by pretreatment with an opiate receptor antagonist, naltrexone. In hypothalamus, the increased dopamine uptake represents a primary effect of beta-endorphin on hypothalamic dopamine neurons and is not secondary to the opioid peptide-induced stimulation of prolactin secretion, since identical effects of beta-endorphin administration are seen in hypophysectomized and intact animals. The effect of beta-endorphin to increase hypothalamic dopamine uptake was not reflected by a change in the affinity constant for dopamine, but involved an increase in maximal initial velocity of uptake. Naltrexone blocked the effect of beta-endorphin to increase the Vmax for [3H]dopamine uptake by hypothalamic dopamine neurons in both intact and hypophysectomized rats. In vitro exposure of hypothalamic and striatal dopaminergic nerve terminals to a wide range of concentrations of beta-endorphin failed to reproduce the in vivo results; some concentrations of beta-endorphin produced small decreases in [3H]dopamine uptake which were not reversed by naloxone. The data of this study provide evidence for a further mechanism by which beta-endorphin may alter dopaminergic neurotransmission, namely by increasing dopamine reuptake into dopaminergic nerve endings.

Absorption↗

Discriminant analysis of the localization of aggression-inducing electrode placements in the hypothalamus of male rats.

Over 400 sites in the hypothalami of 270 male CPB/WE-zob rats were electrically stimulated in order to induce fights between males. The localization of electrodes inducing fights seems to differ from the localization of electrodes in which no fights can be induced. The differences in localization were detected and tested by a non-parametric discriminant analysis. The results were plotted by computer in a stereotaxic atlas of the hypothalamus of the CPB/WE strain. The method delimits areas within the hypothalamus where the probability to induce aggression is high, intermediate or low. Moreover, the procedure allows discrimination between areas where the thresholds for attack behaviour are generally lower than elsewhere and where the fiercest forms of attack are induced. None of the areas delimited coincide with a classical subdivision of the hypothalamus. Parts of the perifornical, anterior, lateral and ventromedial hypothalamus seem to be involved. The methods developed here may help to relate stimulation-induced aggression to other characteristics of the 'aggressive' area which cannot be obtained directly from fighting rats such as cytological, endocrinological, biochemical or physiological data. In addition, the procedure may help to settle disputes on the specificity of the localization of neural substrates of other stimulation-induced behaviours. The methods to discriminate between overlapping 3-dimensional reconstructions validated here for aggressive responses, can also be applied to other types of stereotaxic data and other types of effects, such as electrical, hormonal or other physiological responses. They may be especially useful if the localization of the neural population involved is not yet known, and unknown current-spread or diffusion of substances complicates the interpretation of stereotaxic data.

Aggression↗

Regional distribution of gastrin-releasing peptide- and somatostatin-like immunoreactivity in the rabbit hypothalamus.

Regional distribution of gastrin-releasing peptide- (GRP) and somatostatin (SRIF)-like immunoreactivity in the discrete nuclei of the hypothalamus was examined in the rabbit according to Palkovits' microdissection method. GRP-like immunoreactivity (LI) was detected abundantly in the hypothalamus as compared with the cerebral cortex when measured by radioimmunoassay using the antiserum recognizing the C-terminal portion of synthetic porcine GRP. On gel-filtration chromatography of the hypothalamic extracts, two major peaks of GRP-LI were eluted; the peak with larger molecular size corresponded to synthetic porcine GRP1-27 and the smaller size to porcine GRP14-27. A concentration of GRP-LI was highest in the infundibular nuclei (IFN) as well as the ventromedial nuclei (VMN), and next high in the paraventricular nuclei (PVN), suprachiasmatic nuclei (SCN) and periventricular nuclei (PEV). The content of GRP-LI in the median eminence was not so much when compared with them. On the other hand, SRIF was localized in the highest concentration in the ME, followed by the VMN and IFN, as well as the PEV. The findings indicate that porcine GRP-LI exists in the hypothalamus of rabbits with characteristic regional distribution. Concurrent localization of GRP-LI and SRIF in some parts of the hypothalamus may suggest the interaction of both peptides in these areas under various physiological and pathological status.

Animals↗

Hypothalamus, frontal cortex and lymphocyte beta 2-adrenergic receptors in acute and chronic starvation in rat.

Hypothalamus and frontal cortex beta-adrenergic receptors, as measured by [125I]cyanopindolol binding, were investigated in male rats both after 4 days of acute starvation and after 2 weeks of semistarvation with dietary manipulation. Moreover, to test whether lymphocyte beta 2-adrenergic receptors can be used as a marker for brain beta-receptors, the parallel measurement of beta-adrenoceptors of lymphocyte, hypothalamus and frontal cortex was carried out in acutely starved rats. T3 and corticosterone in rat serum were also determined in this study. Our experiments showed that beta-adrenergic receptors in hypothalamus and frontal cortex, as well as those in lymphocytes remain unaltered in rats starved acutely for 4 days when compared with controls, despite reduced T3 and increased corticosterone levels. Chronic semistarvation on either a protein-rich or a carbohydrate-rich diet also resulted in decreased T3, increased corticosterone and no alterations of beta-adrenergic receptors in hypothalamus and frontal cortex.

Acute Disease↗

Immunohistochemical distribution of somatostatin in the infant hypothalamus.

Somatostatin (SS)-containing neurons were mapped in the normal infant hypothalamus with immunohistochemistry, using the peroxidase anti-peroxidase technique. Neurons displaying SS immunoreactivity show a widespread distribution throughout the hypothalamic region. Principal SS-immunoreactive like (SS-IL) perikarya are located in the paraventricular, infundibular and posterior nuclei and in the preoptic region. High SS innervation is also found in the ventromedial and in the lateral mammillary nuclei, and in the median eminence. In general this distribution of SS-IL agrees well with that reported for rat. Compared to the immunohistochemical distribution of SS in human adult hypothalamus, this mapping in the infant hypothalamus is grossly similar. However some differences may be underlined: the presence of a moderately dense group of SS-IL perikarya in the tuberal and posterior nuclei, and a dense innervation of the ventromedial nucleus and in the median eminence. This first detailed distribution of SS immunoreactivity in infant hypothalamus can provide basic knowledge for further studies of infant neuropathology.

Humans↗

The effects of serotonergic and dopaminergic lesions on sodium-sensitive [3H]mazindol binding in rat hypothalamus and corpus striatum.

The effects of intracerebroventricular administration of 6-hydroxydopamine (6-OHDA) and 5,7-dihydroxytryptamine (5,7-DHT) on sodium-sensitive [3H]mazindol binding were investigated in the rat hypothalamus and corpus striatum. In the hypothalamus, specific [3H]mazindol binding was inhibited by low concentrations of sodium and stimulated by high-sodium concentrations, whereas in the corpus striatum, only a sodium-dependent stimulation of [3H]mazindol binding was observed. Lesions with 6-OHDA significantly reduced sodium-dependent [3H]mazindol binding in the corpus striatum, but had no effect on the binding of [3H]mazindol in the absence of sodium. Lesions of serotonergic neurons with 5,7-DHT, however, had no effect on [3H]mazindol binding in the striatum, but resulted in a significant increase in the number of [3H]mazindol binding sites in the hypothalamus. These data suggest that [3H]mazindol may bind to two anatomically distinct binding sites, one that is stimulated and the other inhibited by sodium. The sodium-stimulated binding sites appear to be located on dopaminergic terminals in the striatum, and in the hypothalamus, the sodium-inhibited sites appear to be regulated by serotonergic neuronal activity.

5,7-Dihydroxytryptamine↗

Distribution of mu, delta, and kappa opioid receptors in the hypothalamus of the rat.

The radioautographic distribution of mu, delta and kappa opioid binding sites was examined by in vitro radioautography in the rat hypothalamus using the highly selective ligands [125I]-FK 33-824, [125I]azidoDTLET and [125I]DPDYN, respectively. Levels of mu opioid binding sites varied considerably amongst hypothalamic nuclei. mu Opioid labeling was dense in the medial preoptic area, medial preoptic nucleus, suprachiasmatic nucleus and ventromedial nucleus, whilst the supraoptic nucleus, paraventricular nucleus, arcuate nucleus and dorsomedial nucleus were devoid of labeling. Delta opioid labeling was sparse throughout most of the hypothalamus; however, moderate binding densities were detected in the suprachiasmatic and ventromedial nucleus. kappa Opioid labeling was also scant throughout the hypothalamus with the exception of the suprachiasmatic nucleus which was very densely labeled. Our results indicate that the 3 opioid receptors types are differentially distributed within the hypothalamus, although a significant overlap exists. In general, the distribution of hypothalamic opioid receptors correlates well with that of opioid-containing terminal fibers and may represent the anatomical substrate for opioid involvement in the hypothalamic regulation of autonomic, behavioral and neuroendocrine functions.

Animals↗

Release of histamine in rat hypothalamus and corpus striatum in vivo.

Histamine has remained a putative neurotransmitter for many years, partially because some of the criteria necessary to define it as a central nervous system neurotransmitter have not been established. The demonstration of in vitro release and the quantification of turnover as an indirect measure of release have been complicated by the histological evidence for multiple histamine pools in the central nervous system. In brain, there are multiple cell types which probably contain histamine. These cells include mast cells, neurolipomastocytoid cells, microvascular endothelial cells, and a histaminergic neuronal system which has been visualized using immunocytochemical methods. Using in situ brain microdialysis and a sensitive and specific radioenzymatic assay for histamine, we have identified histamine in the extracellular space of the rat hypothalamus and corpus striatum in vivo. Following neuronal selective stimuli, significant increases in extracellular histamine levels only were observed in the posterior hypothalamus, where dense histaminergic neuronal terminals have been described. However, after manipulations targeted towards histamine-containing mast cells, such increases were seen in both the posterior hypothalamus and corpus striatum. In summary, this study demonstrates that endogenous histamine can be released from the posterior hypothalamus by stimuli targeted towards histamine neurons and that histamine may also be released by non-neuronal mast cell elements.

Animals↗

Neurons in the sacral parasympathetic nucleus that project to the hypothalamus do not also project through the pelvic nerve--a double labeling study combining Fluoro-gold and cholera toxin B in the rat.

We recently reported that neurons in the sacral parasympathetic nucleus (SPN) project directly to the hypothalamus. In the present study, we examined the possibility that individual neurons in SPN send both an axon into the pelvic nerve and an ascending projection to the hypothalamus. We used a new double-labeling technique in which two sensitive retrograde tracers (Fluoro-gold and cholera toxin subunit B immunocytochemically stained with rhodamine-labeled antibodies) were combined. The effectiveness of this combination for singly and doubly labeling neurons was established in experiments in which both tracers were injected into overlapping areas of the tongue or ventrobasal thalamus. These injections doubly labeled large numbers of neurons in the hypoglossal or dorsal column nuclei, respectively. In studies of the projections of neurons in the SPN, injection of one tracer into the hypothalamus and the other into the pelvic nerve and/or pelvic ganglion singly labeled many neurons (more than 3300 in the 7 examined cases). However, no SPN neurons were doubly labeled. These findings indicate that the SPN in the rat consists of at least two distinct groups of cells, parasympathetic preganglionic neurons and neurons that project to the hypothalamus.

Animals↗

Localization of the substance P-induced cardiovascular responses in the rat hypothalamus.

Intracerebroventricular injection of substance P (SP) has been reported to induce a typical cardiovascular defense response characterized by an increase in blood pressure, heart rate, sympathetic efferent activity, hindlimb vasodilatation and mesenteric vasoconstriction. In this study we employed microinjections of SP to localize the hypothalamic areas in which SP elicits the activation of the cardiovascular system. SP (550 pmol) injected into the anterior hypothalamus (AH) produced, after a short latency, a marked increase in mean arterial pressure and heart rate. In the ventromedial hypothalamus, the magnitude of the cardiovascular response to SP was identical to that in the AH, but the response was delayed. SP injected into the posterior hypothalamus failed to induce any cardiovascular response. These results suggest that the anterior and ventromedial parts of the hypothalamus are responsible for eliciting the central cardiovascular effects of SP in conscious rats.

Animals↗

Proteolytic degradation of rat growth hormone-releasing factor(1-29) amide in rat pituitary and hypothalamus.

The identification of peptide bonds vulnerable to tissue peptidases is a valuable approach to design peptide agonists which exhibit a longer duration of action than the native molecules. Therefore, the kinetic of disappearance of rat growth hormone-releasing factor (rGRF(1-29)NH2) and the identification of its metabolites were studied in rat pituitary and hypothalamus. Synthetic rGRF(1-29)NH2 (10 microM) was incubated (0-120 min, 37 degrees C) in the presence of a pituitary (237 +/- 51 micrograms protein/ml) or hypothalamus homogenate (576 +/- 27 micrograms protein/ml). Using analytical high pressure liquid chromatography (HPLC), apparent half-lives of 22 +/- 3 min and 25 +/- 4 min were found in pituitary and hypothalamus, respectively. In both tissues, three degradation products, all less hydrophobic than the native peptide, were detected and isolated by preparative HPLC. The identification of the purified metabolites was ascertained by amino acid analysis, sequencing and chromatography with synthetic homologs. These results indicate that the main sites of cleavage in the pituitary and hypothalamus are Lys21-Leu22 (trypsin-like cleavage site), Leu14-Gly15 and Tyr10-Arg11 (chymotrypsin-like cleavage sites). TLCK and leupeptin did not affect the formation of fragment (1-21)OH while TPCK blocked the cleavage of Leu14-Gly15. The low affinity of fragment (1-21)NH2 for pituitary GRF binding sites suggests that hydrolysis of the Lys21-Leu22 bond inactivates rGRF(1-29)NH2 in this target tissue.

Amino Acid Sequence↗

Behavioural responses of bicucculline methiodide injections into the ventral hypothalamus of freely moving, socially interacting rats.

Several studies, using electrical stimulation of parts of the hypothalamus, have shown, that different parts of the hypothalamus yield different behavioural responses upon stimulation. In order to differentiate between stimulation of neuronal cell bodies and passing fibres and to investigate the role of GABA in hypothalamically elicited behaviour, 25 local injections with bicucculline methiodide, a GABA antagonist, (35 ng/0.2 microliter) were performed in the ventral parts of the hypothalamus of 16 freely moving rats in a social environment. A cannula system was used that allowed injection without interruption of the ongoing social interactions. Digging, gnawing, drinking and attack behaviour were elicited in different animals. By plotting the behavioural responses of the animals into a detailed hypothalamic atlas, we assessed the hypothalamic distribution of the elicited behavioural responses. A number of injections elicited a combination of two or three different responses, probably due to diffusion of the substance, thus disinhibiting more than one behavioural system. Our results are in general agreement with previous electrical stimulation data and show that, in an overlapping pattern, different populations of neurons are involved in the elicitation of digging, gnawing, drinking and attack behaviour. In the hypothalamus, a tonic GABAergic inhibition of neurons involved in the display of these types of behaviour appears to exist.

Aggression↗