Expression of the P/Q (Cav2.1) calcium channel in nodose sensory neurons and arterial baroreceptors

Abstract

The predominant calcium current in nodose sensory neurons, including the subpopulation of baroreceptor neurons, is the N-type channel, Cav2.2. It is also the primary calcium channel responsible for transmitter release at their presynaptic terminals in the nucleus of the solitary tract in the brainstem. The P/Q channel, Cav2.1, the other major calcium channel responsible for transmitter release at mammalian synapses, represents only 15–20% of total calcium current in the general population of sensory neurons and makes a minor contribution to transmitter release at the presynaptic terminal. In the present study we identified a subpopulation of the largest nodose neurons (capacitance > 50pF) in which, surprisingly, Cav2.1 represents over 50% of the total calcium current, differing from the remainder of the population. Consistent with these electrophysiological data, anti-Cav2.1 antibody labeling was more membrane delimited in a subgroup of the large neurons in slices of nodose ganglia. Data reported in other synapses in the central nervous system assign different roles in synaptic information transfer to the P/Q-type versus N-type calcium channels. The study raises the possibility that the P/Q channel which has been associated with high fidelity transmission at other central synapses serves a similar function in this group of large myelinated sensory afferents, including arterial baroreceptors where a high frequency regular discharge pattern signals the pressure pulse. This contrasts to the irregular lower frequency discharge of the unmyelinated fibers that make up the majority of the sensory population and that utilize the N-type channel in synaptic transmission.

Cellular and Molecular Mechanisms Underlying Arterial Baroreceptor Remodeling in Cardiovascular Diseases and Diabetes

“…(Kv)] are the basis of neuronal electrical excitability [156,157]. Many studies have recorded voltage-gated ion currents in arterial baroreceptor neurons, and analyzed the modulation of voltage-gated ion channels and their contributions to the initiation and propagation of the nerve impulse under normal conditions [99,102,[158][159][160][161][162][163][164][165][166][167][168]. Under pathophysiological conditions, however, only the roles and related modulation of Nav and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels have been elucidated in detail in arterial baroreceptor neurons [4,11,12,15,23,[169][170][171][172].…”

“…In primary viscerosensory neurons in the nodose ganglia, Nav-1.7, -1.8, and -1.9 are abundantly expressed [23,165,176,177]. Based on the expression of Nav-1.7, -1.8, and -1.9 channels, aortic baroreceptor neurons in the nodose ganglia are divided into A-type and C-type [166]. Neurons with only TTX-sensitive Nav channels (Nav-1.7) are defined as A-type, whereas neurons with both TTX-sensitive (Nav-1.7) and TTXresistant Nav channels (Nav-1.8 and -1.9) are defined as C-type [23,165,176,177].…”

Morphology of P2X3‐immunoreactive nerve endings in the rat tracheal mucosa

“…The antibodies were used for both immunoblotting and immunohistochemistry of the rat spinal cord (Xiao et al, 2010) and mouse brain (Wong, Xiao, Kemper, Kilpatrick, & Murray, 2013). This antibody has also used for labeling the myelin sheath of the aortic baroreceptors of the rat (Tatalovic, Glazebrook, & Kunze, 2012).…”

Angiotensin II-superoxide-NFκB signaling and aortic baroreceptor dysfunction in chronic heart failure

“…Using path-clamp and molecular biological techniques, all major subtypes of sodium, calcium, and potassium voltage-gated channels have been functionally characterized in NG neurons including aortic baroreceptor neurons. These major subtypes of voltage-gated ion channels include: (1) tetrodotoxin (TTX)-sensitive and TTX-resistant Na v channels; (2) N-type, L-type, T-type, and R-type calcium voltage-gated channels; (3) 4-aminopyridine-sensitive, tetraethylammonium-sensitive, and calcium-activated potassium voltage-gated channels (Li et al, 1998 ; Lancaster et al, 2002 ; Schild and Kunze, 2012 ; Tatalovic et al, 2012 ; Xu et al, 2015 ).…”