Theta-bursts induce a shift in reversal potentials for GABA-A receptor-mediated postsynaptic currents in rat hippocampal CA1 neurons

Xu, Jiake; Sastry, B.R.

doi:10.1016/j.expneurol.2007.01.004

Cited by 9 publications

(13 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The receptors are abundant in stratum pyramidale and proximal stratum radiatum (Danglot et al, 2004), a location through which excitatory signals would pass, and therefore be affected by the shunt from these receptors. The chloride Nernst potential measured in CA1 pyramidal cells at this age is approximately -60 mV (Xu and Sastry, 2007), consistent with a shunting role.…”

Section: Discussionsupporting

confidence: 62%

Frequency-Dependent Glycinergic Inhibition Modulates Plasticity in Hippocampus

Keck¹,

Lillis²,

Zhou³

et al. 2008

J. Neurosci.

View full text Add to dashboard Cite

Previous studies have demonstrated the presence of functional glycine receptors (GlyRs) in hippocampus. In this work, we examine the baseline activity and activity-dependent modulation of GlyRs in region CA1. We find that strychnine-sensitive GlyRs are open in the resting CA1 pyramidal cell, creating a state of tonic inhibition that "shunts" the magnitude of EPSPs evoked by electrical stimulation of the Schaffer collateral inputs. This GlyR-mediated shunting conductance is independent of the presynaptic stimulation rate; however, pairs of presynaptic and postsynaptic action potentials, repeated at frequencies above 5 Hz, reduce the GlyR-mediated conductance and increase peak EPSP magnitudes to levels at least 20% larger than those seen with presynaptic stimulation alone. We refer to this phenomenon as rate-dependent efficacy (RDE). Exogenous GlyR agonists (glycine, taurine) block RDE by preventing the closure of postsynaptic GlyRs. The GlyR antagonist strychnine blocks postsynaptic GlyRs under all conditions, occluding RDE. During RDE, GlyRs are less responsive to local glycine application, suggesting that a reduction in the number or sensitivity of membrane-inserted GlyRs underlies RDE. By extending the RDE induction protocol to include 500 paired presynaptic and postsynaptic spikes, we can induce long-term synaptic depression (LTD). Manipulations that lead to reduced functionality of GlyRs, either pharmacologically or through RDE, also lead to increased LTD. This result suggests that RDE contributes to long-term synaptic plasticity in the hippocampus.

show abstract

Section: Discussionsupporting

confidence: 62%

Frequency-Dependent Glycinergic Inhibition Modulates Plasticity in Hippocampus

Keck¹,

Lillis²,

Zhou³

et al. 2008

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…However, the GABAergic currents in CA1 hippocampus produce a shunting inhibition because the reversal potential for chloride is close to the membrane potential (Xu and Sastry, 2007) and produces less of a driving force on inhibitory currents than exists for excitatory currents (Fig 4B). Therefore, a change in input resistance would have a greater impact on the ability of excitatory currents to generate an action potential (Fig.…”

Section: 2 Plasticity Of the α4ββ Gabars At Pubertymentioning

confidence: 99%

The influence of stress at puberty on mood and learning: Role of the α4βδ GABAA receptor

Smith¹

2013

Neuroscience

View full text Add to dashboard Cite

It is well-known that the onset of puberty is associated with changes in mood as well as cognition. Stress can have an impact on these outcomes, which in many cases, can be more influential in females, suggesting that gender differences exist. The adolescent period is a vulnerable time for the onset of certain psychopathologies, including anxiety disorders, depression and eating disorders, which are also more prevalent in females. One factor which may contribute to stress-triggered anxiety at puberty is the GABAA receptor (GABAR), which is known to play a pivotal role in anxiety. Expression of α4βδ GABARs increases on the dendrites of CA1 pyramidal cells at the onset of puberty in the hippocampus, part of the limbic circuitry which governs emotion. This receptor is a sensitive target for the stress steroid THP (3α-OH-5[α]β-pregnan-20-one), which paradoxically reduces inhibition and increases anxiety during the pubertal period (~PND 35–44) of female mice in contrast to its usual effect to enhance inhibition and reduce anxiety. Spatial learning and synaptic plasticity are also adversely impacted at puberty, likely a result of increased expression of α4βδ GABARs on the dendritic spines of CA1 hippocampal pyramidal cells, which are essential for consolidation of memory. This review will focus on the role of these receptors in mediating behavioral changes at puberty. Stress-mediated changes in mood and cognition in early adolescence may have relevance for the expression of psychopathologies in adulthood.

show abstract

“…γ-aminobutyric acid (GABA) plays an important role in regulating neuronal excitability in mammalian central nervous system (CNS). Since the amplitude and direction of GABA A mediated postsynaptic currents (PSCs) are subject to changes in their equilibrium potential (E GABA ), either activity-mediated shifts [ 1 , 2 , 3 ] or age-related changes [ 1 , 4 , 5 , 6 ] in E GABA can affect GABAergic synaptic transmission, the excitability of target neurons, excitatory synaptic plasticity, and thus, the balance between excitation and inhibition in the CNS.…”

Section: Introductionmentioning

confidence: 99%

Regulation of GABA Equilibrium Potential by mGluRs in Rat Hippocampal CA1 Neurons

et al. 2015

View full text Add to dashboard Cite

The equilibrium potential for GABA-A receptor mediated currents (EGABA) in neonatal central neurons is set at a relatively depolarized level, which is suggested to be caused by a low expression of K+/Cl- co-transporter (KCC2) but a relatively high expression of Na+-K+-Cl- cotransporter (NKCC1). Theta-burst stimulation (TBS) in stratum radiatum induces a negative shift in EGABA in juvenile hippocampal CA1 pyramidal neurons. In the current study, the effects of TBS on EGABA in neonatal and juvenile hippocampal CA1 neurons and the underlying mechanisms were examined. Metabotropic glutamate receptors (mGluRs) are suggested to modulate KCC2 and NKCC1 levels in cortical neurons. Therefore, the involvement of mGluRs in the regulation of KCC2 or NKCC1 activity, and thus EGABA, following TBS was also investigated. Whole-cell patch recordings were made from Wistar rat hippocampal CA1 pyramidal neurons, in a slice preparation. In neonates, TBS induces a positive shift in EGABA, which was prevented by NKCC1 antisense but not NKCC1 sense mRNA. (RS)-a-Methyl-4-carboxyphenylglycine (MCPG), a group I and II mGluR antagonist, blocked TBS-induced shifts in both juvenile and neonatal hippocampal neurons. While blockade of mGluR1 or mGluR5 alone could interfere with TBS-induced shifts in EGABA in neonates, only a combined blockade could do the same in juveniles. These results indicate that TBS induces a negative shift in EGABA in juvenile hippocampal neurons but a positive shift in neonatal hippocampal neurons via corresponding changes in KCC2 and NKCC1 expressions, respectively. mGluR activation seems to be necessary for both shifts to occur while the specific receptor subtype involved seems to vary.

show abstract

Theta-bursts induce a shift in reversal potentials for GABA-A receptor-mediated postsynaptic currents in rat hippocampal CA1 neurons

Cited by 9 publications

References 22 publications

Frequency-Dependent Glycinergic Inhibition Modulates Plasticity in Hippocampus

Frequency-Dependent Glycinergic Inhibition Modulates Plasticity in Hippocampus

The influence of stress at puberty on mood and learning: Role of the α4βδ GABAA receptor

Regulation of GABA Equilibrium Potential by mGluRs in Rat Hippocampal CA1 Neurons

Contact Info

Product

Resources

About