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梁淑鈴

 

梁淑鈴 (Shu-Ling Liang)

Appointment:Assistant Professor

Lab:Astrocytic and neuronal synaptic transmission laboratory

Education:Ph.D.

University/Nation:National Yang-Ming Univ./Taiwan

Tel:+886-3-2118800 ext. 3688

E-mail: slliang@mail.cgu.edu.tw

Research website:under construction

Laboratory personnel:

Postdoctoral fellow:  ; Ph.D. student:  ; Master student: 2 ; Res. Assistant: 1 ; undergraduate:1

Research interests:

GABA and glutamate, which mediate inhibitory and excitatory transmission, are the most prevalent neurotransmitters in central nervous system (CNS). Imbalance between inhibitory and excitatory transmissions has been implicated in the pathogenesis of various CNS diseases, such as epilepsy. In CNS, neurons are often surrounded by astrocytic processes, in which transporters located on astrocyte membrane, play a pivotal role in the inactivation of GABAergic and glutamatergic neuronal transmissions via uptake of GABA and glutamate. Glutamate transported into astrocyte can then be converted into glutamine, and subsequently be transported back to neurons. In neurons, the glutamine is then converted in to glutamate or GABA. This process is named the astrocytic glutamate-glutamine cycle (GGC, refer cartoon below).

 

Vesicular GABA originating from the glutamate-glutamine cycle depends on astrocytic synthesis and transport. Illustrated are the three cellular components of a GABAergic synapse: the pre- and post-synaptic elements, which are often surrounded by astrocytic processes. The primary transporters regulating presynaptic uptake of glutamate (Glu, n ; EAAC-1) and reuptake of GABA ( l ; GAT-1) are shown on the face of the synapse. The machinery for synthesizing GABA from glutamate (L-glutamic acid decarboxylase; GAD), and packaging GABA into the vesicle (VIAAT) are drawn associated with the vesicle. The glutamate from the glutamate-glutamine cycle pathway is indicated by the thick arrows, starting with glutamate uptake through GLT-1 into the astrocyte, is glutamine synthetase generates glutamine (Gln, l). Glutamine can then be transported out through System-N transporters (SN-1) and into the neuron through System-A transporters (SA-1). Inhibitors of the glutamate-glutamine cycle are also indicated blocking their targets: DHK at GLT-1, MSO at Glutamine synthetase, and MeAIB at SA-1.

Using various electrophysiology techniques in conjunction with pharmacology, qualitative and quantitative protein analysis as well as behavioral testings, three research topics are currently on going in my lab:

1. Cellular mechanism of GGC on estrogen-induced sex differentiation and reproductive behavior in rats.

2. Cellular mechanism of CART peptides on firing rates and synaptic inputs of DMV neurons innervating stomach and cecum in rats.

3. Neuro-physiological mechanism of interactions between D2-like dopamine receptors and GGC on the regulations of sex differentiation and reproductive behavior in rats.

Research approach:

1. Adapting visualized whole-cell voltage and current clamp recordings techniques, inhibitory and excitatory postsynaptic currents (IPSCs; EPSCs), firing activity used cell-attached technique are routinely used to examine the synaptic functions. In addition, several parameters are also used to further test synaptic efficacy, including:

a. Miniature IPSCs (mIPSCs), miniature EPSCs (mEPSCs) for testing changes in synaptic efficacy under basal condition of synaptic activities.

b. Strontium evoked IPSCs and Strontium evoked EPSCs; Miniature evoked IPSCs (meIPSCs) and miniature evoked EPSCs (meEPSCs) for testing changes in potency and release probability under active synapses.

c. Recording spontaneous IPSCs (sIPSCs), spontaneous EPSCs (sEPSCs), evoked IPSCs (eIPSCs), evoked EPSCs (eEPSCs) and field excitatory postsynaptic potential (fEPSP) to assess synaptic efficacy.

d. Paired-pulse stimulation recordings to determine changes in synaptic vesicle’s release probability.

e. Puffed GABA or glutamate for testing changes in postsynaptic receptors’ numbers or sensitivity.

f. Pair-recordings to directly assess synaptic interaction between pre- and post-synaptic neurons.

g. Astrocytic GABA and glutamate transporter currents recordings to reflex extracellular GABA and glutamate concentrations.

2. Western blotting analysis for quantifying protein expression of enzymes or transporters involved in the GGC.

3. Quantitative RT-PCR for evaluating mRNA expression.

4. Immunocytochemistry for post hoc analysis.

5. Animal behavior observation and identification including reproductive behavioral tests.

  Publications (2008-present):

Peer-reviewed

1. Liang SL* (2017) Sex-differential dependency of glutamate-glutamine cycle for sustaining synaptic glutamate release in neonatal hypothalamus. (Submitted).

2. Liang SL*, Alger BE, McCarthy MM (2014) Developmental increase in hippocampal endocannabinoid mobilization: roles of metabotropic glutamate receptor subtype 5 and phospholipase C. J. Neurophysiol. 112:2605-2615. (*, corresponding author).

3. Liang SL*, Hsu SC, Pan JT (2014) Involvement of dopamine D2 receptor in the diurnal changes of tuberoinfundibular dopaminergic neuron activity and prolactin secretion in female rats. J. BioMed. Sci. 21:37 (*, corresponding author).

4. Liang SL*, Pan JT (2012) An endogenous dopaminergic tone acting on dopamine D3 receptors may be involved in diurnal changes of tuberoinfundibular dopaminergic neuron activity and prolactin secretion in estrogen-primed ovariectomized rats. Brain Res. Bull. 87:334-339. (*, corresponding author).

5. Liang SL*, Pan JT (2011) The spontaneous firing rates of dopamine-responsive dorsomedial arcuate neurons exhibit a diurnal rhythm in brain slices obtained from ovariectomized plus estrogen-treated rats. Brain Res. Bull. 85:189-193. (*, corresponding author)

6. Schwarz JM, Liang SL, Thompson, SM, McCarthy MM (2008) Estradiol induces dendritic spines on developing hypothalamic neurons by enhancing glutamate release independent of transcription: A novel mechanism for an organizational sex difference. Neuron 58:584-598.

Published Abstracts

1. Tong YS, Hwang LL, Chen CY, Liang SL: Different regulations of CART peptides on firing rates and synaptic inputs of DMV neurons innervating stomach and cecum in rats. The 32th Joint Annual Conference of Biomedical Science, Taiwan, Taipei, Mar 25-26, 2017. (Submitted).

2. Tong YS, Hwang LL, Chen CY, Liang SL: Retrograde Labeling in vivo of vagal preganglionic neurons innervating stomach and cecum in rats by the carbocyanine dye DiO. The 31th Joint Annual Conference of Biomedical Science, Taiwan, Taipei, Mar 26-27, 2016. (P138).

3. Yeh CY, Liang SL: Sex differential effects of neonatal pretreatments of fluoroacetate or MSO to disrupt glutamate-glutamine cycle on adult reproductive behaviors in rats. EMBO Conference on neural development- function and dysregulation. Taiwan, Taipei, Dec 4-8, 2015. (p32)

4. Liang SL, Hsu SC: Diurnal changes of dopamine D2 and D3 receptor mRNA expression in medial basal hypothalamus of estrogen-primed ovariectomized rats. The 28th Joint Annual Conference of Biomedical Science, Taiwan, Taipei, Mar 23-24, 2013. (P564)

5. Liang SL, Lim SC: Blockade of neuronal glutamine uptake reduces quantal GABA content under active synapse in the mediobasal hypothalamus of neonatal rats. The 27th Joint Annual Conference of Biomedical Science, Taiwan, Taipei, Mar 17-18, 2012. (P415)

6. Liang SL: Blockade of glutamate-glutamine cycle does not change vesicular GABA content in neurons of neonatal hypothalamus under basal neuronal activities. The 7th Federation of Asian-Oceanian Physiology Society (FAOPS) Congress, Taiwan, Taipei, Sep 11-14, 2011. (PT05)

7. Liang SL, Huang YH: Sex differences in astrocyte glutamine synthetase and neuronal spinophilin protein expressions in neonatal hypothalamic brain slices. The 26th Joint Annual Conference of Biomedical Science, Taiwan, Taipei, Mar 19-20, 2011. (P848)

 

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