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W. Hamish Mehaffey  PhD
BSc University of Victoria
PhD Neuroscience University of Calgary 2008
PhD Dissertation: Synaptic regulation of burst discharge

Current Gig:
Postdoctoral Fellow
Keck Center for Integrative Neuroscience
HSE 804, Box 0444
513 Parnassus Ave
San Francisco CA
whmehaff@phy.ucsf.edu

Training
1999
BSc Psychology
University of Victoria
Victoria BC

2001 - 2008
PhD Neuroscience
University of Calgary
Calgary Alberta
Supervisor: R.W. Turner

2006
Teaching Asst. - Methods Computational Neuroscience
                         Wood's Hole MA
2007
Teaching Asst. - Computational Neuroscience Ottawa ON
Special Courses
2005
Wood's Hole Marine Biological Laboratories
Methods in Computational Neuroscience

2006 Center for Non-linear dynamics, McGill Univ.
Non-Linear Dynamics in Physiology and Medicine
Awards
MSc
Province of Alberta Graduate Scholarship
Faculty of Gradute Studies Scholarship
Alberta Learning Scholarship


PhD
CIHR Doctoral Award
Dean's Research Excellence Award
AHFMR Studentship
Society Neuroscience Chapter Graduate Student Travel Award

PDF
Grass Fellowship - Independent Project at Wood's Hole MA
CIHR Postdoctoral Fellowship, UCSF

Research Focus: The synaptic regulation of input-output relations
Approach: I use a combination of intracellular recordings in vitro and conductance-based modeling to determine the relative contribution of voltage- or ligand-gated channels to the input-output relation of ELL pyramidal cells.
Techniques: In vitro slice preparations, computational neuroscience
Below are short summaries of my projects published from the lab.
Backpropagation in ELL pyramidal cells

Model - ELL pyramidal cell burst discharge
    Pyramidal cells of the electrosensory lobe (ELL) of weakly electric fish encode modulations in external electric fields by generating spike bursts. These bursts arise by a "conditional backpropagation" of sodium spikes from the soma and over the proximal apical dendrites that re-excite the soma as a depolarizing afterpotential (DAP). A frequency-dependent mismatch in refractory period between soma and dendrite leads to burst discharge through a cyclic failure of backpropagation. PDF

Scanning EM image of Spread-printed ELL Obtaining patch clamp recordings in the adult CNS
    Patch clamp recordings are often difficult to obtain beyond P17 due to a peri-neuronal net in the extracellular space. I helped develop a method of "spread-printing", a novel approach to partially dissociate tissue slices and remove the peri-neuronal net. We showed that spread-printing allows recordings from identified cells down to the single channel level in animals that are months old without the need for proteolytic enzymes. See Morales et al. (2004).  PDF

Kv3 K+ currents in ELL pyramidal cell Kv3 potassium channels exhibit frequency-dependent effects on cell output
    This study describes a frequency-dependent effect of high threshold Kv3 potassium channels on the input-output relation of pyramidal cells and determined its underlying basis. A combination of patch recordings and modeling show that Kv3 channels rescue spike trains at high frequencies by decreasing both sodium channel inactivation and a cumulative increase in a low threshold potassium current. See Fernandez et al. (2005) PDF
Kv1 K+ channels regulate the climbing fiber EPSP Kv1 potassium channels optimize rebound discharge in deep cerebellar neurons
    In this study we examined the role of low threshold Kv1 K+ channels in controlling Purkinje cell discharge and its effect on the activity of postsynaptic deep cerebellar neurons. We show that Kv1 channels lower Na+ spike frequency and raise the threshold for Ca2+ spike discharge. When these spike patterns are applied as stimulus templates to Purkinje cell axons, we found that Kv1 channels lower Purkinje cell output frequency to a range that optimizes rebound discharge in deep cerebellar neurons. See McKay et al. (2005) PDF
Kv3 K+ currents in ELL pyramidal cell A decrease in dendritic excitability can increase cell output
    This study describes how a progressive inactivation of dendritic Na+ channels during repetitive activity can shift the relation between somatic and dendritic spike timing. A progressive delay in dendritic spike latency increases its effectiveness at generating a depolarizing afterpotential at the soma, leading to a paradoxical increase in somatic spike output in the face of a decrease in dendritic excitability. See Fernandez et al. (2005) PDF
Gain control in ELL pyramidal cell Dendritic inhibition mediates a deterministic gain control
    This study describes a novel mechanism of multiplicative gain control that involves active dendritic membrane. Most gain control mechanisms require noisy inputs, however this mechanism allows a modulation of gain in a purely deterministic fashion. This allows gain control in the absence of the deleterious effects of noise. See Mehaffey et al. (2005) PDF
Measurement of stellate first spike latency A-type K+ and T-type Ca2+ channels generate a novel first spike latency relationship
    In this study we examined the mechanism underlying a non-monotonic voltage - first spike latency relationship in cerebellar stellate cells. We show through current and voltage clamp analysis and modeling that A-type and T-type inactivating channels interact to produce a voltage-dependent increase or decrease in first spike latency. The effect depends critically on the voltage-dependence of inactivation and relative density of the respective currents. See Molineux et al. (2005) PDF
Rebound burst discharge in deep cerebellar neurons T-type Ca2+ channel isoforms correlate with distinct burst phenotypes
    In this study we determined the distribution of the three isoforms of T-type currents (Cav3.1, 3.2, 3.3) in rat cerebellar neurons, revealing a greater range of expression and contribution to rebound discharge than realized. Moreover, a distinct expession pattern for Cav3 isoforms in deep cerebellar nuclear neurons is shown to correlate to either a strong or weak rebound discharge capability. See Molineux et al. (2006). PDF
CF discharge converts Purkinje cell output Climbing fiber input regulates intrinsic properties of Purkinje cells
    In this study we show that climbing fiber input activated at physiological frequencies blocks an intrinsic trimodal pattern inherent to Purkinje cells studied in vitro, restoring tonic Na+ spike discharge similar to that found in vivo. Moreover, all the effects of direct climbing fiber stimulation were reproduced by simulating climbing fiber input with an injected EPSC in the presence of synaptic blockers, emphasizing a key role for the postsynaptic complex spike depolarization in determining Purkinje cell activity. See McKay et al. (2007).
Dendritic GABA-B activation promotes burst discharge Dendritic GABA-B receptors delay dendritic spikes to enhance burst output
    In this study I show that activation of dendritic GABAB receptors by a feedback inhibitory pathway delays the onset of a backpropagating dendritic spike to shift the soma-dendritic temporal relationship in spike discharge. A resulting increase in burst output ultimately serves to increase spike train segregation to improve the encoding of fast frequency inputs. See Mehaffey et al. (2007).
SK potassium channels underlie a component of frequency tuning across multiple sensory maps SK channel-mediated AHPs differentially regulate frequency tuning
    This study describes how a selective expression of SK2 channels can shift the frequency preference of principle sensory neurons. By regulating burst discharge, somatic SK2 channels selectively decrease the low-frequency response of ELL pyramidal cells, creating a comparatively broadband response. In support of this, SK2 channel expression is localized to cells that exhibit broadband frequency responses but is absent in cells with a low-frequency preference. See Ellis, Mehaffey et al. (2007).
Coherence plot of ELL pyramidal cell Pyramidal cell firing characteristics differ across multiple sensory maps
    The ELL of weakly electric fish has multiple sensory maps that have specific behavioural functions related to their frequency tuning. In this study we show that the intrinsic spike generating mechanism can contribute significantly to determining which specific frequency components of a broadband input a neuron responds to. As such, it reveals a direct relationship between ion channels controlling spike discharge and sensory processing. See Mehaffey et al. (2008).
Coherence plot of ELL pyramidal cell Distinct ion channel contributions to burst phenotype in deep cerebellar neurons
    The large diameter putative projection neurons of rat deep cerebellar nuclei have been shown to generate either a Transient or Weak rebound Burst phenotype that was linked to the selective expression of T-type calcium channel isoforms. Here we show that the two burst phenotypes also reflect a differential functional availability of LVA T type calcium current at burst threshold, and different contributions of repolarizing potassium currents that shape burst properties. See Molineux et al. (2008). PDF
On-cell and Whole-cell recording of DCN cell rebound Synaptically evoked rebound bursts in deep cerebellar neurons
    Rebound burst discharge in deep cerebellar nuclear (DCN) cells is readily evoked through direct current injection, but the probability of evoking rebounds with inhibitory synaptic stimulation is less certain. Here we show that stimulation of Purkinje cell inhibitory inputs to DCN neurons in vitro evokes rebound bursts that can be distinguished according to two phenotypes of burst output. Reliable rebound burst generation can be evoked with moderate stimulus intensities, indicating the potential for this activity to contribute to cerebellar output in response to physiological activity in vivo. See Tadayonnejad et al. (2009). PDF
KChiP3 mediated shift in Kv4 inactivation A Cav3-Kv4 signaling complex regulates A type current and neuronal activity
   A-type potassium channels of the Kv4 family regulate the latency and frequency of spike output in numerous CNS cells. Kv4 channels complex with Potassium Channel Interacting Proteins (KChIPs), a family of calcium sensor proteins that should confer calcium sensitivity. However, neither the physiological source for calcium nor its effects on A-type current were known. Here we show that T-type (Cav3) calcium channels associate with the Kv4 complex to selectively modulate Kv4 inactivation and establish function in a physiological range. See Anderson et al. (2010).
Cav3.1 channels link to Kv4.2 channels The Cav3.1 calcium channel modulates Kv4.2 voltage for inactivation
   Here we show that the Cav3.1 (T-type) calcium channel isoform also associates with the Kv4.2 complex to selectively right-shift Kv4 inactivation, but to a lesser extent than for other Cav3 channel isoforms. A link between Cav3.1 and Kv4.2 is further indicated through coimmunoprecipitation and pulldowns with Cav3.1 fusion proteins.
See Anderson et al. (2010b), Addendum.
IT and IH have distinct roles in DCN cell rebound responses Distinct roles for IT and IH in controlling deep cerebellar rebound responses
   Here we examined the role for IT and IH in generating the rebound responses that are evoked in deep cerebellar neurons in response to inhibitory input from Purkinje cells. We used recordings in vitro and modeling to find that only a small fraction of the total IT and IH available to a cell are activated by physiological levels of hyperpolarization. However, the currents activated are still sufficient to differentially control the latency, frequency and precision of spike firing during the immediate phase of a rebound response. See Engbers et al. (2011).
Charybdotoxin slows the rate or repolarization of the parallel fiber-evoked EPSP An intermediate conductance KCa channel modifies parallel fiber EPSPs in Purkinje cells
   Purkinje cells were known to express the two KCa channels typically found in central neurons (SK and BK channels). This study reports that the intermediate conductance KCa channel (KCa3.1) is also expressed in Purkinje cells and is linked to Cav3.2 T-type calcium channels. KCa3.1 is activated during the parallel fiber EPSP to increase the EPSP rate of decay and generate a long duration AHP to suppress temporal summation of low frequency EPSPs, allowing Purkinje cells to respond to sensory-like bursts of parallel fiber input. See Engbers et al. (2012).
A Cav3-Kv4 complex acts as a novel calcium sensor in stellate cells A novel calcium sensor dynamically adjusts inhibitory charge transfer to Purkinje cells
   Stellate cells were known to inhibit complex spikes of Purkinje cells but a mechanism that would allow them to respond to local repetitive climbing fiber input was unknown. This study shows that a Cav3-Kv4 complex expressed in stellate cells acts as a novel calcium sensor to dynamically adjust stellate cell frequency in relation to changes in [Ca]o during complex spike discharge. Inhibitory charge transfer to Purkinje cells is thus maintained in the face of a synaptically evoked decrease in [Ca]o that would otherwise alter network function. See Anderson et al. (2013).

Peer-reviewed Publications

Morales E, Fernandez FR, Sinclair S, Molineux ML, Mehaffey WH and Turner RW. (2004)   Releasing the peri-neuronal net to patch clamp neurons in the adult CNS. Pflugers Archiv 448(2): 248-58. PDF

McKay BE , Molineux ML, Mehaffey WH and Turner RW. (2005) Kv1 potassium channels control Purkinje cell output to facilitate post-synaptic rebound discharge in deep cerebellar neurons. J. Neuroscience 25(6): 1481-1492. PDF

Fernandez FR*, Mehaffey WH*, Molineux ML and Turner RW. (2005) High threshold potassium channels increase gain by offsetting a frequency-dependent increase in low threshold potassium current. (*shared first author) J. Neuroscience 25(2): 363-371. PDF    Faculty of 1000 citation.

Fernandez FR, Mehaffey WH and Turner RW. (2005) Dendritic Na+ current inactivation can increase cell excitability by delaying a somatic depolarizing afterpotential. J. Neurophysiology 94: 3836-3848.PDF

Mehaffey WH, Doiron B, Maler L and Turner RW. (2005) Deterministic multiplicative gain control with active dendrites. J. Neuroscience 25(43): 9968-9977. PDF

Molineux ML*, Fernandez FR*, Mehaffey WH and Turner RW (2005) A-type and T-type currents interact to produce a novel spike latency-voltage relationship in cerebellar stellate cells. J. Neuroscience 25(47): 10863-10873. * Shared first author. PDF

Molineux ML, McRory JE, McKay BE, Hamid J, Mehaffey WH, Snutch TP, Zamponi GW and Turner RW (2006) Specific T-type calcium channel isoforms are associated with distinct burst phenotypes in deep cerebellar nuclear neurons. PNAS 103(14): 5555-5560. PDF Supplementary data

McKay BE, Engbers JT, Mehaffey WH, Gordon G, Molineux ML, Bains J and Turner RW (2007) Climbing fiber discharge regulates cerebellar functions by controlling the intrinsic characteristics of Purkinje cell output. J. Neurophysiology
97: 2590-2604. PDF

Mehaffey WH, Fernandez FR, Maler L and Turner RW (2007) Regulation of burst dynamics improves differential encoding of stimulus frequency by spike train segregation. J. Neurophysiology 98(2): 939-951. PDF

Ellis L*, Mehaffey WH*, Harvey-Girard E, Turner RW, Maler L and Dunn RJ (2007) SK channels provide a novel mechanism for the control of frequency tuning in electrosensory neurons. J. Neuroscience 27 (35): 9491-9502. *Shared first author. PDF

Mehaffey, W.H., Maler, L. and Turner, R.W. (2008) Intrinsic frequency tuning in ELL pyramidal cells varies across electrosensory maps. J. Neurophysiology
99(5): 2641-2655. PDF

Molineux, M.L., Mehaffey, W.H., Tadayonnejad, R., Anderson, D., Tennent, A.F. and Turner, R.W. (2008) Ionic factors governing rebound burst phenotype in rat deep cerebellar neurons. J. Neurophysiology 100:2684-2701. PDF

Tadayonnejad, R., Mehaffey, W.H., Anderson, D. and Turner, R.W. (2009) Reliability of triggering postinhibitory rebound bursts in deep cerebellar neurons. Channels 3(3):149-155. PDF

Anderson, D.M., Mehaffey, W.H., Iftinca, M., Rehak, R., Engbers, J.D.T., Hameed, S., Zamponi, G.W. and Turner, R.W.  (2010) Regulation of neuronal activity by Cav3-Kv4 channel signaling complexes.  Nature Neuroscience 13: 333-337. Link   Faculty of 1000 citation.

Anderson, D., Rehak, R., Hameed, S., Mehaffey, W.H., Zamponi, G.W. and Turner, R.W. (2010) Regulation of the Kv4.2 complex by Cav3.1 channels. Channels
4(3): 163-167. Open Access PDF.

Engbers, J.D.T.*, Anderson, D.*, Tadayonnejad, R.*, Mehaffey, W.H., Molineux, M.L. and Turner, R.W. (2011) Distinct roles for IT and IH in controlling the frequency and timing of rebound spike responses. J. Physiol (Lond.), 589 (Pt 22): 5391-413. * Shared first authors.

Engbers, J.D.T.*, Anderson, D.*, Asmara, H., Rehak, R., Mehaffey, W.H., Hameed, S., McKay, B.E., Kruskic, M., Zamponi, G.W. and Turner, R.W. (2012) Intermediate conductance calcium-activated potassium channels modulate summation of parallel fiber input in cerebellar Purkinje cells. PNAS 109 (7): 2601-2606. * Shared first authors. Faculty of 1000 citation. PDF

Anderson, D.*, Engbers, J.D.T.*, Heath, N.C., Bartoletti, T.M., Mehaffey, W.H., Zamponi, G.W., and Turner, R.W. (2013) The Cav3-Kv4 complex acts as a calcium sensor to maintain inhibitory charge transfer during extracellular calcium fluctuations. J. Neuroscience 33: 7811-7824. * Shared first authors. PDF


Invited Chapters

Mehaffey WH*, Fernandez FR*, Rashid AJ, Dunn RJ and Turner RW (2006) The distribution and function of potassium channels in aperonotid electrosensory lateral line lobe. J. Comp. Physiol. A, Neuroethol Sens Neural Behav Physiol. 20:1-12. *Shared first authorship. PDF

Mehaffey WH, Fernandez FR, Doiron B, and Turner RW. (2008) Regulation of somatic firing dynamics by backpropagating dendritic spikes. J. Physiol. (Paris) 102: 181-194. PDF

Mehaffey WH*, Ellis LD*, Krahe R, Maler L, Dunn RJ and Chacron MJ. (2008) Ionic and neuromodulatory regulation of burst discharge. J. Physiol. (Paris) 102: 195–208. *Shared Authorship. PDF

Tadayonnejad, R., Anderson, D., Molineux, M.L., Mehaffey, W.H., Jayasuriya, K. and Turner, R.W. (2011) Rebound discharge in deep cerebellar nuclear neurons in vitro. Cerebellum 9(3): 352-374. PDF


Invited Talks

- 2005 - Deterministic Multiplicative Gain Control From Active Dendrites, Computational Neuroscience 2005, Madison, WI.

- 2006 - Burst regulation alters spike segregation in the ELL of electric fish, Institute for Theoretical Biology, Humboldt University, Berlin.

- 2007 - Regulation of spike train segregation in electrosensory processing, Stanford University, CA.

Key Abstracts
Fernandez FR, Mehaffey WH, Rashid AJ, Dunn RJ and Turner RW. Kv3 channel contribution to repetitive spike activity. Ann Proc Soc Neurosci 2003.

Fernandez FR,
Mehaffey WH, Molineux ML and Turner RW. High threshold K+ channels increase gain by offsetting a cumulative activation of low threshold K+ current. Ann Proc Soc Neurosci, 2004.

Mehaffey WH, Doiron B, Maler L and Turner RW. Deterministic multiplicative gain control by active dendrites. Ann Proc Soc Neurosci, 2004.

Fernandez FR, Mehaffey WH and Turner, RW. Dendritic Na+ current inactivation can increase cell excitability by delaying a somatic depolarizing afterpotential. Proc Soc Neurosci 2005.

Mehaffey WH, Fernandez FR, and Turner RW. Inhibitory GABA-B conductances cause a shift to burst firing mode. Proc Soc Neurosci, 2005.

Mehaffey WH, Fernandez FR and Turner RW. Inhibitory Dendritic GABAb Conductances can Shift Cells to Burst Firing in the ELL of electric fish. Comp Neurosci (CNS) 2006.

Mehaffey WH, Fernandez FR and Turner RW. Burst regulation regulates spike train segregation in the ELL of electric fish.Proc Soc Neurosci, 2006.

Mehaffey WH, Maler L and Turner RW. Feedback modulation of intrinsic firing dynamics restores feature detection in electrosensory processes. Comp Neurosci (CNS) 2007.

McKay BE, Engbers JDT, Mehaffey WH, Gordon GRJ, Molineux ML, Bains JS and Turner, RW. Climbing fibre control of Purkinje cell spike output. Can Assoc Neurosci 2007 [Can J. Neurol. Sci., 34 (Supplement 3): S87].

Molineux ML, Tennent AF, Mehaffey WH and Turner RW. Ionic mechanisms of spike firing in two distinct types of rat deep cerebellar neurons. Proc. Soc. Neurosci. 2007.

Tadayonnejad R, Molineux ML, Mehaffey WH and Turner RW. Transient and Weak Bursting Deep Cerebellar neurons exhibit differential coding properties for membrane hyperpolarizations. Proc. Soc. Neurosci. 2007.

Mehaffey WH, Maler L and Turner RW. Distribution of intrinsic and bursting properties of basilar and non-basilar pyramidal cells across the maps of the electrosensory lateral line lobe. Proc. Soc. Neurosci. 2007.

Tadayonnejad R, Mehaffey WH, Jayasuriya K and Turner RW. Rate and temporal coding properties of deep cerebellar neurons. Can. Assoc. Neurosci. 2008.

Mehaffey WH and Turner R.W. Feedback modulation of firing dynamics restores feature detection in electrosensory processing. Can. Assoc. Neurosci. 2008.

Engbers, J.D.T., Mehaffey, W.H., Fernandez, F.R. and Turner, R.W. Synaptic noise modulates the probability of climbing fibre-induced state transitions in cerebellar Purkinje cells. Proc. Soc. Neurosci. 2008.

Tadayonnejad, R., Mehaffey, W.H. and Turner, R.W. Deep cerebellar nuclear neurons use different strategies for coding physiological patterns of Purkinje cell activity. Proc. Soc. Neurosci. 2008.

Mehaffey, W.H. and Turner, R.W. Interaction between network and intrinsic oscillatory dynamics in electrosensory processing. Proc. Soc. Neurosci. 2008.

Tadayonnejad, R., Mehaffey, W.H., Jayasuriya, K. and Turner, R.W. Rebound burst phenotypes in Deep Cerebellar Nuclear cells define the response to synaptically evoked mem brane hyperpolarizations. Can Assoc. Neurosci. 2009.

Anderson, D.M., Mehaffey, W.H., Engbers, J.D.T., Rehak, R., Hamid, S., Zamponi, G.W. and Turner, R.W. T-type mediated calcium influx dynamically modulates Kv4 inactivation. Can Assoc. Neurosci. 2009.

Engbers, J.D.T., Mehaffey, W.H. Fernandez, F.R. and Turner, R.W. Synaptic noise modulates the probability of climbing fibre-induced state transitions in cerebellar Purkinje cells. Can Assoc. Neurosci. 2009.

Engbers, J.D.T., Mehaffey, W.H. Fernandez, F.R. and Turner, R.W. Synaptic noise modulates the probability of climbing fiber-induced state transitions in cerebellar Purkinje cells. IUPS, Kyoto 2009.

Anderson, D.M., Mehaffey, W.H., Rehak, R., Hamid, S., Zamponi, G.W. and Turner R.W. A-type potassium channels are dynamically regulated by T-type calcium current. IUPS, Kyoto 2009.

Tadayonnejad, R., Mehaffey, W.H. and Turner, R.W. Rate and temporal neural codes in deep cerebellar neurons translate Purkinje cell inhibitory input. IUPS, Kyoto 2009.

Tadayonnejad, R., Engbers, J.D.T., Anderson, D., Mehaffey, W.H. and Turner, R.W. The role of IH and IT in controlling rebound burst properties of Deep Cerebellar Nuclear cells. Can Assoc. Neurosci., 2010.

Tadayonnejad, R., Engbers, J.D.T., Anderson, D., Mehaffey, W.H. and Turner, R.W. IT and IH selectively regulate rate coding and spike precision in deep cerebellar nuclear cells. Proc. Soc. Neurosci., 2010.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Zamponi, G.W. and Turner, R.W.   T-type/IK channel signalling complex modulates summation of parallel fiber inputs in cerebellar Purkinje cells.  Can. Assoc. Neurosci. 2010.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Zamponi, G.W. and Turner, R.W.   IKCa channels establish a high pass filter for parallel fiber input in cerebellar Purkinje cells.  Gordon Conference, Cerebellum in Health and Disease, New London, NH, 2011.

Engbers, J.D.T., Anderson, D., Rehak, R., Asmara, H., Mehaffey, W.H., Hameed, S., McKay, B.E., Kruskic, M., Zamponi, G.W., Turner, R.W.  IKCa-Cav3 complex reduces temporal summation of parallel fiber input in cerebellar Purkinje cells. IBRO World Congress of Neuroscience, Florence, Italy, 2011.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Kruskic, M., Zamponi, G.W., Turner, R.W.  IKCa-Cav3 complex creates a high pass filter for parallel fiber input in cerebellar Purkinje cells. Comp. Neurosci., Stockholm, Sweden, 2011. Prize, Student Poster Presentation.

Anderson, D.*, Engbers*, J.D.T., Heath, N.C., Bartoletti, T.M., Mehaffey, W.H., Zamponi, G.W. and Turner, R.W. The Cav3-Kv4 complex acts as a calcium sensor to adaptively modulate inhibitory network function during repetitive excitatory input. Can. Assoc. Neurosci., 2013.

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