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H M Edinger

Publications and source records attributed to H M Edinger.

16 recordsLinked to original sources
PubMed1988

Carbamazepine regulates feline aggression elicited from the midbrain periaqueductal gray.

Carbamazepine has been utilized both as an anticonvulsant and as a psychotropic drug for the treatment of complex partial seizures and various mood and other emotional disorders such as the episodic dyscontrol syndrome. In the present study, we sought to identify the role of carbamazepine in the regulation of two forms of aggressive behavior--affective defense and quiet biting attack behavior--elicited by electrical stimulation of the midbrain periaqueductal gray matter of the cat in the absence of convulsive activity. The experimental paradigm involved establishment of stable baseline thresholds for affective defense and quiet biting attack responses. Following establishment of a stable baseline, carbamazepine (2.5, 5, or 10 mg/kg) and propylene glycol (vehicle control) were administered peripherally (IP). The response thresholds were tested 5-30, 30-60, 60-90, 120-150, 1440-1470, and 2160-2190 minutes following drug administration. It was observed that carbamazepine administration at 5 and 10 mg/kg dose levels preferentially suppressed affective defense behavior but had no effect upon quiet biting attack, indicating that the selective effects of carbamazepine upon affective attack are not due to any possible sedative effects upon motor responses. The effects of carbamazepine upon affective defense were dose dependent and of long duration when administered at the highest dose level (10 mg/kg).

Aggression↗
PubMed1985

The organization of the hypothalamic pathways mediating affective defense behavior in the cat.

The purpose of this study was to describe the hypothalamic pathways which mediate affective defense in the cat utilizing the methods of [14C]2-deoxyglucose (2-DG) and [3H]leucine radioautography in concert with the technique of electrical brain stimulation. The feline affective defense response, characterized by pupillary dilatation, piloerection, ear retraction, hissing, growling and striking with the forepaws, was elicited consistently by stimulation of sites within the ventromedial hypothalamus and anterior aspect of the medial hypothalamus. In one series of experiments, 2-DG autoradiography was employed to describe the brain regions activated following stimulation of sites in the region of the ventromedial hypothalamus from which affective defense had been elicited. Ventromedial hypothalamic stimulation produced activation primarily in forebrain regions situated rostral to the level of the stimulating electrode. These structures included principally the anteromedial hypothalamus and medial preoptic area, as well as the bed nuclei of the stria terminalis and anterior commissure, diagonal band and lateral septal area. The caudal extent of activation included only the dorsal and perifornical hypothalamus at the level of the stimulation site. In a second series of experiments, affective defense sites in the anteromedial hypothalamus were stimulated and the regional distribution of 2-DG label was identified. In contrast to the results obtained from ventromedial hypothalamic stimulation, these experiments revealed a marked descending distribution of label within the posterior hypothalamus, midbrain central gray and ventral tegmental area. Results obtained from studies in which tritiated amino acids were injected into affective defense sites in both the ventromedial nucleus and anteromedial hypothalamus confirmed the general findings observed with 2-DG autoradiography. From these observations, we have concluded that the organization of the pathway mediating affective defense behavior from the ventromedial hypothalamus to the midbrain involves an initial synapse within the region of the anteromedial hypothalamus and a second synapse in the midbrain central gray substance. The significance of the anteromedial hypothalamus for the expression of affective defense behavior was considered in the Discussion.

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↗
PubMed1983

An analysis of the mechanisms underlying hippocampal control of hypothalamically-elicited aggression in the cat.

An experiment was performed to determine the role of the hippocampal formation in the regulation of quiet biting attach behavior elicited from electrical stimulation of the hypothalamus. The results showed clearly that stimulation of the dorsal hippocampus resulted in an increased latency to quiet biting attack and that ventral hippocampal stimulation resulted in a decreased latency to quiet biting attack. In addition, the results indicate that those sites in the ventral hippocampal formation from which facilitation of attack can be produced are linked to sensory mechanisms associated with trigeminal reflexes established during hypothalamic stimulation inasmuch as stimulation of these sites increase the lateral extent of the effective sensory field of the lipline. No effect was observed upon a motor component of the jaw-opening response--the latency to jaw-opening-during ventral hippocampal stimulation. In contrast, no effects were observed upon either sensory or motor components of the hypothalamically-elicited jaw-opening response as a result of stimulation of dorsal hippocampal sites. Deoxyglucose autoradiography revealed that the major effect of stimulation of modulatory sites in both the dorsal and ventral hippocampal formation was exerted upon the lateral septal nucleus. Thus, it is proposed that hippocampal modulation of hypothalamically-elicited quiet biting attack is mediated primarily through the lateral septal nucleus.

Aggression↗
PubMed1983

The effects of stimulation of substantia innominata and sensory receiving areas of the forebrain upon the activity of neurons within the amygdala of the anesthetized cat.

The present study investigated the response characteristics of individual neurons in the amygdala following stimulation of the substantia innominata (SI), and compared these responses with those elicited by stimulation of insular and temporal polar cortices and the lateral olfactory tract (LOT). Recordings were made from single units within the medial, central, basal, and lateral amygdaloid nuclei of anesthetized, male cats. Stimulating electrodes were located in the SI, LOT, and sylvian cortex (SG). Unit responses were classified as either excitation or inhibition. Excitatory responses were further divided into fixed latency excitation (FLE) and variable latency excitation (VLE) based on the variability of the onset latency of the response. The majority of responses to SI stimulation were of the FLE type, implying a direct orthodromic, monosynaptic activation of amygdaloid units. Proportionally more FLE responses were recorded laterally, especially in the magnocellular basal nucleus, compared to VLE responses which were more common in the medial and central nuclei. SI stimulation consistently affected the activity of many more units than did SG or LOT stimulation. The onset latencies of the population of cells exhibiting excitatory responses elicited by SI stimulation were distributed bimodally, and this may reflect a dual projection pathway of amygdaloid afferents from this basal forebrain region. This correlates with anatomical descriptions indicating that SI projections to amygdala pass via the ventral amygdalofugal pathway as well as in the stria terminalis. Excitatory onset latencies of responses to SI stimulation were the shortest in the lateral and magnocellular basal nuclei and the longest in the parvocellular basal nucleus. Amygdaloid units exhibited convergent input from the stimulus sites. A clear topographical distribution of units was not demonstrated. The data suggests that units receiving a convergent input were rarely driven monosynaptically by more than one stimulus site. The basal nucleus contained the smallest fraction of units exhibiting a convergent input. A small population of antidromic responses was recorded and indicates that within the system studied the caudal aspect of the basal nucleus is a major source of amygdaloid efferents. Antidromically driven units did not exhibit transynaptic responses following stimulation of any of the test sites.

Afferent Pathways↗
PubMed1983

Role of the limbic system in hypothalamically elicited attack behavior.

The present review summarizes our research findings concerning the role of the limbic system in hypothalamically-elicited aggression in the cat. Utilizing a dual-stimulation procedure, our results indicate that much of the limbic system suppresses quiet biting attack behavior. The most potent inhibitory effects were obtained from the basomedial amygdala and the prefrontal cortex. Other structures displaying suppression of attack following electrical stimulation include the dorsal hippocampus, pyriform cortex, lateral septal nucleus, lateral aspect of substantia innominata, and anterior cingulate gyrus. Sites producing facilitation of attack include the ventral hippocampus, far lateral aspect of the lateral septal nucleus, medial aspect of the substantia innominata, and lateral amygdaloid nucleus. Anatomical studies suggest that the medial forebrain bundle and stria terminalis are utilized by limbic structures to provide direct modulation of the hypothalamus while the substantia innominata, mediodorsal thalamic nucleus and bed nucleus of the stria terminalis contain important interneurons in the control of quiet biting attack. Further studies indicate that the amygdala, ventral hippocampus, and substantia innominata may control aggressive behavior by modulating the trigeminal sensory components of the attack response.

Aggression↗
PubMed1981

Temporary desynchronization among circadian rhythms with lateral fornix ablation.

Lateral or medial fornix suction ablations were performed on adult male rats in order to selectively ablate or leave intact, respectively, fibers which terminate in the region of the suprachiasmatic nucleus and hypophysiotropic area of the hypothalamus. Plasma adrenal corticosteroid secretion, locomotor activity, body temperature, and food and water intake were recorded at 4 h intervals over a period of 48 h in individual animals 7-10 days postoperatively. Lateral fornix ablation specifically disrupted adrenal corticosteroid periodicity. A least-squares spectrum analysis of the data indicated that corticosteroid may be under ultradian control after this lesion. All animals, regardless of treatment, exhibited normal circadian locomotor activity patterns. Aberrations in feeding, drinking and body temperature rhythms were occasionally observed. This represents a temporary dissociation between the rhythmic expression of corticosteroid secretion and activity, temperature, feeding and drinking. The evidence presented lends support to the multi-oscillator theory of circadian organization, and suggests that the anteroventral subiculum, via the medial corticohypothalamic tract, is important in the regulation of some, but not all, circadian parameters. In addition to the observations on the rhythmicity of locomotor activity, the extent to which the animals are active is also significantly different between groups; ie., the hyperactivity of fornix-transected animals previously reported by others was found to be associated with lateral and not medial fornix ablation.

Animals↗
PubMed1980

Effects of stimulation of the substantia innominata upon attack behavior elicited from the hypothalamus in the cat.

Experiments were undertaken in order to determine the role of the substantia innominata and surrounding regions in quiet biting attack elicited from electrical stimulation of the hypothalamus in the cat. Stimulation from sites in the lateral aspect of the substantia innominata resulted in a suppression of quiet biting attack and in a constriction of the 'effective trigeminal sensory fields' established during hypothalamic attack site stimulation. Stimulation from sites situated more medially in the substantia innominata resulted in a facilitation of quiet biting attack and in an expansion of the 'effective trigeminal sensory fields'. The motor component of the jaw opening response was altered in only 50% of the cases in contrast to the consistent effects observed upon the 'effective sensory fields'. Electrical stimulation of the substantia innominata had little effect upon affective display elicited from the ventromedial hypothalamus. Stimulation from sites located in the nucleus accumbens had no effect upon hypothalamically-elicited quiet biting attack and inhibited the occurrence of affective display in 2 to 5 animals tested. These studied suggest that the substantia innominata differentially modulates quiet biting attack and accomplishes this, at least in part, through its effects upon sensory mechanisms associated with the jaw opening reflex.

Affect↗
PubMed1980

Differential fornix ablations and the circadian rhythmicity of adrenal corticosteroid secretion.

Suction ablations of the medial or lateral fornix were performed in order to transect selectively the medial corticohypothalamic tract (mcht) which originates in the anteroventral subiculum and travels in the lateral fornix terminating in the basal hypothalamus. The circadian rhythmicity of plasma adrenal corticosteroid levels was assessed in individual animals 1--2 weeks postoperatively. Ablation of the lateral fornix disrupted the periodicity of corticosteroid secretion which is normally synchronized with the light--dark cycle, whereas medial fornix ablation or neocortical ablation caused no such disruption. Group mean levels of plasma adrenal corticoids were higher in the lateral fornix-ablated animals than in the medial fornix-ablated, neocortically ablated, or intact control animals. These findings suggest that the anteroventral subiculum is important in the regulation of adrenal corticosteroid rhythmicity, and that it exerts an inhibitory influence upon corticosteroid release.

Adrenal Cortex Hormones↗
PubMed1975

Effect of stimulation of prefrontal cortex and amygdala on diencephalic neurons.

Extracellular unit recordings were obtained from the nucleus medialis dorsalis (MD) and adjacent thalamic nuclei and from the hypothalamus of anesthetized cats. Electrical stimulation of the prefrontal cortex produces suppression of unit activity and rebound excitation in MD. In addition antidromic and short latency excitation was found which was followed by prolonged suppression of firing. This suppression was also followed by a strong postinihibitory activation of unit firing which was, in some cases, again followed by a second phase of inhibition. Amygdala stimulation produced similar results except that antidromic responses were found only in the intralaminar nuclei, and short-latency transynaptic excitation occurred somewhat later. The results are in consonance with the hypothesis that the same interneuronal mechanism is engaged by both afferent sources to MD. In the hypothalamus, fewer units responded to cortical and amygdalar stimulation and alternating sequences of excitation-inhibition-excitation were not found.

Amygdala↗