PubMed · 1107868
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E S Valenstein. 1975. Brain stimulation and behavior control.. https://pubmed.ncbi.nlm.nih.gov/1107868/
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The influence of dl-tetrahydropalmatine (THP), an active component isolated from a Chinese herbal medicine corydalis, was tested on the development of electrically kindled amygdala. The seizure activity was quantified by a ultrasonic system for vertical motion measurements. Intraperitoneal injection of THP (20 or 30 mg kg(-1)) 30 min before applying the daily kindling stimulus prevented the development of the kindling process. The behavioral seizure score and the motion responses which normally develop during electrical kindling were reduced below their initial values. The results suggest that THP is a very effective antiepileptogenic and anticonvulsant agent when applied to electrically kindled rats.
Incentive motivation for cocaine, elicited by cocaine-associated stimuli, is thought to be involved in craving and relapse. To examine the role of the basolateral amygdala complex (BLC) in this phenomenon, we assessed the effects of post-training BLC lesions on extinction of cocaine-seeking behavior and cocaine-conditioned place preference (CPP) and the effects of pre-training BLC lesions on acquisition of cocaine-CPP. In Experiment 1, rats were first trained to self-administer cocaine and then received bilateral infusions of the excitotoxin, N-methyl-D-aspartic acid (NMDA, 0.12 M; 0.3 microl/side), or vehicle into the BLC. They were then tested repeatedly for extinction of cocaine-seeking behavior (i.e. nonreinforced responses in the presence of cocaine-paired stimuli). Subsequently, they were trained and tested for acquisition of cocaine-CPP (i.e. increased time spent in a previously cocaine-paired, relative to a saline-paired, environment). Locomotion and compartment entries were also measured. In Experiment 2, rats were first trained and tested for cocaine-CPP, and then received NMDA or vehicle infusions into the BLC. Subsequently, they were tested repeatedly for extinction of cocaine-CPP. Post-training BLC lesions retarded extinction of cocaine-seeking behavior and cocaine-CPP, whereas pre-training lesions disrupted acquisition of cocaine-CPP. These effects did not appear to be related to changes in general activity. We suggest that pre-training BLC lesions disrupted acquisition of cocaine-CPP by impairing assignment of incentive value to cocaine-paired stimuli, whereas post-training BLC lesions disrupted extinction of cocaine-conditioned behaviors by impairing the assessment of the current incentive value of cocaine-paired stimuli.
R-type Ca2+ channels play a critical role in coupling excitability to dendritic Ca2+ influx and neuronal secretion. Unlike other types of voltage-sensitive Ca2+ channels (L, N, P/Q, and T type), the molecular basis for the R-type Ca2+ channel is still unclear, thereby limiting further detailed analyses of R-type Ca2+ channel physiology. The prevailing hypothesis is that alpha(1E) (Ca(V)2.3) gene encodes for R-type Ca2+ channels, but the dearth of critical evidence has rendered this hypothesis controversial. Here we generated alpha1E-deficient mice (alpha1E-/-) and examined the status of voltage-sensitive Ca2+ currents in central amygdala (CeA) neurons that exhibit abundant alpha1E expression and R-type Ca2+ currents. The majority of R-type currents in CeA neurons were eliminated in alpha1E-/- mice whereas other Ca2+ channel types were unaffected. These data clearly indicate that the expression of alpha1E gene underlies R-type Ca2+ channels in CeA neurons. Furthermore, the alpha1E-/- sign mice exhibited signs of enhanced fear as evidenced by their vigorous escaping behavior and aversion to open-field conditions. These latter findings imply a possible role of alpha1E-based R-type Ca2+ currents in amygdala physiology associated with fear.