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Bao-Ming Li

Publications and source records attributed to Bao-Ming Li.

13 recordsLinked to original sources
PubMed2006

SNAP-25 in hippocampal CA3 region is required for long-term memory formation.

SNAP-25 is a synaptosomal protein of 25 kDa, a key component of synaptic vesicle-docking/fusion machinery, and plays a critical role in exocytosis and neurotransmitter release. We previously reported that SNAP-25 in the hippocampal CA1 region is involved in consolidation of contextual fear memory and water-maze spatial memory (Hou et al. European J Neuroscience, 20: 1593-1603, 2004). SNAP-25 is expressed not only in the CA1 region, but also in the CA3 region, and the SNAP-25 mRNA level in the CA3 region is higher than in the CA1 region. Here, we provide evidence that SNAP-25 in the CA3 region is also involved in learning/memory. Intra-CA3 infusion of SNAP-25 antisense oligonucleotide impaired both long-term contextual fear memory and water-maze spatial memory, with short-term memory intact. Furthermore, the SNAP-25 antisense oligonucleotide suppressed the long-term potentiation (LTP) of field excitatory post-synaptic potential (fEPSP) in the mossy-fiber pathway (DG-CA3 pathway), with no effect on paired-pulse facilitation of the fEPSP. These results are consistent with the notion that SNAP-25 in the hippocampal CA3 region is required for long-term memory formation.

Animals↗
PubMed2006

The negative cell cycle regulator, Tob (transducer of ErbB-2), is involved in motor skill learning.

Tob (transducer of ErbB-2) is a negative cell cycle regulator with anti-proliferative activity in peripheral tissues. Our previous study identified Tob as a protein involved in hippocampus-dependent memory consolidation (M.L. Jin, X.M. Wang, Y.Y. Tu, X.H. Zhang, X. Gao, N. Guo, Z.Q. Xie, G.P. Zhao, N.H. Jing, B.M. Li, Y.Yu, The negative cell cycle regulator, Tob (Transducer of ErbB-2), is a multifunctional protein involved in hippocampus-dependent learning and memory, Neuroscience 131 (2005) 647-659). Here, we provide evidence that Tob in the central nervous system is engaged in acquisition of motor skill. Tob has a relatively high expression in the cerebellum. Tob expression is up-regulated in the cerebellum after rats receive training on a rotarod-running task. Rats infused with Tob antisense oligonucleotides into the 4th ventricle exhibit a severe deficit in running on a rotating rod or walking across a horizontally elevated beam.

Animals↗
PubMed2005

Roles of NMDA NR2B subtype receptor in prefrontal long-term potentiation and contextual fear memory.

Cortical plasticity is thought to be important for the establishment, consolidation, and retrieval of permanent memory. Hippocampal long-term potentiation (LTP), a cellular mechanism of learning and memory, requires the activation of glutamate N-methyl-D-aspartate (NMDA) receptors. In particular, it has been suggested that NR2A-containing NMDA receptors are involved in LTP induction, whereas NR2B-containing receptors are involved in LTD induction in the hippocampus. However, LTP in the prefrontal cortex is less well characterized than in the hippocampus. Here we report that the activation of the NR2B and NR2A subunits of the NMDA receptor is critical for the induction of cingulate LTP, regardless of the induction protocol. Furthermore, pharmacological or genetic blockade of the NR2B subunit in the cingulate cortex impaired the formation of early contextual fear memory. Our results demonstrate that the NR2B subunit of the NMDA receptor in the prefrontal cortex is critically involved in both LTP and contextual memory.

Animals↗
PubMed2005

Identification of a novel protein for memory regulation in the hippocampus.

Memory formation, maintenance, and retrieval are a dynamic process, reflecting a combined outcome of new memory formation on one hand, and older memory suppression/clearance on the other. Although much knowledge has been gained regarding new memory formation, less is known about the molecular components and processes that serve the function of memory suppression/clearance. Here, we report the identification of a novel protein, termed hippyragranin (HGN), that is expressed in the rat hippocampus and its expression is reduced by hippocampal denervation. Inhibition of HGN by antisense oligonucleotide in area CA1 results in enhanced performance in Morris water maze, as well as elevated long-term potentiation. These results suggest that HGN is involved in negative memory regulation.

Animals↗
PubMed2005

Neurobiology of executive functions: catecholamine influences on prefrontal cortical functions.

The prefrontal cortex guides behaviors, thoughts, and feelings using representational knowledge, i.e., working memory. These fundamental cognitive abilities subserve the so-called executive functions: the ability to inhibit inappropriate behaviors and thoughts, regulate our attention, monitor our actions, and plan and organize for the future. Neuropsychological and imaging studies indicate that these prefrontal cortex functions are weaker in patients with attention-deficit/hyperactivity disorder and contribute substantially to attention-deficit/hyperactivity disorder symptomology. Research in animals indicates that the prefrontal cortex is very sensitive to its neurochemical environment and that small changes in catecholamine modulation of prefrontal cortex cells can have profound effects on the ability of the prefrontal cortex to guide behavior. Optimal levels of norepinephrine acting at postsynaptic alpha-2A-adrenoceptors and dopamine acting at D1 receptors are essential to prefrontal cortex function. Blockade of norepinephrine alpha-2-adrenoceptors in prefrontal cortex markedly impairs prefrontal cortex function and mimics most of the symptoms of attention-deficit/hyperactivity disorder, including impulsivity and locomotor hyperactivity. Conversely, stimulation of alpha-2-adrenoceptors in prefrontal cortex strengthens prefrontal cortex regulation of behavior and reduces distractibility. Most effective treatments for attention-deficit/hyperactivity disorder facilitate catecholamine transmission and likely have their therapeutic actions by optimizing catecholamine actions in prefrontal cortex.

Adamantane↗
PubMed2005

Locomotor hyperactivity induced by blockade of prefrontal cortical alpha2-adrenoceptors in monkeys.

BACKGROUND: Stimulation of alpha(2)-adrenergic receptors (alpha(2)-ARs) in the prefrontal cortex (PFC) has a beneficial effect on working memory and attentional regulation in monkeys. alpha(2)-adrenergic agonists like clonidine and guanfacine have been used experimentally and clinically for the treatment of attention deficit and hyperactivity disorder (ADHD). However, it is unknown if alpha(2)-ARs in the PFC are involved in the neural mechanisms underlying regulation of locomotor activity. METHODS: The alpha(2)-adrenergic antagonist yohimbine was infused bilaterally and chronically into the dorsolateral PFC (dlPFC) in two monkeys, using mini-osmotic pumps. Spontaneous locomotor activity was measured continuously before, during and after drug administration, using an activity monitor. RESULTS: The monkeys exhibited a dramatic increase in motoric activity during infusion of yohimbine into the dlPFC. Similar treatment with saline was without effect. Thus, the locomotor hyperactivity was due to blockade of alpha(2)-ARs, not because of nonspecific factors such as cortical damage by drug administration. CONCLUSIONS: The present study suggests that alpha(2)-ARs in the dlPFC are involved in inhibitory control of locomotor activity.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed2005

Beta-arrestin1 and beta-arrestin2 are differentially required for phosphorylation-dependent and -independent internalization of delta-opioid receptors.

Beta-arrestins are key negative regulators and scaffolds of G protein-coupled receptor (GPCR) signalling. Beta-arrestin1 and beta-arrestin2 preferentially bind to the phosphorylated GPCRs in response to agonist stimulation, resulting in receptor internalization and desensitization. The critical roles of GPCR kinases (GRKs)-catalyzed receptor phosphorylation and interaction of beta-arrestins with the phosphorylated receptor in receptor internalization are well established. However, emerging evidence suggests that an agonist-stimulated internalization mechanism that is independent of receptor phosphorylation may also be employed in some cases, although the molecular mechanism for the phosphorylation-independent GPCR internalization is not clear. The current study investigated the role of receptor phosphorylation and the involvement of different beta-arrestin subtypes in agonist-induced delta-opioid receptor (DOR) internalization in HEK293 cells. Results from flow cytometry, fluorescence microscopy, and surface biotin labelling experiments showed that elimination of agonist-induced DOR phosphorylation by mutation GRK binding or phosphorylation sites only partially blocked agonist-induced receptor internalization, indicating the presence of an agonist-induced, GRK-independent mechanism for DOR internalization. Fluorescence and co-immunoprecipitation studies indicated that both the wild-type DOR and the phosphorylation-deficient mutant receptor could bind and recruit beta-arrestin1 and beta-arrestin2 to the plasma membrane in an agonist-stimulated manner. Furthermore, internalization of both the wild-type and phosphorylation-deficient receptors was increased by overexpression of either type of beta-arrestins and blocked by dominant-negative mutants of beta-arrestin-mediated internalization, demonstrating that both phosphorylation-dependent and -independent internalization require beta-arrestin. Moreover, double-stranded RNA-mediated interference experiments showed that either beta-arrestin1 or beta-arrestin2 subtype-specific RNAi only partially inhibited agonist-induced internalization of the wild-type DOR. However, agonist-induced internalization of the phosphorylation-deficient DOR was not affected by beta-arrestin1-specific RNAi but was blocked by RNAi against beta-arrestin2 subtype. These data indicate that endogenous beta-arrestin1 functions exclusively in the phosphorylation-dependent receptor internalization, whereas endogenous beta-arrestin2, but not beta-arrestin1, is required for the phosphorylation-independent receptor internalization. These results thus provide the first evidence of different requirement for beta-arrestin isoforms in the agonist induced phosphorylation-dependent and -independent GPCR internalization.

Arrestins↗
PubMed2004

[Progress in study on animal's numerical competence].

Animal's numerical competence has been one of the central issues in comparative psychology, cognitive psychology and cognitive neuroscience. A great number of studies indicate that animals have the capability to subitize small numerousness and judge relative numerousness. However, it is pendent if they have the counting ability. There is no evidence that animals can estimate numerousness. Neurophysiological studies show that the posterior parietal cortex and the prefrontal cortex in monkeys are involved in the neural mechanisms underlying numerical competence.

Animals↗
PubMed2004

Enhanced visuomotor associative learning following stimulation of alpha 2A-adrenoceptors in the ventral prefrontal cortex in monkeys.

The present study investigated the effect of locally infused guanfacine, an alpha2A-adrenergic agonist, into the ventral prefrontal cortex (PFv) on visuomotor associative learning. Two monkeys were well trained on a two-problem visuomotor associative task: the monkeys performed movement A if presented with a circle pattern, or movement B if presented with a triangle pattern. For learning of new visuomotor associations, the monkeys were presented with a new set of four patterns in each and every daily session, two of which instructed movement A and the other two movement B. Bilaterally infused guanfacine (2.5 microg/microl; 3 microl on each side) improved the monkeys' ability to learn new visuomotor associations: trials and errors to learning criterion of 90% correct decreased significantly. The monkeys showed an enhanced capability to use win-stay/lose-shift strategy on 'repeat trials' and change-stay/change-shift strategy on 'change trials.' The present results indicate that alpha2A-adrenoceptor in the PFv is involved in regulating visuomotor associative learning.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2004

The alpha(2A)-adrenergic agonist guanfacine improves visuomotor associative learning in monkeys.

Two monkeys were trained on two-problem visuomotor associations: if the cue was a circle pattern, move a handle to the left ('go-left'), and if it was a triangle pattern, move the handle to the right ('go-right'). These two visuomotor associations were unchanged throughout all the experiments and therefore were very familiar to the monkeys. For learning of new visuomotor associations, each monkey was presented with a new set of four novel patterns in each and every daily session, two of which instructed 'go-left' response and the other two 'go-right' response. Systemically administered guanfacine, a selective alpha(2A)-adrenergic agonist, improved the monkeys' learning ability: trials and errors to the learning criterion of 90% correct decreased significantly. The monkeys showed an enhanced capability of using at least three response strategies: win-stay on 'repeat trial', change-stay and change-shift on 'change trial'. The beneficial effect could be reversed by the coadministered idaxozan, an alpha(2)-adrenergic antagonist, which had no effect when administered alone. Similar treatment with guanfacine had no beneficial effect on visual discriminative learning, a task that involves the inferotemporal cortex. The present results indicate that stimulation by guanfacine of alpha(2A)-adrenoceptors improves visuomotor associative learning, probably through actions at alpha(2A)-adrenoceptors in the prefrontal cortex.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2003

Selective deficit in no-go performance induced by blockade of prefrontal cortical alpha 2-adrenoceptors in monkeys.

Two monkeys (Macaca mulatta) were trained to make a go response (go to touch a computer screen) when a red signal (go signal) was presented or a no-go response (inhibit the screen-touching action) when a green signal (no-go signal) was given. The alpha2-adrenergic antagonist yohimbine was infused locally, bilaterally and continuously for 8 days into the prefrontal cortex (PFC) by using mini-osmotic pump. The no-go but not go performance was selectively impaired during the 8-day administration of yohimbine: the monkeys showed an inability to inhibit the touching response to the no-go signal, indicating that there was a deficit in the inhibitory ability of the animals. Similar infusion of saline into the same cortical area was without effect. The present study provides behavioral pharmacological evidence that alpha2-adrenoceptors in the PFC are involved in the neural mechanisms underlying response inhibition.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed2003

Deficit in long-term contextual fear memory induced by blockade of beta-adrenoceptors in hippocampal CA1 region.

The present study investigated the effects of intra-CA1 infusion of d,l-propranolol, the beta-adrenergic antagonist, on memory for contextual fear conditioning. d,l-Propranolol administered 5 min ('0 h') postconditioning impaired long-term but not short-term contextual fear memory, while it was ineffective when administered 6 h postconditioning, suggesting that there is a time window for beta-adrenoceptors to play a role. Thus, we conclude that beta-adrenoceptors in area CA1 are involved in regulating consolidation of contextual fear memory, with '0 h' but not 6 h post-training, a sensitive time point for the beta-adrenergic involvement.

Adrenergic beta-Antagonists↗