Meera Pratap, Ph.D.

Meera Pratap, Ph.D.


(310) 206-5274

Department of Neurobiology 10833 Le Conte Avenue, Rm 63-234 CHS Los Angeles, CA 90095-1763 (Campus Mail Code 176318)


Dr. Meera Pratap’s primary interest is to understand how membrane proteins (ion channels, transporters and receptors) contribute to membrane and signaling properties of neurons and muscle cells. As a postdoctoral fellow with Drs. Toro and Stefani (Anesthesiology UCLA), she characterized large conductance voltage and calcium-activated potassium channels (MaxiK) in heterologous expression systems (oocytes and mammalian cell lines) and showed that four tissue specific modulatory beta subunits are to large extent responsible for the key functional properties of MaxiK channels found in native tissues (series of four PNAS papers). After joining Tom Otis in the Department of Neurobiology in 2002, she tagged the glutamate transporters with GFP to understand how they are trafficked into peri/postsynaptic neuronal membranes in response to metabotropic Glutamate receptor activation.

In collaboration with Drs. Wallner and Olsen (ULCA, Pharmacology) she characterized the unique pharmacology of extrasynaptic GABA(A) receptors containing the delta subunit, in particular their involvement in the actions of alcohol and anesthetics. She characterized three ataxic mouse models in native neurons in brain slices. One induced ataxia (irregular pacing-making and death of cerebellar Purkinje neurons (PN) in collaboration with Dr. Black, UCLA) by deleting the alternative splicing factor Rbfox (1,2,3) proteins (Gehman et al., Genes and Development 2012), the other is a triplet repeat mouse model of spinocerebellar ataxia (SCA2, in collaboration with Dr. Pulst, Univ. of Utah) (Hansen & Meera (co-first author) et al., Human Mol. Genetics, 2013), where decreased intrinsic firing frequency precedes degeneration of Purkinje cells and phenotypic disease progression. Further, she showed the mechanism contributing to PN dysfunction and loss in SCA2 (Meera et al. eLife 2017). The team achieved a true breakthrough showing that antisense oligonucleotides (Ionis Pharmaceuticals) against SCA2 normalizes Purkinje cell firing frequency and the ataxic phenotype in the SCA2 mouse model, paving the way for clinical trials to treat patients suffering from devastating ataxias (Scoles D, Meera P et al., Nature 2017) and nucleotide repeat expansion diseases in general, by reducing the amounts of accumulating toxic mRNAs (Sareen …Meera  et al., Sci Transl Med 2013). The third ataxic model she characterized is the Missing-in-Metastasis (MIM/MTSS1) KO mouse in collaboration with Dr. Oro (Stanford University). She showed that the tyrosine-kinase inhibitor Dasatinib (a leukemia drug) leads to an almost complete rescue of the MIM-KO electrophysiological phenotype. Most excitingly, she showed that Dasatinib also partially rescues PN firing frequency in SCA2, suggesting that tyrosine kinase hyperactivity might be a common mechanism of cerebellar ataxias, an exciting finding that potentially could lead to clinical treatments of these devastating diseases (Brown AS, Meera P, et al, PNAS 2018; Brown AS, Meera  P, et al., Cell Cycle 2020).

Most recently her collaborations have included Drs. Krantz, Donlea and Lawal where she works on challenging electrophysiologidal recordings from GFP labeled neurons in Drosophila melanogaster. With Drs. Krantz and Schweizer she studied the effects of Ziram, a fungicide that increases the risk for Parkinson’s disease in humans. She showed that Ziram increases the excitability of octopaminergic neurons in the adult abdominal ganglion of Drosophila melanogaster (Harrigan, Neurobiology of Disease, 2020). With Dr. Donlea, she records from neurons involved in sleep in Drosophila to unravel the molecular mechanisms of sleep and study the effects of aging and neurotransmitters on sleep (Dr..Donlea) and projection neurons in aging (Dr. Lawal).

In collaboration with Drs. Lipshutz and Wallner she has been instrumental to show that some guanidino compounds, like guanidinoacetate, that accumulate in the brain in a urea-cycle disorders and creatine deficiency disorders are highly potent GABA(A) receptor agonists and mimetics, and this likely mediates the neurotoxic action of guanidinoacetate accumulation in the brain (Meera et al., J Neurochem 2023).

In addition to her research activities, she has also contributed significant service to the Department, safety compliance and overseeing core research facilities used by dozens of Departmental staff.

A full list of Dr. Meera Pratap’s  publications is available online: or