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Voltage‐dependent amplification of synaptic inputs in respiratory motoneurones
Author(s) -
Enríquez Denton M.,
Wienecke J.,
Zhang M.,
Hultborn H.,
Kirkwood P. A.
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.225789
Subject(s) - neuroscience , excitatory postsynaptic potential , motor neuron , inhibitory postsynaptic potential , respiratory system , spinal cord , phrenic nerve , strychnine , chemistry , biology , anatomy
Key points• The processes whereby various excitatory and inhibitory inputs are integrated in spinal motoneurones during naturally occurring motor acts are not well understood, largely because there are amplifying mechanisms within the motoneurone that can control the effective strengths of the inputs. • Knowledge of these processes is important in understanding conditions such as motoneurone disease, or the spasticity that can follow spinal cord injury or stroke • Respiration is a natural motor act that continues normally under experimental conditions, and this study investigated, for the first time, the likely amplifying processes at work in respiratory motoneurones. • In phrenic motoneurones, which control the most important respiratory muscle, the diaphragm, we found that the mechanism most favoured by investigations in other motoneurones, the activation of persistent inward currents via calcium channels, appears to make a very small contribution. Instead, modulation of synaptic currents (through NMDA channels) appears to be more important.Abstract The role of persistent inward currents (PICs) in cat respiratory motoneurones (phrenic inspiratory and thoracic expiratory) was investigated by studying the voltage‐dependent amplification of central respiratory drive potentials (CRDPs), recorded intracellularly, with action potentials blocked with the local anaesthetic derivative, QX‐314. Decerebrate unanaesthetized or barbiturate‐anaesthetized preparations were used. In expiratory motoneurones, plateau potentials were observed in the decerebrates, but not under anaesthesia. For phrenic motoneurones, no plateau potentials were observed in either state (except in one motoneurone after the abolition of the respiratory drive by means of a medullary lesion), but all motoneurones showed voltage‐dependent amplification of the CRDPs, over a wide range of membrane potentials, too wide to result mainly from PIC activation. The measurements of the amplification were restricted to the phase of excitation, thus excluding the inhibitory phase. Amplification was found to be greatest for the smallest CRDPs in the lowest resistance motoneurones and was reduced or abolished following intracellular injection of the NMDA channel blocker, MK‐801. Plateau potentials were readily evoked in non‐phrenic cervical motoneurones in the same (decerebrate) preparations. We conclude that the voltage‐dependent amplification of synaptic excitation in phrenic motoneurones is mainly the result of NMDA channel modulation rather than the activation of Ca 2+ channel mediated PICs, despite phrenic motoneurones being strongly immunohistochemically labelled for Ca V 1.3 channels. The differential PIC activation in different motoneurones, all of which are Ca V 1.3 positive, leads us to postulate that the descending modulation of PICs is more selective than has hitherto been believed.