Differential effects of septal, preoptic, and habenula ablations on thirst-motivated behaviors in rats.

Two experiments used a total of 59 male Sprague-Dawley rats. Bilateral septal lesions dramatically enhanced barpressing rates generated under progressive ratio schedules of reinforcement. This increased barpressing was dependent on deprivation level but independent of the type of deprivation (i.e., food or water). Equivalent effects on barpressing were observed in Ss with bilateral medial forebrain bundle lesions at the level of the lateral preoptic area. Septal lesions, medial forebrain bundle lesions, and habenula lesions did not result in a hyperreactivity to bitter quinine solutions. Hyperreactivity to quinine was observed only in Ss with medial preoptic lesions. This medial preoptic lesion also impaired operant responding for water on a progressive ratio schedule of reinforcement. It is suggested that the medial preoptic lesion produced a deficit in thirst-motivated behavior. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Limbic lesions and the energizing, aversive, and inhibitory effects of non-reward in rats.

Tested 30 male albino Wistar rats with bilateral lesions in the amygdala, septum, hippocampus, stria terminalis, and fornix on a multiple reinforcement schedule in which barpressing in one component was associated with VI reinforcement (S+) and the other with extinction (S–). Responses on a 2nd lever turned off S– for 5-sec periods during the extinction component. All groups, with the exception of Ss with amygdaloid lesions exhibited behavioral contrast. Ss with hippocampal or fornical lesions showed greater resistance to extinction. Response rates on the lever that turned off S– were higher after stria terminalis and septal lesions, whereas lower rates were obtained from Ss with amygdaloid lesions. It is concluded that amygdaloid lesions attenuate the energizing and aversive effects of nonreward, septal and stria terminalis lesions increase the aversive effects, and hippocampal and fornical lesions interfere with the inhibitory effects of nonreward. (French summary) (28 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Food-deprivation-induced behavioral arousal: Mediation by hypothalamus and amygdala.

Conducted 5 experiments, using a total of 238 male albino Sprague-Dawley rats. Electrolytic lesions of the basomedial hypothalamus eliminated food-deprivation-induced stabilimeter activity in Ss that were prevented from becoming obese. Knife cuts lateral to the basomedial area (separating the medial and lateral hypothalamus) potentiated this activity, as did transections posterior to the basomedial region. Anterior transections (between anterior and medial hypothalamus), however, eliminated the effect. Lesions of the stria terminalis and amygdala likewise abolished deprivation-induced locomotor activity, but elevated ad lib activity to a level comparable with that after deprivation in intact Ss. Ss with combined basomedial-stria terminalis lesions behaved like Ss with basomedial lesions. Results suggest that food-deprivation-induced locomotor activity in stabilimeter cages was due to a disinhibition of the basomedial hypothalamus by the amygdala via the stria terminalis. (79 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Localization of the septal rage syndrome in Long-Evans rats.

Used lesion methods to study the anatomical localization of the septal rage syndrome in 38 male hooded Long-Evans rats. Previous studies have attributed this syndrome to incidental damage of structures peripheral to the septal nuclei, to the stria terminalis, and to the central core of the septal structures. Lesions were systematically varied so as to destroy different parts of the septum. Analyses show that the dorsal nuclei and structures of the anterior septal area mediate mechanisms pertaining to septal rage. Lesions of the posterior septal area resulted in rage scores that were similar to those of control Ss. (16 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Septal influences on operant responding in the rat.

In 3 experiments with a total of 74 male albino Sprague-Dawley rats, the afferent and efferent connections of the septum with the hippocampus (fornix) or with the hypothalamus and lower brain stem (medial forebrain bundle) were transected by means of an encephalotome near the point where these pathways enter or leave the septal area. A transection of the fornix that produced minimal direct damage to cellular components of the septum or hippocampus reproduced the effects of large septal lesions on responding in several temporally defined paradigms that involve periods of response suppression (DRL, discriminated Sidman avoidance, FI). Transection of the medial forebrain bundle fibers that interconnect the septum with the hypothalamus and lower brain stem did not affect behavior in any of these paradigms. It is suggested that these observations be viewed in the context of the results of earlier investigations by the authors (see record 1974-27002-001), R. J. Carey (see record 1969-13784-001), and J. M. McDougall et al (see record 1969-13791-001), which showed that transection of the medial forebrain bundle reproduces several other components of the septal lesion syndrome. (28 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Lateral septal lesions enhance conditioned bradycardia in the rabbit.

52 New Zealand albino rabbits received sham lesions or complete, medial, lateral, or posterior septal lesions and were subjected to differential conditioning in which tones of different frequencies served as CSs, and paraorbital electric shock was the UCS. EMG, heart rate (HR), blood pressure (BP) CRs, and hippocampal rhythmic slow wave activity (RSA) were recorded. Lateral or complete septal lesions enhanced the bradycardiac HR CR but had no effect on the BP depressor response. Both unconditioned and conditioned EMG responses occurred infrequently and were unaffected by any lesion. Unconditioned HR responses and somatomotor threshold determinations to unsignaled electric shock were also unaffected by the lesions. Complete septal lesions increased locomotor activity relative to sham or other septal lesions. Little hippocampal RSA was detected in Ss with medial lesions, but the HR CR was unimpaired in these Ss. Data implicate the septo-hippocampal circuit in classical conditioning of cardiovascular changes and further suggest that diencephalic forebrain structures may modulate forebrain processing of sensory stimulation, perhaps in terms of assessing its biological significance. (41 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Motivational and neuroanatomical specificity of hypodipsia for aversive solutions produced by medial preoptic injury to the rat.

In an experiment with a total of 28 Sprague-Dawley rats, bilateral medial preoptic lesions dramatically lowered the rejection threshold for quinine-adulterated water but not for food in 24-hr forced-choice tests. The detection threshold for quinine in a 2-bottle choice test, however, was unaffected by the medial preoptic lesion. Bilateral septal and lateral preoptic lesions had no effect on any quinine adulteration tests. The enhanced rejection of quinine-adulterated water in a forced-choice test by medial-preoptic-damaged Ss was also observed after 24 hrs of water deprivation. The plasma osmolality of medial preoptic Ss was significantly elevated above controls after 24 hrs of water deprivation. Findings suggest that a medial preoptic lesion produces a deficit in thirst-motivated behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Increased ipsilateral expression of Fos following lateral hypothalamic self-stimulation

Immunohistochemical labeling of Fos protein was used to visualize neurons activated by rewarding stimulation of the lateral hypothalamic level of the medial forebrain bundle (MFB). Following training and stabilization of performance, seven rats were allowed to self-stimulate for 1 h prior to anesthesia and perfusion. Brains were then processed for immunohistochemistry. Two control subjects were trained and tested in an identical manner except that the stimulator was disconnected during the final 1 h test. Among the structures showing a greater density of labeled neurons on the stimulated side of the brains of the experimental subjects were the septum, lateral preoptic area (LPO), medial preoptic area, bed nucleus of the stria terminalis, substantia innominata (SI), and the lateral hypothalamus (LH). Several of these structures, the LPO, SI, and LH, have been implicated in MFB self-stimulation by the results of psychophysical, electrophysiological, and lesion studies.     

Self-stimulation in 7- and 10-day-old rats.

It has been shown that the infant rat exhibits learned behaviors characteristic of the adult. With a modified self-stimulation paradigm, the present study explored whether 7- and 10-day-old Long-Evans rat pups could learn a discriminated operant to obtain direct electrical stimulation in neural sites that support self-stimulation in adults. By nudging 1 of 2 response manipulanda, at 2 ages (7 and 10 days) and temperatures (22 and 35°C), Ss self-stimulated with electrodes implanted in a variety of forebrain sites, including the prefrontal cortex, bed nucleus of the stria terminalis, medial nucleus of the amygdala, and the medial forebrain bundle. The only temperature-sensitive site might be the nucleus accumbens, which was positive only at the higher temperature in 10-day-olds. Results indicate that several forebrain sites demonstrate rewarding properties of stimulation in the preweanling rat pup. (40 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Running-wheel avoidance behavior following septal area lesions in rats.

Studied acquisition of a running-wheel avoidance response in 52 male Wistar rats with (a) septal lesions, (b) septal and postcommissural fornix lesions, or (c) septal, postcommissural fornix, and anterior thalamic damage. Ss with lesions confined to the septum were deficient in acquiring the avoidance response compared with both normal Ss and Ss with the more posterior lesions. Ss sustaining combined septal-fornical and septal-fornical-thalamic lesions did not differ from normal Ss or from each other in their acquisition scores. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Thalamocortical relations in taste aversion learning: II. Involvement of the medial ventrobasal thalamic complex in taste aversion learning.

Examined the involvement of the gustatory thalamic nuclei in fundamental taste reactivity, gastrointestinal reactivity, and conditioned taste aversion (CTA) learning. In Exp I, using 72 male Long-Evans rats, bilateral electrolytic lesions were produced in the medial ventrobasal thalamic complex (VBm), including the thalamic gustatory nuclei, in 1 group of Ss. For a 2nd group, at the conclusion of conditioning, lesions were produced in the anterior insular gustatory neocortex (AIGN). Results indicate that destruction of VBm thalamus attenuated taste reactivity to sucrose, citric acid, and quinine hydrochloride. Elimination of VBm thalamus markedly attenuated CTA learning. Results of neocortical lesion manipulations showed that the AIGN contributed to initial CTA learning in Ss lacking a mediodorsal-periventricular thalamus. Whether Ss lacking VBm thalamus used olfactory cues associated with drinking solutions to acquire CTAs was evaluated in Exp II, using 72 male Long-Evans rats. Results demonstrate that Ss lacking VBm thalamus and the olfactory bulbs could not acquire aversions to ingested LiCl following 8 conditioning trials. (54 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Hyperreactivity, muricide, and intraspecific aggression in the rat produced by infusion of local anesthetic into the lateral septum or surroundng areas.

Intracranial infusions of a local anesthetic (lidocaine, 2%) were made bilaterally (4 μl over 20 min) through permanently implanted cannulas ending in the lateral septum or adjacent areas in 167 male hooded rats. Increases in irritability and reactivity to the experimenter, muricide, and intermale aggression were produced by injections into the lateral septum and the region ventral to it. The increase in reactivity and interanimal aggression occurred in varying degrees and were independent of one another, but intermale aggression occurred only in Ss showing muricide. The most effective site for eliciting the entire spectrum of aggressive behaviors was the region ventral to the anterior septum. The region ventral to the posterior septum tended to produce a high incidence of muricide with only modest increases in reactivity. No changes in behavior were noted with infusions into the medial septum or the medial forebrain bundle/lateral preoptic area ventrolateral to the septum. It is suggested that the hyperreactivity and irritability may be related to hyperdefensiveness and that muricide and intermale aggression are points on a continuum of interanimal aggressiveness. (39 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of septal and amygdaloid lesions on social behavior of the cat.

Tested 3 male and 43 female cats for social behavior and activity in an open field. Ss were then subjected to either septal or amygdaloid lesions and retested. Ss with septal lesions exhibited dramatic increases in social awareness as measured by the percentage of time they watched the Ss with which they were paired. Ss with amygdaloid lesions were twice as active postoperatively as they had been preoperatively. Both the enhanced social behavior of Ss with septal lesions and the enhanced activity with amygdalectomized Ss were independent of the locus of the lesion in the Ss with which they were paired. Results are discussed in terms of an alteration in disposition as opposed to an alteration of the response system after lesions of the septal region in the forebrain. (24 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste agnosia following gustatory neocortex ablation: Dissociation from odor and generality across taste qualities.

In Exp I, 18 male Long-Evans hooded rats trained to avoid drinking in the presence of a compound odor (benzyl acetate) and taste (sucrose) CS lost the taste habit but retained the odor habit following gustatory neocortex (GN) ablation. Conversely, olfactory bulb ablation resulted in loss of the odor habit but retention of the taste habit. In Exp II, with 60 Ss, Ss lacking GN did not retain preoperatively instated learned aversions to a suprathreshold quinine hydrochloride (bitter) taste solution that had been employed as a CS. However, Ss with GN lesions that were virtually identical to those of the bitter-trained group retained a preoperatively learned aversion to a hydrochloric acid (sour) CS. Exp III, with 60 Ss, demonstrated that reliable agnosia for an acid CS could be produced by lesions that extended more deeply into perirhinal areas near the claustrum at the level of the GN. It is concluded that the agnosia following GN ablation is relatively specific to gustation and that agnosia for preoperatively acquired tasted aversion habits occurs for all 4 basic gustatory stimuli following anterolateral cortex ablations centered on the GN. (49 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Suppression of VMH-lesion-induced reactivity and aggressiveness in the rat by stimulation of lateral septum, but not medial septum or cingulate cortex.

32 male hooded rats made vicious with bilateral ventromedial hypothalamic lesions had bipolar electrodes implanted unilaterally in the lateral septum, medial septum, or cingulate cortex. Four days later, the Ss' reactivity and aggressiveness were evaluated 5 min before, during, and 5 min after stimulation at 20 muA (60 Hz, sine wave). Lateral septal stimulation suppressed reactivity and aggressiveness by almost 80% compared with pre- and poststimulation levels. Stimulation of neither the cingulate cortex nor the medial septum produced a change reliably different from that seen in unstimulated control Ss. Further tests with stimulation of the lateral septum at the 20 muA level showed that neither rewarding self-stimulation nor disruption of ongoing water drinking was produced. These results are congruent with evidence from lesion studies that the lateral septum normally acts to suppress reactivity and aggressiveness in the rat; they do not support previous suggestions that the medial septum is involved in the modulation of these behaviors. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of lesions in the medial forebrain bundle on three measures of pain sensitivity and noise-elicited startle.

Subjected 137 male Holtzman albino rats to bilateral lesions of the medial forebrain bundle (MFB) or to surgical control procedures. Lesions produced equivalent decreases in paw-lick latency to heat and in jump and high-magnitude-response thresholds to footshock. Flinch and detection thresholds to footshock were also significantly decreased, though the lesion did not alter the magnitude or habituation of noise-elicited startle. Injection of 75 mg/kg serotonin into lesioned Ss returned the high-magnitude-response threshold to normal values but did not affect detection threshold. It is concluded that the increased sensitivity to painful stimuli resulted from the decrease in telencephalic content of serotonin following MFB lesions. Previous exposure of lesioned Ss to footshock resulted in a potentiation of the startle response to noise, further suggesting that the lesion had increased the aversiveness of footshock. (27 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lesions of the gustatory neocortex on taste aversion learning in the rat.

In 5 experiments, 110 normal male Long-Evans hooded rats and 125 Ss with lesions of the gustatory neocortex (GN) were compared for their ability to learn aversions to taste cues paired with toxicosis. When the taste presentation was followed immediately by toxicosis, normal Ss and 8 Ss with lesions of the posterior (visual) neocortex learned aversions to sucrose, sodium chloride, quinine hydrochloride, and hydrochloric acid solutions. Ss with GN lesions learned aversions to all solutions except sucrose. In preference tests, all solutions were shown to be discriminable from water by both normal and GN-lesioned Ss. Under conditions in which a 6-hr delay separated taste presentation and toxicosis, normals again learned specific aversions to all 4 solutions, but Ss with GN lesions failed to learn specific aversions to sucrose, sodium chloride, and hydrochloric acid solutions. It was shown that the ability of Ss with GN lesions to learn aversions to sucrose and quinine depended on stimulus concentration. It is proposed that the data can be accounted for by postulating a change in the threshold for taste illness associations following GN lesions. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Organization of inputs to the dorsomedial nucleus of the hypothalamus: a reexamination with Fluorogold and PHAL in the rat

Possible inputs to the DMH were studied first using the fluorescent retrograde tracer Fluorogold, and identified cell groups were then injected with the anterograde tracer PHAL to examine the distribution of labeled axons in and around the DMH. From this work, we conclude that the majority of inputs to the DMH arise in the hypothalamus, although there are a few significant projections from the telencephalon and brainstem. With few exceptions, each major nucleus and area of the hypothalamus provides inputs to the DMH. Telencephalic inputs arise mainly in the ventral subiculum, infralimbic area of the prefrontal cortex, lateral septal nucleus, and bed nuclei of the stria terminalis. The majority of brainstem inputs arise in the periaqueductal gray, parabrachial nucleus, and ventrolateral medulla. In addition, it now seems clear that inputs to the DMH use only a few discrete pathways. Descending inputs course through a periventricular pathway through the hypothalamic periventricular zone, a medial pathway that follows the medial corticohypothalamic tract, and a lateral pathway traveling through medial parts of the medial forebrain bundle. Ascending inputs arrive through a midbrain periventricular pathway that travels adjacent to the cerebral aqueduct in the periaqueductal gray, and through a brainstem lateral pathway that travels through central and ventral midbrain tegmental fields and enters the hypothalamus, and then the DMH from more lateral parts of the medial forebrain bundle. The results are discussed in relation to evidence for involvement of the DMH in ingestive behavior, and diurnal and stress-induced corticosterone secretion.     

Medial forebrain bundle lesions: Specific loss of feeding to decreased glucose utilization in rats.

Found that bilateral destruction of the medial forebrain bundle in female Sherman rats eliminated feeding to decreased intracellular glucose utilization (glucoprivation). The deficit was specific. Feeding was enhanced by dietary dilution and reduced by dietary concentration. More was eaten in the cold and less in the heat. The Ss were not differentially sensitive to quinine adulteration. They returned to normal body weight following regimens of gavage or of restricted feeding. Moreover, they did not differ from normal Ss in drinking to various thirst stimuli. It is suggested that the glucoprivic mechanism makes but a minor contribution to the initiation of spontaneous feeding. (39 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Recognition and management of childhood cardiac arrhythmias

Axonal connections between the amygdala and the hypothalamic paraventricular nucleus were examined by combined anterograde-retrograde tract tracing. Iontophoretic injections of the retrograde tracer Fluorogold were placed in the paraventricular nucleus, and the anterograde tracer PHA-L in the ipsilateral central or medial amygdaloid nuclei. Single and double-label immunohistochemistry were used to detect tracers. Single label anterograde and retrograde tracing suggest limited evidence for direct connections between the central or medial amygdala and the paraventricular nucleus. In general, scattered PHA-L-positive terminals were seen in autonomic subdivisions of the paraventricular nucleus (lateral parvocellular, dorsal parvocellular and ventral medial parvocellular subnuclei) following central or medial amygdaloid nucleus injection. Double-label studies indicate that central and medial amygdaloid nucleus efferents contact paraventricular nucleus-projecting cells in several forebrain nuclei. In the case of central nucleus injections, PHA-L positive fibers occasionally contacted Fluorogold-labeled neurons in the anteromedial, ventromedial and preoptic subnuclei of the bed nucleus of the stria terminalis. Overall, such contacts were quite rare, and did not occur in the bed nucleus of the stria terminalis regions showing greatest innervation by the central amygdaloid nucleus. In contrast, medial amygdala injections resulted in a significantly greater overlap of PHA-L labeling and Fluorogold-labeled neurons, with axosomatic appositions observed in medial divisions of the bed nucleus of the stria terminalis, anterior hypothalamic area and preoptic area. The results provide anatomical evidence that a substantial proportion of amygdaloid connections with hypophysiotrophic paraventricular nucleus neurons are likely multisynaptic, relaying in different subregions of the bed nucleus of the stria terminalis and hypothalamus.