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Behavioral pharmacological investiga...
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Woods, Vanessa Erin Blythe.
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Behavioral pharmacological investigations of basolateral amygdala modulation of amphetamine-induced behaviors.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Behavioral pharmacological investigations of basolateral amygdala modulation of amphetamine-induced behaviors./
作者:
Woods, Vanessa Erin Blythe.
面頁冊數:
123 p.
附註:
Adviser: Aaron Ettenberg.
Contained By:
Dissertation Abstracts International67-10B.
標題:
Biology, Neuroscience. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3238811
ISBN:
9780542929731
Behavioral pharmacological investigations of basolateral amygdala modulation of amphetamine-induced behaviors.
Woods, Vanessa Erin Blythe.
Behavioral pharmacological investigations of basolateral amygdala modulation of amphetamine-induced behaviors.
- 123 p.
Adviser: Aaron Ettenberg.
Thesis (Ph.D.)--University of California, Santa Barbara, 2006.
The focus of this dissertation was to explore the nature of the functional relationship between the basolateral amygdala (BLA) and nucleus accumbens (NAC) with respect to dopamine (DA)-dependent behaviors. Male rats were given intra-BLA injections of either lidocaine, (to induce temporary lesions), or NMDA, (to chemically activate), during amphetamine (AMP) challenge in the locomotor activity chambers, in a circling paradigm, and after stable AMP self-administration had been achieved. Pharmacological manipulation of the BLA by itself had no effect on spontaneous locomotion or circling behavior, however intra-BLA lidocaine resulted in an increase, while stimulation of glutamatergic receptors in the BLA served to decrease, AMP-induced hyperactivity. These results suggest that removing the input from the BLA releases the NAC from inhibition, thereby potentiating NAC-mediated stimulant-induced activity. Also consistent with this view was the demonstration that unilateral inactivation of the BLA led to contralateral circling behavior in AMP-but not APO-treated rats. Intra-BLA lidocaine was without measurable effect on lever pressing behavior. Intra-BLA infusions of NMDA (low dose) tended to increase responding, whereas the higher dose attenuated lever-pressing for AMP. It is suggested that the low dose of NMDA may have slightly increased, and the high dose decreased, the motivation to seek AMP while leaving the reinforcing efficacy of AMP intact. In conclusion, BLA inactivation or stimulation on its own is insufficient to alter NAC-dependent behaviors; such modulations occur when NAC DA is activated. In a motivated behavioral paradigm, BLA stimulation is altering NAC function in such a way as to modulate the motivation to seek AM while leaving the reinforcing capacity of AMP intact. Inactivation of the BLA had no such effects. It is acknowledged that a motivational interpretation is without an associated mechanism of action so it remains a preliminary one. Lastly, there is an indirect route and a direct route by which the BLA could be modulating NAC function, and a clear understanding of the BLA-NAC functional relationship requires a more global "circuit" based investigation of brain-behavior relationships that includes an understanding of the relative contributions of these two routes.
ISBN: 9780542929731Subjects--Topical Terms:
1017680
Biology, Neuroscience.
Behavioral pharmacological investigations of basolateral amygdala modulation of amphetamine-induced behaviors.
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The focus of this dissertation was to explore the nature of the functional relationship between the basolateral amygdala (BLA) and nucleus accumbens (NAC) with respect to dopamine (DA)-dependent behaviors. Male rats were given intra-BLA injections of either lidocaine, (to induce temporary lesions), or NMDA, (to chemically activate), during amphetamine (AMP) challenge in the locomotor activity chambers, in a circling paradigm, and after stable AMP self-administration had been achieved. Pharmacological manipulation of the BLA by itself had no effect on spontaneous locomotion or circling behavior, however intra-BLA lidocaine resulted in an increase, while stimulation of glutamatergic receptors in the BLA served to decrease, AMP-induced hyperactivity. These results suggest that removing the input from the BLA releases the NAC from inhibition, thereby potentiating NAC-mediated stimulant-induced activity. Also consistent with this view was the demonstration that unilateral inactivation of the BLA led to contralateral circling behavior in AMP-but not APO-treated rats. Intra-BLA lidocaine was without measurable effect on lever pressing behavior. Intra-BLA infusions of NMDA (low dose) tended to increase responding, whereas the higher dose attenuated lever-pressing for AMP. It is suggested that the low dose of NMDA may have slightly increased, and the high dose decreased, the motivation to seek AMP while leaving the reinforcing efficacy of AMP intact. In conclusion, BLA inactivation or stimulation on its own is insufficient to alter NAC-dependent behaviors; such modulations occur when NAC DA is activated. In a motivated behavioral paradigm, BLA stimulation is altering NAC function in such a way as to modulate the motivation to seek AM while leaving the reinforcing capacity of AMP intact. Inactivation of the BLA had no such effects. It is acknowledged that a motivational interpretation is without an associated mechanism of action so it remains a preliminary one. Lastly, there is an indirect route and a direct route by which the BLA could be modulating NAC function, and a clear understanding of the BLA-NAC functional relationship requires a more global "circuit" based investigation of brain-behavior relationships that includes an understanding of the relative contributions of these two routes.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3238811
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