Transcript substrates for vestibular input to head direction cells

Polysynaptic pathways from the
vestibular nuclei to the lateral mamillary
nucleus of the rat: substrates for
vestibular input to head direction cells
J. E. Brown, J. P. Card, B. J. Yates
Exp Brain Res (2005) 161: 47-61
Presented by Lianne K. Morris-Smith
NS&B275, 3/1/2005
Abstract
The activity of some neurons in the lateral mammillary nucleus (LMN)
of the rat corresponds with the animal’s current head direction (HD). HD cells
have been studied extensively but the circuitry responsible for the generation and
maintenance of the HD signal has not been established. The present study tested
the hypothesis that a polysynaptic pathway connects the vestibular nuclei with
the LMN via one or more relay nuclei. This circuitry could provide a substrate
for the integration of sensory input necessary for HD cell activity. This
hypothesis is based upon the prior demonstration that labyrinthectomy abolishes
HD selectivity in thalamic neurons. Viral transneuronal tracing with
pseudorabies virus (PRV) was used to test this hypothesis. We injected
recombinants of PRV into the LMN and surrounding nuclei of adult male rats
and defined the patterns of retrograde transneuronal infection at survival intervals
of 60 and 72 h. Infected medial vestibular neurons (MVN) were only observed
at the longest postinoculation interval in animals in which the injection site was
localized largely to the LMN. Robust infection of the dorsal tegmental nucleus
(DTN) and nucleus prepositus hypoglossi (PH) in these cases, but not in
controls, at both survival intervals identified these nuclei as potential relays of
vestibular input to the LMN. These data are consistent with the conclusion that
vestibular information that contributes to the LMN HD cell activity is relayed to
this caudal hypothalamic cell group via a polysynaptic brainstem circuit.
(From: J. E. Brown, J. P. Card, B. J. Yates
Exp. Brain Res (2005) 161: 47-61)
Hypothesis
“A polysynaptic pathway connects the
vestibular nuclei with the LMN via one
or more relay nuclei.”
Areas that were of particular interest
(and why)

LMN: bilateral lesions of LMN lead to loss of directional specificity of
ADN HD cells (Blair et al, 1999)

Vestibular nuclei: abolishing labyrinthine input eliminates directional
sensitivity of HD cells in ADN (Stackman and Taube, 1997)

DTN: known to receive vestibular input; some DTN neurons code for
angular head velocity; small percentage of DTN are “classic” HD cells

SUG and PH: receive vestibular input; project to DTN; thought to be
involved in oculomotor pathways
Study used Pseudorabies Virus (PRV)

PRV is taken up by axon terminals and transported
retrogradely from injection site

PRV can “jump” synapses

Brown et al. used two different recombinants of
PRV: PRV BaBlu (expresses β-gal) and PRV-152
(expresses enhanced GFP)
Photomicrographs of an injection site (a) and
retrogradely infected brainstem nuclei (b-d),
60-hour survival time animal
Photomicrographs of an injection site (a) and
retrogradely infected brainstem nuclei (b-f),
72-hour survival time animal
Distribution of infected neurons from case
shown in Fig. 2
Conclusion