National Institutes of Health
Weizmann Institute of Science
Degree: Doctor of Philosophy in Biophysics
University of California
Degree: Bachelor of Science in Biochemistry
Memory acquisition, retention and learning is influenced by various neurological and
neuropsychiatric conditions. My laboratory is focused on elucidating functional changes
in signaling and circuitry in different parts of the brain as a result of normal aging,
or as a result of neuropsychiatric disease such as depression or neurological disease
such as epilepsy.
Modulation of Synaptic and Extra-Synaptic Plasticity
Long term changes in rapid electrical signaling between neurons (plasticity) may be
a mode of memory storage within our brains. Memory acquisition, retention and learning
is influenced by various neurological and neuropsychiatric conditions. My laboratory
is focused on elucidating functional changes in signaling and circuitry in different
parts of the brain as a result of normal aging, or as a result of neuropsychiatric
disease such as depression or neurological disease such as epilepsy. We use electrophysiological
techniques combined with optogenetics and mouse models to measure changes in postsynaptic
potentials as well as action potentials in the prefrontal cortex and hippocampus.
The hippocampus is associated with spatial and temporal learning and memory, while
the prefrontal cortex is involved in higher brain function including facets of memory
and attention. Among the projects currently running in the laboratory are:
Cognitive Impairment in Epilepsy - The epileptic state is caused by an imbalance of excitation and inhibition in brain
circuitry, such that excitation exceeds inhibition. Often, patients with epilepsy
have co-morbid cognitive impairment which can affect their quality of life. Using
animal models of epilepsy, we investigate what differences exist in induction of long-term
plastic changes in rapid electrical signaling within and between neurons.
Cognitive Impairment in Depression - Lack of Serotonin is associated with a clinically depressed state, as SSRIs (selective
serotonin reuptake inhibitors) can be used as anti-depressants. How does serotonin
affect neuronal communication? Is the ability to cause long term changes in plasticity
influenced by serotonin?
Cognitive Impairment in Alzheimers Disease - Amyloid Beta is a protein associated with the pathophysiology of Alzheimers Disease.
Various animal models exist to mimic the human pathology. One of the hallmark features
of Alzheimers Disease is the inability to acquire new memories. What causes Alzheimers
Disease to express itself behaviorally later in life? We are testing one such model
to determine if circuitry changes associated with memory acquisition coincide with
behavioral testing of memory over the lifespan of the animal.
Other projects also available.
Carpenter-Hyland E, Bichler EK, Smith M, Sloviter RS, Benveniste M (2017) Epileptic pilocarpine-treated rats exhibit aberrant hippocampal EPSP-spike
potentiation but retain long-term potentiation. Physiol Rep 5:e13490.
Weeks AM, Harms JE, Partin KM, Benveniste M (2014) Functional insight into development of positive allosteric modulators of AMPA receptors. Neuropharmacology 85:57-66.
Inagaki A, Frank CA, Usachev YM, Benveniste M, Lee A (2014) Pharmacological Correction of Gating Defects in the Voltage-Gated Cav2.1 Ca2+ Channel due to a Familial Hemiplegic Migraine Mutation. Neuron 81:91-102.
Harms JE, Benveniste M, Kessler M, Stone LM, Arai AC, Partin KM (2014) A Charge-inverting Mutation in the "Linker" Region of alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptors Alters Agonist Binding and Gating Kinetics Independently of Allosteric Modulators. The Journal of biological chemistry 289:10702-10714.
Harms JE, Benveniste M, Maclean JKF, Partin KM, Jamieson C (2013) Functional analysis of a novel positive allosteric modulator of AMPA receptors derived from a structure-based drug design strategy. Neuropharmacology 64:45-52.
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