# Enhancing the function of hippocampal neurons after TBI

> **NIH NIH R01** · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · 2021 · $545,095

## Abstract

Abstract. The cognitive impairments that occur after a concussion (or mild TBI) can be long-lasting, and can
interfere with every day activities. These deficits, especially memory dysfunction, are often due to perturbations
of hippocampal function. In vivo recordings of neural activity in behaving animals have demonstrated that the
firing of a subset of pyramidal neurons in the hippocampus increases when an animal moves through its
environment. These cells, referred to as “place cells”, display localized firing patterns (i.e. place fields) that the
animal uses to recognize an environment. Thus, a failure to form stable place fields has been linked to learning
and memory dysfunction. Evidence has shown that theta oscillations (a rhythmic firing pattern seen in the
hippocampus) play an important role in modulating place field stability, and in learning and memory. This rhythm
is established by connections between inhibitory neurons present in the medial septum and the hippocampus.
We present supportive results to indicate that the number of parvalbumin-expressing inhibitory neurons in the
CA1 subfield of the hippocampus is decreased after a fluid percussion injury (FPI), an effect that occurs in the
absence of overt loss of pyramidal neurons. Associated with this loss, electrophysiological recordings revealed
a decrease in theta power and place cell instability that are evident for weeks after brain injury. The transcription
factor cAMP response element binding protein (CREB) is phosphorylated and increases neuroplasticity-related
gene expression following phosphorylation by specific protein kinases, and has been shown to be critical for
place cell stability. Based on these results, we propose to test the hypothesis that stimulation of hippocampal
CA1 pyramidal neurons at theta frequency or pharmacological potentiation of CREB will increase place cell
function and improve memory formation in the chronic stage of FPI. The results from these proposed studies
will reveal the neural basis for memory dysfunction and potential pharmacological strategy to restore neural
function and improve learning and memory during subacute/chronic stage of traumatic brain injury.

## Key facts

- **NIH application ID:** 10211632
- **Project number:** 1R01NS118329-01A1
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
- **Principal Investigator:** PRAMOD K DASH
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $545,095
- **Award type:** 1
- **Project period:** 2021-06-01 → 2026-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10211632

## Citation

> US National Institutes of Health, RePORTER application 10211632, Enhancing the function of hippocampal neurons after TBI (1R01NS118329-01A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10211632. Licensed CC0.

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