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K C Liang

Publications and source records attributed to K C Liang.

At least 19 recordsLinked to original sources
PubMed2004

Pre- and post-training infusion of prazosin into the bed nucleus of the stria terminalis impaired acquisition and retention in a Morris water maze task.

The bed nucleus of the stria terminalis (BNST) is interconnected with the amygdala that is implicated in memory modulation. In view of the innervation of this structure by the hippocampus and brain stem noradrenergic nuclei, this study examined the role of BNST noradrenergic activity in acquisition, formation and expression of spatial memory. Male Wistar rats with indwelling cannulae in the BNST were trained on a spatial navigation task in the Morris water maze. Groups of rats received intra-BNST infusion of vehicle, norepinephrine, prazosin or both drugs shortly before or after each daily training session, or shortly before retention tests. Results showed that pre- or posttraining infusion of 1.0 microg prazosin impaired acquisition and retention, but the treatment had no effect on a cued response task. Posttraining infusion of 1.0 microg norepinephrine enhanced acquisition and retention, and this enhancing effect was blocked by simultaneous infusion of 0.3 microg prazosin. Pretest intra-BNST of prazosin or norepinephrine at a dose of 1.0 microg did not impair expression of the spatial navigation memory. These findings suggest that the BNST noradrengergic function is involved in modulating acquisition and formation of spatial memory that engage the hippocampus.

Adrenergic alpha-Agonists↗
PubMed2002

Amphetamine induced sensitization in acoustic startle: lack of blockade by adrenalectomy and alpha-helical CRF9-41.

The present study utilized the acoustic startle response to evaluate the sensitization effect of repeated administration of amphetamine (AMPH). Intraperitoneal injections of AMPH induced a dose-dependent enhancement of startle: 5.0 mg/kg caused a robust effect, 1.0 or 3.0 mg/kg caused a negligible effect. Sensitization was generated by repeated administration of 5.0 mg/kg AMPH for 7 consecutive days and tested on the 8th and 9th days with challenge of saline and 3 mg/kg AMPH. The results showed that rats receiving chronic injections of AMPH, but not saline, showed significant enhancement of startle to 3.0 mg/kg AMPH, and this effect lasted at least for a month. To explore the role of the hypothalamo-pituitary-adrenal axis in this sensitization effect, rats received adrenalectomy, adrenal demedullation, or sham adrenal operation, and then were subjected to acute or chronic injections of 5.0 mg/kg AMPH. Removal of the whole adrenal gland or only the medulla abolished neither the startle enhancing effect of AMPH injected acutely nor the sensitization effect of AMPH injected chronically. In addition, intracerebroventricular infusion of a CRF antagonist, alpha-helical CRF9-41, prior to the challenge test failed to alter the sensitization effect of AMPH. These findings suggest that neither adrenal hormones nor CRF was indispensable for induction/expression of AMPH-induced sensitization in acoustic startle.

Acoustic Stimulation↗
PubMed2001

Posttraining infusion of norepinephrine and corticotropin releasing factor into the bed nucleus of the stria terminalis enhanced retention in an inhibitory avoidance task.

The present study investigated whether the bed nucleus of the stria terminalis (BNST) is involved in formation and retrieval of affective memory. Male Wistar rats with cannulae bilaterally implanted into the BNST were trained on a one-trial step-through inhibitory avoidance task. Shortly after training they received bilateral intra-BNST infusion of lidocaine, various noradrenergic drugs, or corticotropin releasing factor (CRF). Results showed that posttraining intra-BNST infusion of lidocaine impaired retention. Posttraining intra-BNST infusion of norepinephrine or the alpha1 antagonist prazosin induced a dose- and time-dependent retention enhancement or deficit, respectively. The enhancing effect of norepinephrine was mimicked by the alpha1 agonist phenylephrine, and antagonized by prazosin at a non-impairing dose. Posttraining intra-BNST infusion of the alpha2 antagonist idazoxan or the beta antagonist propranolol failed to affect retention. Posttraining intra-BNST infusion of CRF also enhanced retention in a dose-dependent manner. Various drugs infused shortly before testing did not significantly influence locomotor activity and retention. These findings, taken together, suggest that the BNST is involved in memory formation processes for affective experience and norepinephrine released in the BNST acting via alpha1 receptors plays a critical role in this function.

Adrenergic alpha-Agonists↗
PubMed2000

Startle responses to electric shocks: measurement of shock sensitivity and effects of morphine, buspirone and brain lesions.

The present study developed a new protocol to assess shock sensitivity in rats. Male Wistar rats were subjected to footshock stimuli ranging from 0 to 1.6 mA (0.1 s) in a startle apparatus and startle responses elicited by shocks were measured. Acoustic stimuli (95, 105, or 115 dB) were dispersed within the shock series serving as a control measurement of motor performance. Results indicated that the magnitude of shock startle responses significantly increased with the shock intensity in a linear trend. Morphine (8.0 mg/kg) and buspirone (1.0, 2.5, or 5.0 mg/kg), both of which possessing analgesic effects, depressed shock startle but had no such effect on acoustic startle. The effect of morphine was readily reversed by pretreatment of naloxone (1.0 mg/kg). To investigate the neural basis underlying this response, radio-frequency lesions of various structures implicated in processing of nociceptive or aversive information were undertaken. Lesions of the ventroposterior thalamic nucleus, insular cortex, or amygdala decreased startle reactivity to electric shocks but not to acoustic stimuli. Lesions of the anterior cingulate gyrus or medial prefrontal cortex, while altered the reactivity to acoustic stimuli, had no effect on the shock-elicited startle. These results suggested that the amplitude of startle in response to electric shocks provide a quantitative measurement of shock sensitivity within an extended range of stimulus intensities. Performing this response may engage the the central nociceptive pathway.

Animals↗
PubMed1999

Pre- or post-training injection of buspirone impaired retention in the inhibitory avoidance task: involvement of amygdala 5-HT1A receptors.

The present study investigated the effect of buspirone on memory formation in an aversive learning task. Male Wistar rats were trained on the inhibitory avoidance task and tested for retention 1 day after training. They received peripheral or intra-amygdala administration of buspirone or other 5-HT1A drugs either before or after training. Results indicated that pretraining systemic injections of buspirone caused a dose-dependent retention deficit; 5. 0 mg/kg had a marked effect and 1.0 mg/kg had no effect. Post-training injections of the drug caused a time-dependent retention deficit, which was not due to a state-dependent effect on retrieval. When training in the inhibitory avoidance task was divided into a context-training phase and a shock-training phase, buspirone impaired retention only when administered in the shock-training phase, suggesting that the drug influenced memory processing of affective events. Further results indicated that post-training intra-amygdala infusion of buspirone or the 5-HT1A agonist 8-hydroxy-di-n-propylaminotetralin (8-OH-DPAT) caused a time-dependent and dose-dependent retention deficit. Post-training intra-amygdala infusion of the 5-HT1A antagonist WAY100635 (N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)-N-(2-pyridyl) cyclohexane carboxamine maleate) attenuated the memory-impairing effects of buspirone. These findings suggest that buspirone may modulate memory storage processes in the inhibitory avoidance task through an action on amygdaloid 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1998

Pretraining infusion of DSP-4 into the amygdala impaired retention in the inhibitory avoidance task: involvement of norepinephrine but not serotonin in memory facilitation.

The present study investigated the involvement of amygdala noradrenergic (NE) and serotonergic (5-HT) systems in memory storage processing. Rats bearing chronic cannulae in the amygdala were trained on a one-trial inhibitory avoidance task and tested for retention 24 hrs later. Five days prior to training, rats received intra-amygdala infusion of vehicle or various doses of N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP-4)-a NE-specific neurotoxin when given peripherally. Results showed that pretraining intra-amygdala infusion of 10.0 micrograms or 30.0 micrograms of DSP-4 impaired retention. Further, 30.0 micrograms of DSP-4 also abolished the memory enhancing effect of epinephrine (E) injected peripherally. However, local infusion of DSP-4 depleted not only NE but also 5-HT and DA substantially. Subsequent experiments found that the retention deficit induced by 30.0 micrograms of DSP-4 could be ameliorated by 0.2 microgram NE but not by 5-HT at a wide range of doses infused into the amygdala shortly after training, which ascribed the deficit to depletion of NE. After protecting the 5-HT terminals by a pretreatment of fluoxetine (15.0 mg/kg), pretraining intra-amygdala infusion of 30.0 micrograms DSP-4 shifted the memory-enhancing dose of E from 0.1 mg/kg to 1.0 mg/kg. In contrast, pretraining intra-amygdala infusion of 15.0 micrograms 5,7-dihydroxytryptamine (5,7-DHT) or DSP-4 with a pretreatment of desipramine (DMI, 25.0 mg/kgx2) to protect NE terminals failed to impair retention or attenuate the memory enhancing effect of 0.1 mg/kg E injected peripherally. These findings, taken together, suggest that the memory modulatory effect of peripheral E involved, at least partially, the amygdala NE system.

5,7-Dihydroxytryptamine↗
PubMed1998

Buspirone impaired acquisition and retention in avoidance tasks: involvement of the hippocampus.

This study investigated the effects of buspirone on acquisition as well as formation and expression of memory in three different types of avoidance tasks. Rats were trained and tested on a one-trial inhibitory avoidance task, an 8-trial active avoidance task or the Morris water maze. Buspirone (5.0 mg/kg) was administered subcutaneously 30 min before training, immediately after training or 30 min before testing. Retention was tested at various times after training. In the inhibitory avoidance task, pretraining injections of buspirone produced a marked impairing effect on retention, posttraining injections of buspirone produced a moderate but time-dependent memory deficit. Pretest injections of buspirone suppressed retention performance. Such an effect was more pronounced in the 1-day test than in the 21-day test. Intra-hippocampal infusion of buspirone (5.0 micrograms) before testing suppressed expression of the 1-day, but not the 21-day, memory. In the active avoidance task and the Morris water maze, an injection of buspirone before training or testing also impaired acquisition or suppressed retention performance. These findings suggest that buspirone given at various times could compromise acquisition, consolidation and retrieval of affective memory and the hippocampus was involved in the retrieval effect.

Affect↗
PubMed1997

Inhibitory avoidance learning alters the amygdala calcium/calmodulin-dependent protein kinase II activity in rats.

This study investigated the role of amygdala CaM-kinase II (calcium/calmodulin-dependent protein kinase II) in affective learning and memory. In Experiment I, two groups of rats were trained on a one-trial step through inhibitory avoidance learning task. The experimental group received a high intensity foot shock contingent upon the stepping-through behavior, whereas the control group received a series of non-contingent low intensity foot shock during training. The experimental rats showed significantly higher retention scores than the control rats. Correspondingly, rats in the experimental group showed significantly higher Ca2+-independent activity of CaM-kinase II than the controls. Intra-amygdala injection of a specific CaM-kinase II inhibitor, KN-62, before the training trial disrupted affective learning. In comparison with the vehicle-injected controls, pretraining injection of KN-62 impaired the acquisition of affective specific learning. These results, taken together, indicated that the activation of amygdala CaM-kinase II in the amygdala is associated with the affective learning behavior, and may be one of the neural mechanisms underlying formation of affective memory.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

Spatial learning alters hippocampal calcium/calmodulin-dependent protein kinase II activity in rats.

This study investigated the role of hippocampal CaM-kinase II (calcium/calmodulin-dependent protein kinase II) in spatial learning. In Experiment I, three groups of rats received 1, 2 or 5 days of training on a spatial task in the Morris water maze with a hidden platform, while a control group was trained on a nonspatial task with a visible platform. The acquisition rate in the spatial task was slower than that in the nonspatial task. However, rats receiving 5 days of spatial training had the highest Ca(2+)-independent activity of CaM-kinase II compared with the controls receiving nonspatial training and rats having 1 or 2 days of spatial training. Furthermore, the level of hippocampal Ca2+-independent CaM-kinase II activity was correlated with the final performance on the spatial task. In Experiment II, rats received intra-hippocampal injections of a specific CaM-kinase II inhibitor-KN-62-before each training session. In comparison with the vehicle-injected controls, pretraining injection of KN-62 retarded acquisition in the spatial task but had no effect on the nonspatial task. These results, taken together, indicated that the activation of CaM-kinase II in the hippocampus is not only correlated to the degree of spatial training on the Morris water maze, but may also underlie the neural mechanism subserving spatial memory.

Animals↗
PubMed1996

Formation and retrieval of inhibitory avoidance memory: differential roles of glutamate receptors in the amygdala and medial prefrontal cortex.

This study investigated the roles of NMDA and AMPA receptors in the amygdala and medial prefrontal cortex in formation and retrieval of affective memory. In a one-trial step-through inhibitory avoidance task, groups of rats with cannulae implanted into these two regions received infusion of 2.5 micrograms APV or 0.3 micrograms CNQX 5 min before training, shortly after training or 5 min prior to the 1-day or 21-day retention test. Results showed that pre- or posttraining intra-amygdala infusion of APV or CNQX induced a persistent retention deficit with the pretraining treatment causing a greater effect. Pre- or posttraining infusion of CNQX into the medial prefrontal cortex also induced a persistent retention deficit with the posttraining treatment causing a greater effect. Pre- or posttraining infusion of APV into the medial prefrontal cortex impaired 21-day retention but not 1-day retention. Pretraining infusion of lidocaine into either structure caused a retention deficit, which was not attenuated by activating the other structure with glutamate. Pretest intra-amygdala infusion of CNQX impaired memory expression in the 1-day test, while infusion of CNQX into the medial prefrontal cortex impaired memory expression in the 21-day test. Pretest APV infusion into either structure had no effect on memory expression. These findings suggest that the amygdala and medial prefrontal cortex may be contained in a circuitry responsible for formation of affective memory. The consolidation process involves the NMDA and AMPA receptors in both structures. Further, retrieval of recent affective memory engages amygdala AMPA receptors, whereas retrieval of remote affective memory engages AMPA receptors in the medial prefrontal cortex.

2-Amino-5-phosphonovalerate↗
PubMed1995

Mineral excretion following furosemide compared with bumetanide therapy in premature infants.

Mineral excretion following single doses of furosemide were compared with bumetanide in a random cross-over trial in 17 premature infants. The mean birthweight and gestational age were 889 +/- 85 g and 27 +/- 2 weeks. Following furosemide therapy, significantly higher chloride losses and urine volumes were noted in the first 8-h period compared with the second or third 8-h periods. Following bumetanide therapy, sodium, calcium, and chloride losses and urine volumes were significantly higher in the first 8 h compared with the second or third 8-h periods. Hourly sodium and chloride losses were significantly lower following bumetanide than furosemide during the first two 8-h periods. During the final 8-h period sodium, potassium, chloride, and calcium losses were significantly lower following bumetanide than following furosemide. Sodium loss per urine volume was lower with bumetanide than furosemide but calcium loss tended to be higher. Hence, bumetanide does not appear to be a calcium-sparing diuretic following single-dose therapy.

Bronchopulmonary Dysplasia↗
PubMed1995

The role of amygdala norepinephrine in memory formation: involvement in the memory enhancing effect of peripheral epinephrine.

The present study examined the roles of amygdala alpha 1 and beta noradrenergic receptors in memory formation as well as their involvement in the memory enhancing effect of peripheral epinephrine (E). Male Sprague-Dawley rats with cannulae implanted into the amygdala were trained on the one-trial inhibitory avoidance task and tested for retention 24 hrs later. Immediately after training, they received various treatments to alter amygdala noradrenergic functions and/or peripheral adrenergic functions. Separate groups of animals were decapitated 10 min after training for assays of monoamine levels in various brain regions by the HPLC-EC method. Results indicated that, when infused into the amygdala immediately after training, isoproterenol and 8-bromo-cAMP enhanced retention, while propranolol impaired retention. On the other hand, phenylephrine or prazosin failed to produce statistically significant effects. Posttraining intra-amygdala infusion of propranolol, but not prazosin, abolished the memory enhancing effects of norepinephrine (NE) infused into the amygdala or E given subcutaneously to the adrenal demedullated rats. Depletion of amygdala NE by the selective neurotoxin DSP-4 also abolished the memory modulatory effects of E. These findings support that amygdala noradrenergic beta, but not alpha 1, receptors are involved in both central and peripheral memory modulatory processes. However, since the postmortem tissue NE levels in the amygdala and other brain regions did not differ among various groups, the inhibitory avoidance training and peripheral E may only activate a transient functional increase in the amygdala NE activity.

Amygdala↗
PubMed1994

Pre- and posttraining infusion of N-methyl-D-aspartate receptor antagonists into the amygdala impair memory in an inhibitory avoidance task.

Involvement of amygdaloid N-methyl-D-aspartate (NMDA) receptors in memory processes was investigated. Rats with cannulas implanted in the basolateral amygdala were trained on a 1 trial step-through inhibitory avoidance task and tested for 24-hr retention. Pretraining infusion of 2-amino-5-phosphonovaleric acid (APV) into the amygdala, but not striatum or hippocampus, produced a dose-dependent retention deficit, which was attenuated by immediate posttraining intra-amygdala infusion of NMDA. Posttraining APV infusion also caused a dose- and time-dependent retention deficit. Pretest APV infusion had no effect on performance in the retention test. Further, pre- or posttraining infusion of 5.0 micrograms APV failed to affect acquisition and retention in the Morris water maze task. These findings suggest that amygdala NMDA receptors are normally activated by aversive training and play a critical role in memory formation for affective experience.

2-Amino-5-phosphonovalerate↗
PubMed1994

Involvement of hippocampal NMDA and AMPA receptors in acquisition, formation and retrieval of spatial memory in the Morris water maze.

This study investigated the roles of hippocampal N-methyl-D-aspartate (NMDA) receptors and alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionate (AMPA) receptors in acquisition, consolidation and retrieval processes of spatial memory. Male Wistar rats with indwelling cannulae in the dorsal hippocampus received 4 training trials on the Morris water maze for consecutively 6 days. Rats received infusion of the NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid (AP5) or the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) into the hippocampus under one of the three schedules: 5 min prior to each daily training session, immediately after each daily training session or 5 min prior to the final testing trial. Pretraining intra-hippocampal infusion of 5.0 micrograms AP5 retarded acquisition. The same dose of AP5 given after training had little effect but a higher dose (10.0 micrograms) did slow down progress in the acquisition curve. Pretest infusion AP5 failed to affect memory retrieval. Pretraining intra-hippocampal infusion of 1.0 micrograms CNQX also impaired acquisition, but posttraining infusion of CNQX at 1.0 or 2.0 micrograms had no effect. However, pretest infusion of 1.0 micrograms CNQX markedly impaired retrieval of the already-formed spatial memory. These findings taken together suggest that acquisition in a spatial task involves hippocampal NMDA and AMPA receptors, consolidation of spatial memory involves NMDA receptors and retrieving such memory involves AMPA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1993

Congenital syphilitic skeletal manifestations in a premature infant revisited.

Increasing rates of congenital syphilis have been reported in recent years despite the availability of adequate therapy. In our perinatal-neonatal center, approximately 1.5% of newborns have reactive serologic tests for syphilis. Untreated or partly treated maternal syphilis can adversely affect neonatal outcome since the treponeme can cross the placenta at any time during pregnancy. As a result of hematogenous placental transmission, neonatal manifestations are usually systemic and similar to the secondary stage of syphilis, and include hepatosplenomegaly, jaundice, neurosyphilis, and skeletal changes. A case of early congenital syphilis in an extremely premature infant with primary skeletal involvement is presented.

Gentamicins↗
PubMed1993

Involvement of amygdala N-methyl-D-asparate receptors in long-term retention of an inhibitory avoidance response in rats.

This study examined the involvement of amygdala N-methyl-D-aspartate (NMDA) receptors in long-term retention of an inhibitory avoidance response. Rats bearing chronic cannulae implanted into the basolateral amygdala were trained on a one-trial inhibitory avoidance task and tested for retention 21 days later. They received intra-amygdala injections of vehicle (Veh) or 0.25, 1.25 or 5.0 micrograms of a competitive NMDA antagonist-2-amino-5-phosphonopentoic acid (AP5) either 5 min before training, immediately after training or 5 min before testing. Results indicated that pretraining intra-amygdala injections of AP5 at all doses impaired retention performance profoundly. Intra-amygdala injections of AP5 immediately after training caused a dose-dependent retention deficit: 0.25 microgram induced no deficit and 5.0 micrograms induced a great deficit. Immediate posttraining intra-amygdala injections of a non-competitive NMDA antagonist MK-801, also impaired retention but MK-801 given 2 hrs after training had no significant effect. In contrast to the marked amnestic effect produced by pre- or posttraining intra-amygdala injections of AP5, intra-amygdala injections of AP5 given just before retention tests had no discernible effect on retention performance. The retention deficit induced by pretraining intra-amygdala injections of 1.25 micrograms AP5 was ameliorated completely by N-methyl-DL-aspartate (0.25 microgram), but also partially by norepinephrine (0.2 microgram) infused into the amygdala immediately after training. However, posttraining infusion 0.2 microgram norepinephrine failed to attenuate significantly the amnestic effect induced by 5.0 micrograms AP5. These findings, taken together, suggest that NMDA receptors in the amygdala are normally involved in memory formation processing of affective experience.

2-Amino-5-phosphonovalerate↗
PubMed1992

Fluoxetine and 8-OH-DPAT in the lateral septum enhances and impairs retention of an inhibitory avoidance response in rats.

The present study investigated the role of lateral septal serotonin (5HT) in memory consolidation and the subtype of 5HT receptors involved in this process. Rats with cannulae implanted bilaterally into the lateral septum were trained in an inhibitory avoidance task. Immediately after training, the septal serotonergic function was manipulated by pharmacological agents selectively blocking 5HT reuptake (fluoxetine and zimelidine), antagonizing 5HT2 receptors (ketanserin and ritanserin), or activating 5HT1A receptors, respectively. Results indicated that direct fluoxetine infusions into the lateral septum at a dose of 6 micrograms/0.5 microliter and zimelidine at a dose of 5 micrograms/0.5 microliter both markedly enhanced memory. Intralateral septal injections of ketanserin (0.3 microgram/0.5 microliter and 0.5 microgram/0.5 microliter) and ritanserin (0.3 microgram/0.5 microliter and 0.6 microgram/0.5 microliter) did not have a significant effect by themselves on memory, and neither did they attenuate the memory-facilitating effect of fluoxetine in the same area. Intralateral septal infusions of 8-hydroxy-2-(di-n-propylamino)tetralin at 5 micrograms/0.5 microliter significantly impaired memory retention. These findings altogether support the notion that the lateral septal nuclei of rats are involved in the memory processes of inhibitory avoidance learning. Furthermore, postsynaptic 5HT receptor activation (not the 5HT2 receptor subtype) probably exerts a facilitatory effect while presynaptic 5HT1A receptor activation exerts an impairing effect on the memory consolidation process, probably due to autoreceptor inhibition of 5HT release.

8-Hydroxy-2-(di-n-propylamino)tetralin↗