The septal forebrain and the inhibitory modulation of attack and defense in the rat. A review

Albert, D.J.; Chew, Grace

doi:10.1016/s0163-1047(80)91247-9

Cited by 124 publications

(56 citation statements)

References 175 publications

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“…It has been reported consistently that lesions of the lateral septum induce a hyperdefensive and transient behavior known as septal rage (Brady and Nauta, 1953;Brady and Nauta, 1955;Albert and Chew, 1980). In the latter work, the location of the lesion appeared restricted to the LSr-vl.…”

Section: Implications For Understanding Lateral Septum Functionmentioning

confidence: 73%

“…Ascending connections from the medial septum to the hippocampus are proposed to provide 'pacemaker' control of hippocampal theta rhythm (Vertes and Kocsis, 1997;Hangya et al, 2009), which may underpin goal-oriented behavior (Vinogradova, 1995) and plastic changes occurring during the formation of cognitive maps (O'Keefe, 1993); whereas descending projections from the lateral septum target a wide variety of subcortical circuits related to visceral and metabolic functions, ranging from aggression, social and sexual behavior to circadian rhythms (Albert and Chew, 1980;Risold and Swanson, 1997a;Veenema and Neumann, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Distribution and targets of the relaxin‐3 innervation of the septal area in the rat

Olucha-Bordonau¹,

Otero-García²,

Sánchez-Pérez³

et al. 2012

J of Comparative Neurology

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Neural tracing studies have revealed that the rat medial and lateral septum are targeted by ascending projections from the nucleus incertus, a population of tegmental GABA neurons. These neurons express the relaxin‐family peptide, relaxin‐3, and pharmacological modulation of relaxin‐3 receptors in medial septum alters hippocampal theta rhythm and spatial memory. In an effort to better understand the basis of these interactions, we have characterized the distribution of relaxin‐3 fibers/terminals in relation to different septal neuron populations identified using established protein markers. Dense relaxin‐3 fiber plexuses were observed in regions of medial septum containing hippocampal‐projecting choline acetyltransferase (ChAT)‐, neuronal nitric oxide synthase (nNOS)‐, and parvalbumin (PV)‐positive neurons. In lateral septum (LS), relaxin‐3 fibers were concentrated in the ventrolateral nucleus of rostral LS and the ventral nucleus of caudal LS, with sparse labeling in the dorsolateral and medial nuclei of rostral LS, dorsal nucleus of caudal LS, and ventral portion nuclei. Relaxin‐3 fibers were also observed in the septofimbrial and triangular septal nuclei. In the medial septum, we observed relaxin‐3‐immunoreactive contacts with ChAT‐, PV‐, and glutamate decarboxylase‐67‐positive neurons that projected to hippocampus, and contacts between relaxin‐3 terminals and calbindin‐ and calretinin‐positive neurons. Relaxin‐3 colocalized with synaptophysin in nerve terminals in all septal areas, and ultrastructural analysis revealed these terminals were symmetrical and contacted spines, somata, dendritic shafts, and occasionally other axonal terminals. These data predict that this GABA/peptidergic projection modulates septohippocampal activity and hippocampal theta rhythm related to exploratory navigation, defensive and ingestive behaviors, and responses to neurogenic stressors. J. Comp. Neurol. 520:1903–1939, 2012. © 2011 Wiley Periodicals, Inc.

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Section: Implications For Understanding Lateral Septum Functionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Distribution and targets of the relaxin‐3 innervation of the septal area in the rat

Olucha-Bordonau¹,

Otero-García²,

Sánchez-Pérez³

et al. 2012

J of Comparative Neurology

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“…Because testosterone levels were measured in adulthood after mating and three aggression tests, it is difficult to determine the mechanism behind the reduction of testosterone levels. One possibility is that the ethanol-exposed animals experience more defeat during the aggression tests or during their lifetime (since they are housed in pairs) and this experience results in a lower testosterone level [3,15,34,35]. However, the ethanol-exposed animals were housed with an animal also treated with ethanol, making it unlikely that there are long-term differences across groups in social defeat.…”

Section: Discussionmentioning

confidence: 99%

“…in mice results in an increase in aggression [3][4][5][6]; ethanol exposure from gestation day (GD) 6 to 19 increases offensive aggression in rats [7]. Ethanol exposure during the last four days of pregnancy and from postnatal day (PD) 1 to PD 4 increases aggression, while ethanol exposure confined to the period from PD 1 to 4 did not affect aggressive behavior in mice [8].…”

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confidence: 99%

Ethanol exposure during development reduces resident aggression and testosterone in rats

Lugo

Marino

Gass

et al. 2006

Physiology & Behavior

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Ethanol exposure during development has been shown to alter social behaviors in people, but the range of deficits is not clear. Using an animal model of Fetal Alcohol Spectrum Disorders, intermale aggression and testosterone levels were examined in adult rats. Rats were exposed to ethanol during the entire prenatal period and from postnatal day 2 through 10. Ethanol was administered via intragastric intubation. Two other groups consisted of a nontreated control and an intubated control group that was exposed to the administration procedures but not ethanol. Both offensive and defensive aggression were examined in experimental residents and intruders under three different housing conditions for the resident males: (1) with another male, (2) with a pregnant female, and (3) with a female and litter fathered by the experimental animal. When housed with a female and litter, ethanol-exposed rats displayed reduced offensive aggression compared to control groups under the same condition. Defensive aggression in the non-experimental intruders was reduced in this same condition. There were no differences in duration of non-aggressive social behaviors among the groups in any of the housing conditions. Testosterone levels were reduced in ethanol-exposed rats compared to controls. In summary, ethanol exposure over the combined prenatal and postnatal periods reduces aggressive behavior in a condition where aggressive behavior is normally seen. This reduction may be related to lower testosterone levels. KeywordsFetal alcohol syndrome; Aggression; Resident-intruder paradigm; Social behavior; Prenatal alcohol Fetal Alcohol Spectrum Disorders (FASD) describes those individuals who manifest mild to severe disturbances of physical, behavioral, emotional, and/or social functioning due to in utero ethanol exposure. FASD individuals are found to commit high rate of crimes against others, engage in inappropriate sexual behavior, and are described as having a failure to consider the consequences of their actions [1,2]. Even though FASD individuals show high rates of crime, no direct measures of aggressive behaviors or testosterone in FAS individuals have been conducted. [3][4][5][6]; ethanol exposure from gestation day (GD) 6 to 19 increases offensive aggression in rats [7]. Ethanol exposure during the last four days of pregnancy and from postnatal day (PD) 1 to PD 4 increases aggression, while ethanol exposure confined to the period from PD 1 to 4 did not affect aggressive behavior in mice [8]. However, another study found that ethanol exposure from birth until PD 14 decreases aggression in mice [6]. These studies suggest that prenatal ethanol exposure may increase aggression, while postnatal ethanol exposure may decrease aggression. However, many of the early studies used ethanol administration procedures that were confounded by nutritional effects [4][5][6]8] or resulted in minimal transfer of ethanol to the pup [6]. The effect of ethanol exposure during the entire gestation period and during early postnatal development (i.e...

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“…Additionally, several forebrain structures that project to this region provide tonic inhibitory input to structure. Lesioning the prefrontal cortex, orbitofrontal cortices, or septal forebrain or severing the connections between the forebrain and the hypothalamus leads to the disinhibition of aggression behaviors (47)(48)(49)(50)(51).…”

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confidence: 99%

Applying gene regulatory network logic to the evolution of social behavior

Baran

McGrath

Streelman

2017

Proc. Natl. Acad. Sci. U.S.A.

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Animal behavior is ultimately the product of gene regulatory networks (GRNs) for brain development and neural networks for brain function. The GRN approach has advanced the fields of genomics and development, and we identify organizational similarities between networks of genes that build the brain and networks of neurons that encode brain function. In this perspective, we engage the analogy between developmental networks and neural networks, exploring the advantages of using GRN logic to study behavior. Applying the GRN approach to the brain and behavior provides a quantitative and manipulative framework for discovery. We illustrate features of this framework using the example of social behavior and the neural circuitry of aggression.gene regulatory networks | social behavior network | neural networks | evolution | development

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The septal forebrain and the inhibitory modulation of attack and defense in the rat. A review

Cited by 124 publications

References 175 publications

Distribution and targets of the relaxin‐3 innervation of the septal area in the rat

Distribution and targets of the relaxin‐3 innervation of the septal area in the rat

Ethanol exposure during development reduces resident aggression and testosterone in rats

Applying gene regulatory network logic to the evolution of social behavior

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