Literature DB >> 8876463

Monosynaptic projections from the nucleus tractus solitarii to C1 adrenergic neurons in the rostral ventrolateral medulla: comparison with input from the caudal ventrolateral medulla.

S A Aicher1, R H Saravay, S Cravo, I Jeske, S F Morrison, D J Reis, T A Milner.   

Abstract

The rostral ventrolateral medulla (RVL) contains reticulospinal adrenergic (C1) neurons that are thought to be sympathoexcitatory and that form the medullary efferent limb of the baroreceptor reflex pathway. The RVL receives direct projections from two important autonomic regions, the caudal ventrolateral medulla (CVL) and the nucleus tractus solitarii with immunocytochemical identification of C1 adrenergic neurons in the RVL to compare the morphology of afferent input from these two autonomic regions into the RVL. NTS (n = 203) and CVL (n = 380) efferent terminals had similar morphology and vesicular content, but CVL efferent terminals were slightly larger than NTS efferent terminals. Overall, efferent terminals from either region were equally likely to contact adrenergic neurons in the RVL (21% for NTS, 25% for CVL). Although efferents from both regions formed both symmetric and asymmetric synapses, NTS efferent terminals were statistically more likely to form asymmetric synapses than CVL efferent terminals. CVL efferent terminals were more likely to contact adrenergic somata than were NTS efferents, which usually contacted dendrites. These findings 1) support the hypothesis that a portion of NTS efferents to the RVL may be involved in sympathoexcitatory, e.g., chemoreceptor, reflexes (via asymmetric synapses), whereas those from the CVL mediate sympathoinhibition (via symmetric synapses); and 2) provide an anatomical substrate for differential postsynaptic modulation of C1 neurons by projections from the NTS and CVL. With their more frequent somatic localization, CVL inhibitory inputs may be more influential than excitatory NTS inputs in determining the discharge of RVL neurons.

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Year:  1996        PMID: 8876463     DOI: 10.1002/(SICI)1096-9861(19960909)373:1<62::AID-CNE6>3.0.CO;2-B

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


  40 in total

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