Texas Tech University

Karina Alviña, Ph.D.

Assistant Professor

Email: karina.alvina@ttu.edu

Phone: 806-834-2751


  • Postdoctoral Fellow. Department of Neuroscience. Albert Einstein College of Medicine, Bronx, NY. 2012-2016
  • Postdoctoral Fellow. Department of Neuroscience. Columbia University, New York, NY. 2009-2011
  • Ph.D. in Biological Sciences (Physiological Sciences), Pontifical Catholic University of Chile, 2008
  • B.S. in Biological sciences, Pontifical Catholic University of Chile, 2002

Lab website

Karina Alviña

Research interests

In order to successfully navigate and survive the environment most animals must learn to modify their behavior according to past experiences. This process of learning is mediated by the brain, which controls not only how animals sense their surroundings but also how they respond to changes (both positive and negative). To orchestrate the many different functions of the brain, neurons rely on exquisite communication mechanisms via cellular junctions called synapses.

We are interested in understanding how synapses work, not only in physiological conditions but also in adverse or stressful environments. The brain is central in coordinating the response to stress, and at the same time, a very sensitive target when such response is not controlled. In fact, in humans stress is associated with the onset and exacerbation of a number of brain disorders, including anxiety, depression, drug addiction, post-traumatic stress disorder, and schizophrenia.  

We will use a combination of techniques, including electrophysiology, viral genetic manipulation, optogenetics and behavior in order to characterize synaptic function in animal models (rodents).

Current interest in the lab include:

  1. Modulation of hippocampal function in conditions of chronic stress. The hippocampus is one of the brain regions directly involved in learning and memory formation. It is also one of the most sensitive areas to stress. We will study the effects of chronic and acute stress in specific hippocampal subfields.
  2. Early life stress and hippocampus. It is a well-documented fact that adverse conditions during early development can cause dramatic changes in the brain however the precise mechanism involved are far from clear. We will use a known paradigm for early stress (maternal deprivation) in order to fully characterize changes in synaptic function in the hippocampus of adult rodents exposed to maternal deprivation.
  3. The obese brain. A number of recent findings have shown how signals coming from the gut microbiota can actually modulate hormone systems and the brain. Even though this communication is essential to maintain the health of the host, it has recently been associated with a number of diseases, including obesity and even neurodevelopmental disorders. We will use a rodent model of obesity and will study brain function, both from a behavioral and cellular perspective.

Selected publications

Alviña K*, Tara E, Khodakhah K. Developmental change in the contribution of voltage-gated Ca(2+) channels to the pacemaking of deep cerebellar nuclei neurons. Neuroscience. 2016, 322:171-7. PMID: 26902515 *corresponding author

Ben-Simon Y, Rodenas-Ruano A, Alviña K, Lam AD, Stuenkel EL, Castillo PE, Ashery U. A Combined Optogenetic-Knockdown Strategy Reveals a Major Role of Tomosyn in Mossy Fiber Synaptic Plasticity. Cell Rep. 2015; 12 (3):396-404.PMID: 26166572 3.

Alviña K, Sawtell NB. Sensory processing and corollary discharge effects in posterior caudal lobe Purkinje cells in a weakly electric mormyrid fish. J Neurophysiol. 2014; 112(2):328-39. PMID: 24790163

Kennedy A, Wayne G, Kaifosh P, Alviña K, Abbott LF, Sawtell NB. A temporal basis for predicting the sensory consequences of motor commands in an electric fish. Nat Neurosci. 2014; 17(3):416-22. PMID: 24531306

Alviña K, Khodakhah K. The therapeutic mode of action of 4-aminopyridine in cerebellar ataxia. J Neurosci. 2010; 30(21):7258-68.PMID: 20505092

Alviña K, Khodakhah K. KCa channels as therapeutic targets in episodic ataxia type-2. J Neurosci. 2010; 30(21): 7249-57 PMID: 20505091

Alviña K, Ellis-Davies G, Khodakhah K. T-type calcium channels mediate rebound firing in intact deep cerebellar neurons. Neuroscience. 2009; 158(2):635-41 PMID: 18983899

Alviña K, Walter JT, Kohn A, Ellis-Davies G, Khodakhah K. Questioning the role of rebound firing in the cerebellum. Nat Neurosci. 2008; 11:1256-8. PMID: 18820695

Alviña K, Khodakhah K. Selective regulation of spontaneous activity of neurons of the deep cerebellar nuclei by N-type calcium channels in juvenile rats. J Physiol. 2008; 586 (10):2523-38 PMID: 18372310

Walter JT, Alviña K, Womack MD, Chevez C, Khodakhah K. Decreases in the precision of Purkinje cell pacemaking cause cerebellar dysfunction and ataxia. Nat Neurosci. 2006; 9 (3):389-97 PMID: 16474392

Department of Biological Sciences

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    Department of Biological Sciences, Texas Tech University, Box 43131 Lubbock, TX 79409
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