Role of the Bed Nucleus of the Stria Terminalis on Memory Formation Precesses: Interaction Between Norepinephrine and Glutamate

• Main Authors: Tzu-Lan Liu, 劉姿蘭
• Other Authors: Keng-Chen Liang
• Format: Others
• Language: zh-TW
• Published: 2004
• Online Access: http://ndltd.ncl.edu.tw/handle/14149566910029382942

碩士 === 國立臺灣大學 === 心理學研究所 === 92 === Extensive evidence implicates the amygdala in modulation of memory processes. Previous research indicated that the stria terminalis mediates the memory modulatory influences from the amygdala. The bed nucleus of the stria terminalis (BNST) is a projection target of the stria terminalis. Neuroanatomical and immunohistochemical studies demonstrated a variety of neurotransmitters and neuropeptides, including norepinephrine and glutamate, present in the perikarya or afferent terminals of the BNST. Some of the noradrenergic terminals in the BNST possess presynaptic NMDA receptors. Norephinephrine released in the BNST may be regulated by presynaptic NMDA receptors. Moreover, previous evidence showed that norepinephrine released in the BNST could modulate memory processes through ?-adrenergic receptors. While the NMDA receptor in various brain regions is importanted in neural plasticity, but its role in the BNST in terms of interacting with norepinephrine in modulating memory processing is still obscured. The present study investigated the involvement of NMDA receptors, as well as the interaction of norepinephrine and glutamate in the BNST in memory consolidation processes. Rats with the BNST bilaterally implanted cannula were trained on the inhibitory avoidance task, water maze task, and fear-potentiated startle task. Drugs were bilaterally infused into the BNST shortly after training. Results indicated that immediate post-training intra-BNST infusion of 1.0 μg L-glutamate enhanced retention of the inhibitory avoidance response, and the memory enhancing effect was attenuated by 1.0 μg APV. Post-training intra-BNST infusion of 5.0 μg APV impaired retention of the inhibitory avoidance task. These effects were not observed in either the water maze or the fear-potentiated startle task. Posttraining intra-BNST infusion of 10.0 μg propranolol impaired retention of the inhibitory avoidance response. The memory enhancing effect of 1.0 μg norepinephrine was attenuated by 5.0 μg propranolol. Intra-BNST infusion of 0.02 μg norepinephrine and 0.2 μg L-glutamate, in which either drug by itself had no discernible effect, enhanced inhibitory avoidance retention if given concurrently right after training. The amnestic effect of APV in the inhibitory avoidance task could be ameliorated by 0.02 μg norephinephrine, which by itself caused no enhancing effect. The memory enhancing effect of L-glutamate was not attenuated by prazosin, but ameliorated by propranolol. These findings suggest that in the inhibitory avoidance task, the glutamate released in the BNST could modulate memory processes through NMDA receptors. Furthermore, release of norepinephrine in the BNST, which may be regulated by presynaptic NMDA receptors, could act on postsynapticβ-adrenergic receptors in modulating memory consolieation processes.