Forebrain and Rage Reactions

Spiegel, E. A.; Miller, H.; Oppenheimer, M. J.

doi:10.1152/jn.1940.3.6.538

Cited by 148 publications

(28 citation statements)

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“…A few early specific lesion studies in the 1920s to 1940s similarly found ‘chronic rage’ in cats and dogs after localized lesions in rostral regions of the basal forebrain (which it is tempting to speculate might also have damaged the VP) (Fulton & Ingraham, ; Spiegel et al ., ). By the 1960s, the rough outline of a specific site for disgust induction began to emerge in the results obtained with large electrolytic lesions of the ventral forebrain region containing the LH and GP (which also probably damaged the VP) (Morgane, ; Teitelbaum & Epstein, ).…”

Section: Discussionmentioning

confidence: 97%

Excessive disgust caused by brain lesions or temporary inactivations: mapping hotspots of the nucleus accumbens and ventral pallidum

Berridge

2014

Eur J of Neuroscience

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Disgust is a prototypical type of negative affect. In animal models of excessive disgust, only a few brain sites are known in which localized dysfunction (lesions or neural inactivations) can induce intense ‘disgust reactions’ (e.g., gapes) to a normally pleasant sensation such as sweetness. Here we aimed to map forebrain candidates more precisely to identify where either local neuronal damage (excitotoxin lesions) or local pharmacological inactivation (muscimol-baclofen microinjections) caused rats to emit excessive sensory disgust reactions to sucrose. Our study compared subregions of nucleus accumbens shell, ventral pallidum, lateral hypothalamus and adjacent extended amygdala. Results indicated the posterior half of ventral pallidum to be the only forebrain site where intense sensory disgust gapes to sucrose were induced by both lesions and temporary inactivations (this site was previously identified as a hedonic hotspot for enhancements of sweetness ‘liking’). By comparison, for the nucleus accumbens, temporary GABA inactivations in the caudal half of the medial shell also generated sensory disgust but lesions never did at any site. Further, even inactivations failed to induce disgust in the rostral half of accumbens shell (which also contains a hedonic hotspot). In other structures, neither lesions nor inactivations induced disgust as long as the posterior ventral pallidum remained spared. We conclude that the posterior ventral pallidum is an especially crucial hotspot for producing excessive sensory disgust by local pharmacological/lesion dysfunction. By comparison, the nucleus accumbens appears to segregate sites for pharmacological disgust induction and hedonic enhancement into separate posterior versus rostral halves of medial shell.

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Section: Discussionmentioning

confidence: 97%

Excessive disgust caused by brain lesions or temporary inactivations: mapping hotspots of the nucleus accumbens and ventral pallidum

Berridge

2014

Eur J of Neuroscience

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“…Spiegel (13) reported that lesioning of the olfactory tubercles induced rage reaction in the cat. It is therefore postulated that the afferent fibers in the olfactory tubercles originat ing from the olfactory bulbs and anterior olfactory nuclei degenerate after ablation of these structures, which in turn alters the activity of the olfactory tubercles connected with the septum and hypothalamus, and results in the development of aggressiveness.…”

Section: Resultsmentioning

confidence: 99%

Hyperemotionality Induced by Lesions in the Olfactory System of the Rat

1974

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Abstract-In order to clarify the neural mechanisms underlying the hyperemotion ality induced by bilateral olfactory bulb ablations in rats, changes in emotional be havior were measured after various parts of the secondary olfactory structures had been lesioned and olfactory bulb ablations had been carried out. When the anterior olfactory nuclei, lateral olfactory tracts and prepiriform cortices were bilaterally lesioned simultaneously with olfactory bulb ablations, many rats died from lack of food in take, while on the contrary, the rats with bilateral lesions in the olfactory tubercle, anterior olfactory nuclei and olfactory bulb developed marked hyperemotionality immediately after the lesioning. Hyperemotionality of the latter rats included not only hyperreactivity similar to that observed in the septal rat but also a muricide of 90% in incidence, which is similar to rats with olfactory bulb ablations.From these results, it can be concluded that changes in the activity of the olfactory tubercle were the most important for the development of hyperemotionality following bilateral ablations of the olfactory bulb in the rat.Since Watson (1) reported that bilateral olfactory bulb ablations caused hyperirrit ability in the rat, a number of investigators (2-6) have studied this hyperemotionality, including mouse-killing behavior (muricide) and a comparison has been made with that induced by lesioning in the other brain structures.The present authors (7) have also compared the emotional behavior of the rat with bilateral olfactory bulb ablations (O.B. rat) with that of the rat with septal lesions (septal rat), and clarified that hyperemotionality of the O.B. rat was characterized by gradual development after olfactory bulb removal and offensive aggression in nature, whereas that of the septal rat developed immediately after septal lesioning and was defensive in nature. However, the neural mechanisms underlying such aggressiveness of the O.B.rat are still unknown.The neuroanatomical studies on the neuronal connection in the olfactory system of the rat have revealed that the afferent fibers originating from the olfactory bulbs connected with the secondary olfactory structures such as the anterior olfactory nuclei , olfactory tubercles, amygdaloid complex and prepiriform cortices (8-11) .The authors (7) speculated that hyperemotionality of the O .B. rat could be related to changes in activities of these secondary olfactory structures following removal of the olfactory bulbs, especially due to degeneration of the primary olfactory afferent fibers .The present investigation was therefore undertaken to clarify changes in emotional be

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“…The lateral septum (LS) is a brain region highly implicated in aggression (Spiegel et al, 1940;Brady and Nauta, 1953;Albert and Chew, 1980). LS lesions in mammals lead to dramatic displays of aggression, first coined as "septal rage," and characterized by increased biting, attacks, and defensive behaviors (Spiegel et al, 1940;Nauta, 1953, 1955). Similar behavioral alterations result from injection of local anesthetics into the LS (Albert and Richmond, 1976;Albert and Wong, 1978).…”

Section: Introductionmentioning

confidence: 99%

TMEM16B Calcium-Activated Chloride Channels Regulate Action Potential Firing in Lateral Septum and Aggression in Male Mice

et al. 2019

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The lateral septum (LS) plays an important role in regulating aggression. It is well recognized that LS lesions lead to a dramatic increase in aggressive behaviors. A better understanding of LS neurophysiology and its functional output is therefore important to assess LS involvement in regulating aggression. The LS is a heterogeneous structure that maintains inputs and outputs with multiple brain regions, and is also divided into subregions that innervate one another. Thus, it is challenging to identify the exact cell type and projections for characterization. In this study, we determined the expression pattern of the calcium-activated chloride channel, TMEM16B, in the LS of both male and female mice. We then investigated the physiological contribution of the calcium-activated chloride channel to LS neuronal signaling. By performing whole-cell patch-clamp recording, we showed that TMEM16B alters neurotransmitter release at the hippocampal-LS synapse, and regulates spike frequency and spike frequency adaptation in subpopulations of LS neurons. We further demonstrated that loss of TMEM16B function promotes lengthened displays of aggressive behaviors by male mice during the resident intruder paradigm. In conclusion, our findings suggest that TMEM16B function contributes to neuronal excitability in subpopulations of LS neurons and the regulation of aggression in male mice.

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Forebrain and Rage Reactions

Cited by 148 publications

References 0 publications

Excessive disgust caused by brain lesions or temporary inactivations: mapping hotspots of the nucleus accumbens and ventral pallidum

Excessive disgust caused by brain lesions or temporary inactivations: mapping hotspots of the nucleus accumbens and ventral pallidum

Hyperemotionality Induced by Lesions in the Olfactory System of the Rat

TMEM16B Calcium-Activated Chloride Channels Regulate Action Potential Firing in Lateral Septum and Aggression in Male Mice

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