Role of the Septum in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

Lee, Young Lim; Davis, Michael T.

doi:10.1523/jneurosci.17-16-06424.1997

Cited by 48 publications

(20 citation statements)

References 42 publications

(45 reference statements)

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“…In a recent study, we showed that knife cuts of the fimbria/ fornix blocked CRH-enhanced startle, whereas lesions of the dorsal hippocampus did not (Lee and Davis, 1997). Given the fact that the fimbria /fornix is the major output pathway for the hippocampal formation, the failure to block CRH-enhanced startle by either dorsal hippocampal (Lee and Davis, 1997) or ventral hippocampal lesions (current study) is puzzling.…”

Section: Effects Of Chemical Lesions Of the Hippocampus Bnst And Ammentioning

confidence: 57%

“…Given the fact that the fimbria /fornix is the major output pathway for the hippocampal formation, the failure to block CRH-enhanced startle by either dorsal hippocampal (Lee and Davis, 1997) or ventral hippocampal lesions (current study) is puzzling. Interestingly, although NMDA lesions of the ventral hippocampus overall failed to block CRH-enhanced startle, f urther investigation of the data revealed that there was a clear dichotomy in lesion effects among ventral hippocampal-lesioned animals.…”

Section: Effects Of Chemical Lesions Of the Hippocampus Bnst And Ammentioning

confidence: 82%

“…The startle apparatus is been described in detail in the accompanying article (Lee and Davis, 1997). Briefly, five separate stabilimeters consisting of an 8 ϫ 15 ϫ 15 cm Plexiglas and wire mesh cage suspended between compression springs within a steel frame were used.…”

Section: Startle Apparatusmentioning

confidence: 99%

“…Therefore, the blockade of CRH-enhanced startle by transection of the fimbria/fornix suggests that the hippocampus might be critically involved in CRH-enhanced startle. Among its subdivisions, however, the dorsal hippocampus seems not to be involved, because electrolytic lesions of this area did not block CRH-enhanced startle (Lee and Davis, 1997). A possible involvement of the ventral hippocampus in CRH-enhanced startle has not been investigated.…”

mentioning

confidence: 98%

“…Thus far, however, the exact anatomical sites responsible for these behavioral and physiological actions of CRH after intracerebroventricular administration have not been identified. As part of an effort to delineate the neural circuitry underlying intracerebroventricular CRH effects, recently we investigated a possible involvement of the septum, using increased acoustic startle amplitude after CRH (CRH-enhanced startle) as a behavioral measure (Lee and Davis, 1997). Electrolytic lesions of the whole septum and the medial septum, but not the lateral septum, blocked CRH-enhanced startle.…”

mentioning

confidence: 99%

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Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

1997

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Previously, we demonstrated that transection of the fimbria/ fornix blocked the excitatory effect of corticotropin-releasing hormone (CRH) on startle (CRH-enhanced startle), suggesting that the hippocampus and its efferent target areas that communicate via the fimbria may be critically involved in CRHenhanced startle. The bed nucleus of the stria terminalis (BNST) receives direct projections from the ventral hippocampus via the fimbria/fornix. Therefore, the role of the ventral hippocampus, the BNST, and the amygdala in CRH-enhanced startle was investigated. NMDA lesions of the BNST completely blocked CRH-enhanced startle, whereas chemical lesions of the ventral hippocampus and the amygdala failed to block CRH-enhanced startle. However, the same amygdala-lesioned animals showed a complete blockade of fear-potentiated startle, a conditioned fear response sensitive to manipulations of the amygdala. In contrast, BNST-lesioned rats had normal fear-potentiated startle. This indicates a double dissociation between the BNST and the amygdala in two different paradigms that enhance startle amplitude. Microinfusions of CRH into the BNST, but not into the ventral hippocampus, mimicked intracerebroventricular CRH effects. Furthermore, infusion of a CRH antagonist into the BNST blocked CRH-enhanced startle in a dose-dependent manner. Control studies showed that this blockade did not result from either leakage of the antagonist into the ventricular system or a local anesthetic effect caused by infusion of the antagonist into the BNST. The present studies strongly suggest that CRH in the CSF can activate the BNST, which could lead to activation of brainstem and hypothalamic BNST target areas involved in anxiety and stress responses. Key words: bed nucleus of the stria terminalis (BNST ); amygdala; hippocampus; corticotropin-releasing hormone (CRH); startle; anxiety; fearIntracerebroventricular inf usion of corticotropin-releasing hormone (CRH) elicits a constellation of behavioral, physiological, and endocrinological changes similar to those produced by natural stressors (cf. Dunn and Berridge, 1990). Thus far, however, the exact anatomical sites responsible for these behavioral and physiological actions of CRH after intracerebroventricular administration have not been identified. As part of an effort to delineate the neural circuitry underlying intracerebroventricular CRH effects, recently we investigated a possible involvement of the septum, using increased acoustic startle amplitude after CRH (CRH-enhanced startle) as a behavioral measure (Lee and Davis, 1997). Electrolytic lesions of the whole septum and the medial septum, but not the lateral septum, blocked CRH-enhanced startle. However, fiber-sparing chemical lesions of the medial septum failed to block CRH-enhanced startle, suggesting that the blockade seen with electrolytic lesions was probably caused by damage to fibers of passage, presumably the fornix. Supporting this conclusion, f unctional lesions of the fornix induced by knife cuts of the fimbria /fornix complete...

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Section: Effects Of Chemical Lesions Of the Hippocampus Bnst And Ammentioning

confidence: 57%

Section: Effects Of Chemical Lesions Of the Hippocampus Bnst And Ammentioning

confidence: 82%

Section: Startle Apparatusmentioning

confidence: 99%

mentioning

confidence: 98%

mentioning

confidence: 99%

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Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

1997

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Hippocampus and contextual fear conditioning: Recent controversies and advances

2001

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Dorsal hippocampal (DH) lesions produce a severe deficit in recently, but not remotely, acquired contextual fear without impairing memory of discrete training stimuli, i.e., DH lesions produce an anterograde and time‐limited retrograde amnesia specific to contextual memory. These data are consistent with the standard model which posits temporary involvement of the hippocampus in recent memory maintenance. However, three recent controversies apparently weaken the case for a selective mnemonic role for the hippocampus in contextual fear. First, although retrograde amnesia (from posttraining lesions) is severe, anterograde amnesia (from pretraining lesions) may be mild or nonexistent. Second, a performance, rather than mnemonic, account of contextual freezing deficits in hippocampal‐lesioned animals has been offered. Third, damage to the entire hippocampus, including the ventral hippocampus, can produce a dramatic and temporally stable disruption of context and tone fear. These data are reviewed and explanations are offered as to why they do not necessarily challenge the standard model of hippocampal memory function in contextual fear. Finally, a more complete description of the hippocampus' proposed role in contextual fear is offered, along with new data supporting this view. In summary, the data support a specific mnemonic role for the DH in the acquisition and consolidation of contextual representations. Hippocampus 2001;11:8–17. © 2001 Wiley‐Liss, Inc.

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Hippocampus and contextual fear conditioning: Recent controversies and advances

2001

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ABSTRACT:Dorsal hippocampal (DH) lesions produce a severe deficit in recently, but not remotely, acquired contextual fear without impairing memory of discrete training stimuli, i.e., DH lesions produce an anterograde and time-limited retrograde amnesia specific to contextual memory. These data are consistent with the standard model which posits temporary involvement of the hippocampus in recent memory maintenance. However, three recent controversies apparently weaken the case for a selective mnemonic role for the hippocampus in contextual fear. First, although retrograde amnesia (from posttraining lesions) is severe, anterograde amnesia (from pretraining lesions) may be mild or nonexistent. Second, a performance, rather than mnemonic, account of contextual freezing deficits in hippocampal-lesioned animals has been offered. Third, damage to the entire hippocampus, including the ventral hippocampus, can produce a dramatic and temporally stable disruption of context and tone fear. These data are reviewed and explanations are offered as to why they do not necessarily challenge the standard model of hippocampal memory function in contextual fear. Finally, a more complete description of the hippocampus' proposed role in contextual fear is offered, along with new data supporting this view. In summary, the data support a specific mnemonic role for the DH in the acquisition and consolidation of contextual representations. Hippocampus 2001;11:8 -17.

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Role of the Septum in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

Cited by 48 publications

References 42 publications

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

Hippocampus and contextual fear conditioning: Recent controversies and advances

Hippocampus and contextual fear conditioning: Recent controversies and advances

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