Koganezawa T, Paton JF. Exp Physiol. 2014 Jul 11.
We normally think of the RVLM as something that responds to
incoming signals from other areas and adjusts its activity accordingly.
However, it has been shown that if you block synaptic transmission, the neurons
still fire on their own despite a lack of incoming signals. Other groups have
looked at their “pacemaker” properties, but in this paper, they decided to look
at the intrinsic chemosensitvity of presympathetic neurons – something we haven’t
really looked at. They used a modified version of the working heart brainstem
preparation so that they could record the activity of nerves and neurons while
they switched the perfusion solution to ones that would induce periods of
eucapnia, normoxia, hypercapnia, hypoxia, etc. First, they blocked fast synaptic
transmission and looked at spontaneous activity under the different conditions
and found that in all 26 presympathetic neurons, activity was not significantly
affected. During hypercapnic-hypoxia, they found that all presympathetic
neurons increased their firing rate by an average of 130%. This indicates that
these neurons are themselves chemosensitive, independent of afferents from
chemoreceptors. They also tested the combined effects of cyanide and
hypercapnia on presympathetic neurons during synaptic blockade and found that 7
had their activity depressed by -82%, while 3 were slightly excited by it,
though the effect was not significant due to a wide variability in response. Interestingly,
and in terms of differential control, they found out that if they block a
particular sodium current known to be involved in C1 neuron activity, they can block
the preparation from “gasping” during asphyxia, but sympathetic chain activity
remains unaffected. Personally, my take-home message from this paper is that I
really need to watch my blood gas measurements and make sure that I’m not
putting my rat into a state that could compromise my recordings. -DH
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