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Time course and mechanisms of hippoc...
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Burman, Michael Aaron.
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Time course and mechanisms of hippocampus involvement in trace and delay fear-potentiated startle.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Time course and mechanisms of hippocampus involvement in trace and delay fear-potentiated startle./
作者:
Burman, Michael Aaron.
面頁冊數:
147 p.
附註:
Adviser: Jonathan Gewirtz.
Contained By:
Dissertation Abstracts International67-07B.
標題:
Psychology, Experimental. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3225718
ISBN:
9780542793455
Time course and mechanisms of hippocampus involvement in trace and delay fear-potentiated startle.
Burman, Michael Aaron.
Time course and mechanisms of hippocampus involvement in trace and delay fear-potentiated startle.
- 147 p.
Adviser: Jonathan Gewirtz.
Thesis (Ph.D.)--University of Minnesota, 2006.
Intrusive traumatic memories are a major feature of several human anxiety disorders. While all fearful memories depend critically on the amygdala, the declarative aspect of these traumatic memories depends upon the hippocampus. The hippocampus is also required for a subset of fear conditioning tasks in rodents. One of the hallmarks of hippocampus function in memory is that the hippocampus is required for memory retrieval for only a limited time. Older memories are not impaired by hippocampus damage. However, the neural mechanisms underlying the different stages of memory processing are only beginning to be elucidated. The current experiments developed procedures aimed at further delineating the processes involved in hippocampus-dependent traumatic memory formation and storage by examining fear-potentiated startle following trace and delay fear conditioning. Hippocampus-dependent trace fear conditioning differs from hippocampus-independent delay fear conditioning only by the separation of the conditioned stimulus from the unconditioned stimulus in time. Furthermore, measuring the acoustic startle response allows for an examination of the temporal specificity of the conditioned response. By making lesions varying in their extent along the septo-temporal axis of the hippocampus, the current studies demonstrate that pre-training lesions of the septal hippocampus are sufficient to disrupt acquisition of trace conditioning. However, larger lesions are required to disrupt trace conditioning when made after training. This suggests different neural substrates are required for retrieval than were required for acquisition and identifies the splenial region of the hippocampus as critical for long-term memory storage. In addition, lesions including the temporal pole of the hippocampus disrupt fear conditioning generally. Pharmacological experiments further demonstrated that septal hippocampus inactivation only disrupts memory when made immediately after training. Pre-training inactivation and inactivation 2 hours following training do not impair memory. Finally, while septal hippocampal activity is required for this process, common mechanisms of synaptic plasticity are not. Thus, the septal hippocampus appears to be required only for the earliest phase of the consolidation of trace fear conditioning in other parts of the brain.
ISBN: 9780542793455Subjects--Topical Terms:
517106
Psychology, Experimental.
Time course and mechanisms of hippocampus involvement in trace and delay fear-potentiated startle.
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Intrusive traumatic memories are a major feature of several human anxiety disorders. While all fearful memories depend critically on the amygdala, the declarative aspect of these traumatic memories depends upon the hippocampus. The hippocampus is also required for a subset of fear conditioning tasks in rodents. One of the hallmarks of hippocampus function in memory is that the hippocampus is required for memory retrieval for only a limited time. Older memories are not impaired by hippocampus damage. However, the neural mechanisms underlying the different stages of memory processing are only beginning to be elucidated. The current experiments developed procedures aimed at further delineating the processes involved in hippocampus-dependent traumatic memory formation and storage by examining fear-potentiated startle following trace and delay fear conditioning. Hippocampus-dependent trace fear conditioning differs from hippocampus-independent delay fear conditioning only by the separation of the conditioned stimulus from the unconditioned stimulus in time. Furthermore, measuring the acoustic startle response allows for an examination of the temporal specificity of the conditioned response. By making lesions varying in their extent along the septo-temporal axis of the hippocampus, the current studies demonstrate that pre-training lesions of the septal hippocampus are sufficient to disrupt acquisition of trace conditioning. However, larger lesions are required to disrupt trace conditioning when made after training. This suggests different neural substrates are required for retrieval than were required for acquisition and identifies the splenial region of the hippocampus as critical for long-term memory storage. In addition, lesions including the temporal pole of the hippocampus disrupt fear conditioning generally. Pharmacological experiments further demonstrated that septal hippocampus inactivation only disrupts memory when made immediately after training. Pre-training inactivation and inactivation 2 hours following training do not impair memory. Finally, while septal hippocampal activity is required for this process, common mechanisms of synaptic plasticity are not. Thus, the septal hippocampus appears to be required only for the earliest phase of the consolidation of trace fear conditioning in other parts of the brain.
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