# From Molecules to Behavior: The Role of Homeostatic Synaptic Scaling in Associative Learning and Memory

> **NIH NIH F31** · BRANDEIS UNIVERSITY · 2020 · $31,402

## Abstract

Project Summary
A central goal of neuroscience research is to advance our understanding of the cellular physiology
underlying learning and memory processes. The most extensively studied model for how
associative learning is achieved at the cellular level is the Hebbian modification of synapses.
However, computational modeling studies have demonstrated that these forms of plasticity follow
positive feedback rules, making them inherently destabilizing in nature. Without additional
features, Hebbian plasticity could give way to “unconstrained” changes in synaptic strengths,
resulting in the disruption of associative learning. Homeostatic synaptic plasticity is hypothesized
to be the basis for neural-network stability during learning-driven changes of synaptic strength.
Synaptic scaling, the most extensively studied form of homeostatic synaptic plasticity, functions
as a negative-feedback mechanism, bidirectionally regulating synaptic strengths, in a cell-
autonomous manner, to maintain an activity set point. Synaptic scaling is thus hypothesized to
constrain the positive feedback nature of Hebbian mechanisms while simultaneously preserving
circuit features permissive to learning. Despite its potential to impact our current understanding
of associative learning processes, this hypothesis remains untested and the consequences of
disrupted synaptic scaling on learning remain unknown. This proposal aims to determine
the role of homeostatic synaptic scaling in associative learning and memory using a
conditioned taste aversion (CTA) paradigm in rats. First, I will confirm that I can induce
and block synaptic scaling in gustatory cortex using in-vivo chronic TTX infusions and ex-vivo
acute slice electrophysiology. Second, I aim to characterize the effects of synaptic scaling loss on
engram excitability. I will train rats on a CTA behavior paradigm and then perform
immunofluorescent staining to characterize the time course of learning-driven changes in CTA
engram neuron excitability. Then, I will use a combination of ex-vivo acute slice electrophysiology
and virus mediated targeting of CTA engram neurons to characterize the impact of blocked
homeostatic plasticity on the underlying cellular physiology of associative learning. Lastly, I will
determine the role of homeostatic plasticity in memory acquisition & extinction using behavioral
training and ex-vivo recordings of CTA engram cells. These experiments will elucidate the
behavioral consequences of loss of homeostatic plasticity. Moreover, this research proposal will
advance our current understanding of the associative learning and memory mechanisms
underlying behavior.

## Key facts

- **NIH application ID:** 9978157
- **Project number:** 5F31NS108506-03
- **Recipient organization:** BRANDEIS UNIVERSITY
- **Principal Investigator:** Raul Arturo Ramos
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $31,402
- **Award type:** 5
- **Project period:** 2018-08-01 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9978157

## Citation

> US National Institutes of Health, RePORTER application 9978157, From Molecules to Behavior: The Role of Homeostatic Synaptic Scaling in Associative Learning and Memory (5F31NS108506-03). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/9978157. Licensed CC0.

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