# AGE, AXON INJURY AND MOTOR NEURON SYNAPTOLOGY

> **NIH NIH R01** · BOSTON UNIVERSITY MEDICAL CAMPUS · 1991 · $132,397

## Abstract

When the axon of a motor neuron is injured, the neuron loses much of its
central afferent connectionns.  These central changes are reversed when
the axons restore appropriate peripheral contacts.  This proposal aims
to examine the changing synaptic relationships of injured facial motor
neurons following crush injury of the facial nerve in young (3 month)
and middle aged (15 month) rats.  The model for this analysis is ideal
because the facial nucleus is a homogeneous population of motor neurons,
its afferent innervation is well characterized, and it loses no neurons
with advancing age.  Our preliminary studies suggest that recovery of
central afferent connections may be incomplete in older animals
following peripheral reinnervation.

The facial motor nucleus will be examined using morphometry and electron
microscope immunocytochemistry to determine the identity of terminals
showing GABA-like, serotonin-like and noradrenalin-like
immunoreactivity.  Standard procedures of fine structure morphometry
(including reconstruction from serial thin sections) will establish a
"catalog" of all morphological types of axon boutons in the normal
facial nucleus.  Following axon crush the response of the identified
terminals will be characterized as to their fate and recovery, as will
the response of the neurons and neuroglial cells.  In addition,
autoradiographic analysis will determine the dynamics of loss and
recovery of postsynaptic GABA-A, serotonin IA and 2, and Beta-
adrenoceptor ligand binding.  Receptor dynamics will be correlated with
binding to serotonin and noradrenalin uptake sites and presynaptic
receptors.  These studies will establish a bridge between the results of
anatomical, immunocytochemical and pharmacological approaches to the
investigation of the effects of advancing age on motor neuron response
to injury.

Given the crucial role of these synaptic connections and receptors in
neuronal excitability and calcium mobilization it is important to
understand how advancing age compromises the ability of neurons to
recover from peripheral nerve injury.  Such understanding is important
to the development of therapeutic intervention designed to improve nerve
regeneration.

## Key facts

- **NIH application ID:** 3121804
- **Project number:** 1R01AG009869-01
- **Recipient organization:** BOSTON UNIVERSITY MEDICAL CAMPUS
- **SAM.gov UEI:** FBYMGMHW4X95
- **Principal Investigator:** DEBORAH W VAUGHAN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $132,397
- **Award type:** 1
- **Project period:** 1991-06-01 → 1994-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3121804

## Citation

> US National Institutes of Health, RePORTER application 3121804, AGE, AXON INJURY AND MOTOR NEURON SYNAPTOLOGY (1R01AG009869-01). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3121804. Licensed CC0.

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