Beta-Adrenergic Modulation of Tremor and Corticomuscular Coherence in Humans

Abstract

Coherence between the bioelectric activity of sensorimotor cortex and contralateral muscles can be observed around 20 Hz. By contrast, physiological tremor has a dominant frequency around 10 Hz. Although tremor has multiple sources, it is partly central in origin, reflecting a component of motoneuron discharge at this frequency. The motoneuron response to ∼20 Hz descending input could be altered by non-linear interactions with ∼10 Hz motoneuron firing. We investigated this further in eight healthy human subjects by testing the effects of the beta-adrenergic agents propranolol (non-selective β-antagonist) and salbutamol (β2-agonist), which are known to alter the size of physiological tremor. Corticomuscular coherence was assessed during an auxotonic precision grip task; tremor was quantified using accelerometry during index finger extension. Experiments with propranolol used a double-blind, placebo-controlled crossover design. A single oral dose of propranolol (40 mg) significantly increased beta band (15.3–32.2 Hz) corticomuscular coherence compared with placebo, but reduced tremor in the 6.2–11.9 Hz range. Salbutamol (2.5 mg) was administered by inhalation. Whilst salbutamol significantly increased tremor amplitude as expected, it did not change corticomuscular coherence. The opposite direction of the effects of propranolol on corticomuscular coherence and tremor, and the fact that salbutamol enhances tremor but does not affect coherence, implies that the magnitude of corticomuscular coherence is little influenced by non-linear interactions with 10 Hz oscillations in motoneurons or the periphery. Instead, we suggest that propranolol and salbutamol may affect both tremor and corticomuscular coherence partly via a central site of action.

Alterations of cAMP-dependent signaling in dystrophic skeletal muscle

“…This showed immunohistochemical signals of β 2 -AR in at least four different locations: (1) larger blood vessels (not depicted), (2) motoneurons (Figures 5A,B), (3) muscle fibers (Figure 5E, left panel), and (4) ill-defined anastomotic fibers (Figure 5E, on left panel see central part of the picture). Since the presence of β 2 -AR had been found by staining and anticipated to be present due to functional roles in blood vessels (Daly and McGrath, 2011), motoneurons (Melamed et al, 1976; Wohlberg et al, 1986; Bondok et al, 1988; Adachi et al, 1992; Parkis et al, 1995; Zeman et al, 2004; Tartas et al, 2010; Noga et al, 2011; Baker and Baker, 2012) and muscle fibers (Gross et al, 1976; Cairns and Dulhunty, 1993a,b; Cairns et al, 1993; Kokate et al, 1993; Navegantes et al, 1999, 2000, 2001, 2002, 2003, 2004; Prakash et al, 1999; Decostre et al, 2000; Gonçalves et al, 2012), our findings in wildtype muscles were corroborating previous reports. However, the difference between wildtype and dystrophic mdx muscles was striking, both with respect to neuronal as well as muscle staining: First, while the typical pretzel-shaped postsynaptic AChR signals in wildtype muscle were perfectly mirrored by presynaptic β 2 -AR staining (Figures 5A,B) in almost fibers, this was much rarer the case in mdx synapses (Figures 5C,D), which were also highly fragmented as reported previously (Torres and Duchen, 1987; Lyons and Slater, 1991; Grady et al, 2000).…”

Interação funcional entre o sistema colinérgico e adrenérgico na manutenção da massa muscular e da placa motora

“…This showed immunohistochemical signals of β 2 -AR in at least four different locations: (1) larger blood vessels (not depicted), (2) motoneurons (Figures 5A,B), (3) muscle fibers ( Figure 5E, left panel), and (4) ill-defined anastomotic fibers ( Figure 5E, on left panel see central part of the picture). Since the presence of β 2 -AR had been found by staining and anticipated to be present due to functional roles in blood vessels (Daly and McGrath, 2011), motoneurons (Melamed et al, 1976;Wohlberg et al, 1986;Bondok et al, 1988;Adachi et al, 1992;Parkis et al, 1995;Zeman et al, 2004;Tartas et al, 2010;Noga et al, 2011;Baker and Baker, 2012) and muscle fibers (Gross et al, 1976;Cairns and Dulhunty, 1993a,b;Cairns et al, 1993;Kokate et al, 1993;Navegantes et al, 1999Navegantes et al, , 2000Navegantes et al, , 2001Navegantes et al, , 2002Navegantes et al, , 2003Navegantes et al, , 2004Prakash et al, 1999;Decostre et al, 2000;Gonçalves et al, 2012), our findings in wildtype muscles were corroborating previous reports. However, the difference between wildtype and dystrophic mdx muscles was striking, both with respect to neuronal as well as muscle staining: First, while the typical pretzel-shaped postsynaptic AChR signals in wildtype muscle were perfectly mirrored by presynaptic β 2 -AR staining ( Figures 5A,B) in almost fibers, this was much rarer the case in mdx synapses (Figures 5C,D), which were also highly fragmented as reported previously (Torres and Duchen, 1987;Lyons and Slater, 1991;Grady et al, 2000).…”

Antihypertensive and Statin Medication Use and Motor Function in Community-Dwelling Older Adults

“…8,13,14,15,16 However, our results indicate a similar association across classes of antihypertensive medication, and thus the underlying mechanism would likely involve an effect common to antihypertensive medication in general. Increasing evidence indicates that among the oldest old, use of antihypertensive medications and lower blood pressure may be associated with increased morbidity and mortality, 17,18,19,20 and paradoxically, that hypertension may actually be beneficial among certain subgroups of this population.…”