Insect Nervous System Animation

Jim Kalisch Author

03/11/2019 Added

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video describes the function of an insect's nervous system

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[00:00:04.540]The nervous system is composed of neurons.
[00:00:07.140]The nervous system's functions are
[00:00:08.610]to gather information about the environment,
[00:00:10.590]process this information, and then use the information
[00:00:13.500]to modify neural programs that result
[00:00:15.370]in behavioral performance.
[00:00:18.350]The input to the system is a stimulus captured
[00:00:20.670]by a sensory neuron, which transduces the stimulus energy
[00:00:24.050]into an electrical signal, also called action potential.
[00:00:28.380]This electrical signal travels
[00:00:29.910]in one direction along the neuron membrane,
[00:00:32.600]towards a neuron extremity,
[00:00:34.130]until reaching the synaptic cleft,
[00:00:36.820]which is the junction between two neurons.
[00:00:40.110]There, the action potential triggers
[00:00:41.830]the release of neurotransmitters,
[00:00:43.260]which can either be excitatory
[00:00:44.610]or inhibitory in nature.
[00:00:46.380]The importance of the nervous system
[00:00:47.840]to the functional integrity of animals makes it
[00:00:50.340]an extremely sensitive target to poisons.
[00:00:53.380]During this animation, we will explain how
[00:00:55.410]the stimulus travels as an electrical signal along
[00:00:57.680]the neuron membrane, and how it is chemically transmitted
[00:01:00.490]to a second neuron or cell.
[00:01:02.970]We will also demonstrate how pesticides
[00:01:05.210]can interfere with this process.
[00:01:07.480]Any living cell possesses
[00:01:08.850]a transmembrane electrical potential
[00:01:10.960]so that the outside of the cell
[00:01:12.810]is positive with respect to the inside.
[00:01:15.400]In neurons, the power source used
[00:01:17.450]to transmit the stimulus is
[00:01:19.190]the transmembrane electrical potential generated
[00:01:22.320]by a controlled distribution of different ions.
[00:01:26.530]Using energy from ATP,
[00:01:28.760]an ionic pump creates a charge imbalance across the membrane
[00:01:32.440]by carrying three sodium ions out of the neuron
[00:01:35.900]for every two potassium ions carried in.
[00:01:39.580]In a resting neuron, the sodium ions
[00:01:42.310]and the potassium ions
[00:01:43.740]are therefore asymmetrically distributed across
[00:01:45.970]the cell membrane, making the inside negative relative
[00:01:49.260]to the outside.
[00:01:50.530]The neuron membrane is therefore polarized.
[00:01:55.340]The basis of the nerve excitability resides
[00:01:57.910]in the ability of the membrane
[00:01:59.440]to undergo transient changes in membrane potential
[00:02:02.470]in response to external stimuli.
[00:02:04.700]These changes are caused by inward
[00:02:06.880]and outward currents of the sodium
[00:02:09.380]and potassium ions respectively.
[00:02:11.960]A stimulus to the neuron causes
[00:02:13.730]an action potential to move along the axon.
[00:02:16.870]The first phase of the action potential
[00:02:19.050]is caused by a sharp increase
[00:02:21.010]in sodium ion conductance or permeability.
[00:02:24.380]Leading to its inward movement
[00:02:26.150]through sodium ion channels,
[00:02:28.500]the local depolarization causes
[00:02:30.810]the adjacent sodium channel to open, and so on.
[00:02:34.960]A rapid change in potential differences across
[00:02:37.480]the membrane follows increasing potassium conductance,
[00:02:40.530]leading to its outward movement
[00:02:42.100]through the potassium ion channel.
[00:02:43.920]The sharp increase in outward potassium flux causes
[00:02:47.390]the decrease of sodium conductance
[00:02:49.900]by closing sodium ion channels.
[00:02:53.370]The action potential moves in one direction
[00:02:55.950]as a wave of depolarization
[00:02:57.930]because after each opening of a sodium ion channel,
[00:03:01.240]a short refractory period follows,
[00:03:03.800]during which the sodium ion channel cannot open again.
[00:03:07.100]This signal moves until reaching the synaptic cleft.
[00:03:12.200]Within the central nervous system,
[00:03:14.020]neurons communicate by means of chemical transmitters
[00:03:16.650]across a specialized junction,
[00:03:18.320]which is called a synapse.
[00:03:20.050]In synapses, the electrical signal
[00:03:22.240]is transduced into chemical signal,
[00:03:24.540]which are received at the membranes
[00:03:26.300]of other nerves or muscles.
[00:03:28.320]Chemical transmission is therefore initiated
[00:03:30.980]by depolarization resulting from an action potential.
[00:03:34.360]Both excitatory and inhibitory neurotransmitters
[00:03:37.720]have been identified in synapses.
[00:03:40.490]In the excitatory synaptic transmission
[00:03:42.920]when the wave of depolarization achieves
[00:03:44.960]the synaptic region,
[00:03:46.410]voltage-gated calcium ion channels open,
[00:03:49.580]allowing the inward calcium ion movement
[00:03:52.020]into the presynaptic neuron.
[00:03:54.380]The increase in calcium ions inside
[00:03:56.700]the neuron triggers the exocytosis release
[00:03:59.980]of the acetylcholine neurotransmitter
[00:04:02.550]into the synaptic cleft.
[00:04:05.130]Acetylcholine molecules move randomly
[00:04:07.300]within synaptic clefts,
[00:04:08.910]and it is about equally possible
[00:04:10.620]for any given molecule to meet acetylcholinesterase
[00:04:13.860]or acetylcholine receptor sites.
[00:04:16.210]Molecules that reach the enzyme
[00:04:18.030]are broken into choline and acetate,
[00:04:20.180]which are reabsorbed by the presynaptic membrane
[00:04:23.120]to form new acetylcholine molecules.
[00:04:25.970]Molecules that bind to receptor sites
[00:04:28.070]cause depolarization of the postsynaptic membrane,
[00:04:31.270]which is then transmitted along the axon,
[00:04:34.170]as explained earlier.
[00:04:37.290]The inhibitory synaptic transmission
[00:04:39.410]presents similar processes to the excitatory transmission.
[00:04:42.930]In this case, however,
[00:04:44.230]the GABA receptor is the primary inhibitor receptor
[00:04:47.370]at the insect neuromuscular synapsis.
[00:04:50.140]The inhibitor neurotransmitter GABA binds
[00:04:53.200]to the GABA receptor, causing the opening
[00:04:55.970]of chloride ion channels
[00:04:57.720]and consequent chloride ion inward movement
[00:05:01.000]into the neuron membrane.
[00:05:02.570]This conductance increase causes hyperpolarization
[00:05:05.560]of the membrane, blocking the excitatory stimuli.
[00:05:09.140]The importance of the nervous system
[00:05:10.720]to the functional integrity of animals makes it
[00:05:13.160]an extremely sensitive target to poisons.
[00:05:15.570]Therefore, most insecticides have
[00:05:17.560]been directed primarily at the disruption
[00:05:19.570]of the nervous system functions.
[00:05:22.820]Insecticides that act on the sodium channel
[00:05:25.120]can either work by keeping the channel open,
[00:05:27.210]leading to repetitive discharge,
[00:05:28.820]resulting in excitation, or keeping them closed
[00:05:31.330]for a longer period of time,
[00:05:32.830]resulting in depression.
[00:05:34.590]Other groups of insecticides interact
[00:05:36.520]with acetylcholine in various ways.
[00:05:43.410]Acetylcholine inhibitors bind to acetylcholinesterase,
[00:05:46.580]preventing acetylcholine binding to it,
[00:05:48.970]leading acetylcholine binding
[00:05:50.450]to the receptors more frequently.
[00:05:56.760]Acetylcholine agonists bind to acetylcholine receptors,
[00:05:59.840]mimicking the effect of acetylcholine,
[00:06:02.170]causing an excitatory response.
[00:06:09.030]Acetylcholine antagonists bind to acetylcholine receptors,
[00:06:12.470]blocking the effect of acetylcholine,
[00:06:14.390]leading to paralysis.
[00:06:16.330]Antagonists prevent impulse propagation
[00:06:18.870]across the synapse.
[00:06:21.030]Other insecticides act on GABA receptors or transmitters.
[00:06:24.950]GABA antagonists inhibit effects of GABA,
[00:06:27.860]resulting in excitation.
[00:06:29.910]Since GABA acts to increase chloride conductance,
[00:06:32.910]thereby hyperpolarizing the membrane,
[00:06:34.980]inhibition of this effect would result in excitation,
[00:06:38.520]whereas GABA agonists increase affinity
[00:06:40.900]of receptor for GABA, resulting in depression.

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Insect Nervous System Animation

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