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Imaging the neural circuitry and chemical control of aggressive motivation.

Ferris CF, Stolberg T, Kulkarni P, Murugavel M, Blanchard R, Blanchard DC, Febo M, Brevard M, Simon NG - BMC Neurosci (2008)

Bottom Line: As expected, brain areas previously identified as critical in the organization and expression of aggressive behavior were activated, e.g., lateral hypothalamus, medial basal amygdala.Unexpected was the intense activation of the forebrain cortex and anterior thalamic nuclei.However, the effect of SRX251, but not fluoxetine, was specific to aggression as brain activation in response to a novel sexually receptive female was unaffected.

View Article: PubMed Central - HTML - PubMed

Affiliation: Center for Translational NeuroImaging, Northeastern University, Boston, Massachusetts, USA. c.ferris@neu.edu

ABSTRACT

Background: With the advent of functional magnetic resonance imaging (fMRI) in awake animals it is possible to resolve patterns of neuronal activity across the entire brain with high spatial and temporal resolution. Synchronized changes in neuronal activity across multiple brain areas can be viewed as functional neuroanatomical circuits coordinating the thoughts, memories and emotions for particular behaviors. To this end, fMRI in conscious rats combined with 3D computational analysis was used to identifying the putative distributed neural circuit involved in aggressive motivation and how this circuit is affected by drugs that block aggressive behavior.

Results: To trigger aggressive motivation, male rats were presented with their female cage mate plus a novel male intruder in the bore of the magnet during image acquisition. As expected, brain areas previously identified as critical in the organization and expression of aggressive behavior were activated, e.g., lateral hypothalamus, medial basal amygdala. Unexpected was the intense activation of the forebrain cortex and anterior thalamic nuclei. Oral administration of a selective vasopressin V1a receptor antagonist SRX251 or the selective serotonin reuptake inhibitor fluoxetine, drugs that block aggressive behavior, both caused a general suppression of the distributed neural circuit involved in aggressive motivation. However, the effect of SRX251, but not fluoxetine, was specific to aggression as brain activation in response to a novel sexually receptive female was unaffected.

Conclusion: The putative neural circuit of aggressive motivation identified with fMRI includes neural substrates contributing to emotional expression (i.e. cortical and medial amygdala, BNST, lateral hypothalamus), emotional experience (i.e. hippocampus, forebrain cortex, anterior cingulate, retrosplenial cortex) and the anterior thalamic nuclei that bridge the motor and cognitive components of aggressive responding. Drugs that block vasopressin neurotransmission or enhance serotonin activity suppress activity in this putative neural circuit of aggressive motivation, particularly the anterior thalamic nuclei.

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Anterior thalamic nuclei. Shown is a composite of figures depicting the anatomical details (top) of the dorsal midline thalamus at the level of the anterior thalamus, an autoradiograph (middle) of V1a binding density in the anterior thalamic nuclei (adapted from [100]) and BOLD activation (bottom) in the same thalamic area for aggressive motivation and seizure genesis (adapted from [67]).
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Figure 9: Anterior thalamic nuclei. Shown is a composite of figures depicting the anatomical details (top) of the dorsal midline thalamus at the level of the anterior thalamus, an autoradiograph (middle) of V1a binding density in the anterior thalamic nuclei (adapted from [100]) and BOLD activation (bottom) in the same thalamic area for aggressive motivation and seizure genesis (adapted from [67]).

Mentions: The contribution of the thalamus to aggressive motivation has received little if any attention in the animal and human literature. The robust BOLD signal change in the dorsal thalamus during aggressive motivation (Fig 3D mate/intruder condition) highlights the potential importance of this area as a key trigger region in behavioral activation (see Fig 9). This area of the dorsal thalamus comprises multiple midline nuclei, e.g., paraventricular, central medial, paratenial, medial dorsal, paracentral and medial habenula bordered by the anterior thalamic nuclei, e.g. anteroventral, anteromedial and anterodorsal. When compared to mate alone, only the anterior thalamic nuclei exhibited a robust increase in BOLD signal (Fig 3D &4C, D) and volume of activation (Table 1) in response to mate/intruder. Treatment with SRX251 or fluoxetine dramatically attenuated the increase in BOLD signal change in the anterior thalamic nuclei in response to aggressive or sexual stimuli (Fig 6). The BOLD signal change did not exceed the 2% baseline threshold over most of the imaging period in the presence of SRX251 and only marginally so for fluoxetine with aggressive motivation but not receptive female.


Imaging the neural circuitry and chemical control of aggressive motivation.

Ferris CF, Stolberg T, Kulkarni P, Murugavel M, Blanchard R, Blanchard DC, Febo M, Brevard M, Simon NG - BMC Neurosci (2008)

Anterior thalamic nuclei. Shown is a composite of figures depicting the anatomical details (top) of the dorsal midline thalamus at the level of the anterior thalamus, an autoradiograph (middle) of V1a binding density in the anterior thalamic nuclei (adapted from [100]) and BOLD activation (bottom) in the same thalamic area for aggressive motivation and seizure genesis (adapted from [67]).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2601047&req=5

Figure 9: Anterior thalamic nuclei. Shown is a composite of figures depicting the anatomical details (top) of the dorsal midline thalamus at the level of the anterior thalamus, an autoradiograph (middle) of V1a binding density in the anterior thalamic nuclei (adapted from [100]) and BOLD activation (bottom) in the same thalamic area for aggressive motivation and seizure genesis (adapted from [67]).
Mentions: The contribution of the thalamus to aggressive motivation has received little if any attention in the animal and human literature. The robust BOLD signal change in the dorsal thalamus during aggressive motivation (Fig 3D mate/intruder condition) highlights the potential importance of this area as a key trigger region in behavioral activation (see Fig 9). This area of the dorsal thalamus comprises multiple midline nuclei, e.g., paraventricular, central medial, paratenial, medial dorsal, paracentral and medial habenula bordered by the anterior thalamic nuclei, e.g. anteroventral, anteromedial and anterodorsal. When compared to mate alone, only the anterior thalamic nuclei exhibited a robust increase in BOLD signal (Fig 3D &4C, D) and volume of activation (Table 1) in response to mate/intruder. Treatment with SRX251 or fluoxetine dramatically attenuated the increase in BOLD signal change in the anterior thalamic nuclei in response to aggressive or sexual stimuli (Fig 6). The BOLD signal change did not exceed the 2% baseline threshold over most of the imaging period in the presence of SRX251 and only marginally so for fluoxetine with aggressive motivation but not receptive female.

Bottom Line: As expected, brain areas previously identified as critical in the organization and expression of aggressive behavior were activated, e.g., lateral hypothalamus, medial basal amygdala.Unexpected was the intense activation of the forebrain cortex and anterior thalamic nuclei.However, the effect of SRX251, but not fluoxetine, was specific to aggression as brain activation in response to a novel sexually receptive female was unaffected.

View Article: PubMed Central - HTML - PubMed

Affiliation: Center for Translational NeuroImaging, Northeastern University, Boston, Massachusetts, USA. c.ferris@neu.edu

ABSTRACT

Background: With the advent of functional magnetic resonance imaging (fMRI) in awake animals it is possible to resolve patterns of neuronal activity across the entire brain with high spatial and temporal resolution. Synchronized changes in neuronal activity across multiple brain areas can be viewed as functional neuroanatomical circuits coordinating the thoughts, memories and emotions for particular behaviors. To this end, fMRI in conscious rats combined with 3D computational analysis was used to identifying the putative distributed neural circuit involved in aggressive motivation and how this circuit is affected by drugs that block aggressive behavior.

Results: To trigger aggressive motivation, male rats were presented with their female cage mate plus a novel male intruder in the bore of the magnet during image acquisition. As expected, brain areas previously identified as critical in the organization and expression of aggressive behavior were activated, e.g., lateral hypothalamus, medial basal amygdala. Unexpected was the intense activation of the forebrain cortex and anterior thalamic nuclei. Oral administration of a selective vasopressin V1a receptor antagonist SRX251 or the selective serotonin reuptake inhibitor fluoxetine, drugs that block aggressive behavior, both caused a general suppression of the distributed neural circuit involved in aggressive motivation. However, the effect of SRX251, but not fluoxetine, was specific to aggression as brain activation in response to a novel sexually receptive female was unaffected.

Conclusion: The putative neural circuit of aggressive motivation identified with fMRI includes neural substrates contributing to emotional expression (i.e. cortical and medial amygdala, BNST, lateral hypothalamus), emotional experience (i.e. hippocampus, forebrain cortex, anterior cingulate, retrosplenial cortex) and the anterior thalamic nuclei that bridge the motor and cognitive components of aggressive responding. Drugs that block vasopressin neurotransmission or enhance serotonin activity suppress activity in this putative neural circuit of aggressive motivation, particularly the anterior thalamic nuclei.

Show MeSH
Related in: MedlinePlus