Final answer:
Centrally acting skeletal muscle relaxants like d-tubocurarine inhibit neurotransmitter effects at the neuromuscular junction, reducing activity within the spinal cord and leading to muscle relaxation. These relaxants function differently from botulinum toxin, which inhibits the release of acetylcholine directly from motor neurons.
Step-by-step explanation:
Centrally acting skeletal muscle relaxants, such as d-tubocurarine, work by blocking the action of neurotransmitters at the neuromuscular junction, in particular, inhibiting the effect of acetylcholine. This blockage results in the muscle cell becoming insensitive to motor-nerve impulses and acetylcholine without affecting the muscle fiber's response to direct electrical stimulation and potassium ions. Hence, these muscle relaxants inhibit or reduce activity within the spinal cord (intraneuronal), disrupting the central stimuli required for muscle contraction. This is distinct from the effects of botulinum toxin, which inhibits the release of acetylcholine from the motor neurons, consequently producing muscle relaxation and paralysis.
Concerning the statements provided in your question, option B is an accurate description of how centrally acting skeletal muscle relaxants function. It's important to note that dantrolene is not centrally acting - it works directly on muscle tissue, while cisatracurium is a neuromuscular blocker used during anesthesia and is not a centrally acting muscle relaxant. Options C and D are incorrect traits for this class of drugs, as they can be delivered in various forms and do not always cause systemic release of histamine. As for option E, botulinum toxin (Botox) decreases the release of acetylcholine, inducing muscle relaxation, whereas centrally acting muscle relaxants inhibit neural pathways within the spinal cord, making their interaction with botulinum toxin not one of direct counteraction.