11.
The poison dart frog, or poison arrow frog in the family Dendrobatidae carry
Batrachotoxin, among other agents. The toxin irreversibly binds to voltage-gated sodium
channels and keeps them open. Why does this paralyze and kill you?
a. The ionic gradient gets lost and the nerve cells die
b. Synapses remain active so muscles cannot relax
c. The metabolic cost of pumping sodium ions exhausts the ATP reserves of cells
d. All pain-conducting nerves become active simultaneously
Batrachotoxin from poison dart frogs irreversibly locks open voltage-gated sodium channels, causing persistent sodium influx that disrupts nerve signaling. This leads to paralysis and death primarily by preventing normal muscle relaxation at synapses. The correct answer is option b.
Option Analysis
a. The ionic gradient gets lost and the nerve cells die
Continuous Na⁺ entry depolarizes cells, dissipating gradients, but death occurs faster from signaling failure than outright cell death. Nerve cells do not die immediately; paralysis precedes any necrosis.
b. Synapses remain active so muscles cannot relax (Correct)
Open channels cause persistent depolarization, blocking action potential repolarization needed for neurotransmitter release cycles. Synapses stay in a depolarized state, leading to initial tetanus followed by flaccid paralysis as muscles exhaust.
c. The metabolic cost of pumping sodium ions exhausts the ATP reserves of cells
Na⁺/K⁺-ATPase works overtime, but paralysis is too rapid for ATP depletion to be primary; depolarization halts signaling first.
d. All pain-conducting nerves become active simultaneously
Pain fibers may fire initially, but paralysis affects all nerves/muscles, not just nociceptors; cardiac/respiratory failure kills.
Poison dart frogs (Dendrobatidae) secrete batrachotoxin, a steroidal alkaloid that binds irreversibly to voltage-gated sodium channels, locking them open. This batrachotoxin poison dart frog toxin paralysis mechanism floods cells with Na⁺, causing constant depolarization that halts action potentials. Victims experience rapid muscle paralysis, respiratory failure, and death, with no antidote.
Molecular Action on Sodium Channels
Batrachotoxin shifts activation thresholds negatively and blocks inactivation, keeping channels open at rest. Persistent Na⁺ influx prevents repolarization, so neurons/muscles cannot reset for new signals. This targets peripheral nerves and heart, inducing arrhythmias.
Physiological Effects Leading to Death
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Nerve depolarization: Blocks signal propagation, causing numbness then paralysis.
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Synaptic failure: Depolarized presynaptic terminals disrupt Ca²⁺-dependent release, locking synapses “on” initially then “off”.
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Muscle impact: Respiratory and cardiac muscles fail from inability to relax/contract properly.
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Secondary effects: Swelling and minor necrosis occur later, not primarily.
CSIR NET Relevance
This question tests electrophysiology: option b captures synaptic/muscle dysfunction from persistent activation. Frogs acquire toxin from diet; captive ones are safe.
