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20.01.2015 admin
Tagged 5 paragraph essay format, 5 paragraph essay lesson plan, five paragraph essay, how to write a five paragraph essay, teaching kids to write five paragraph essays. Once you can write a good 5 paragraph essay shorter answers or longer reports are a breeze.
I saw a teacher’s post not long ago on how to teach 5 paragraph essays to young elementary students.
Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. Olds and Milner (1954) conducted the first brain-reinforcement experiments by implanting electrodes in the brains of rats and allowing them to press a lever to produce self-stimulation of the brain. Parents leave their kids to make dinner, make them write five paragraph essays, and make kids wait until they are sixteen to drive a car.
My kids will have dinner served to them every night or maybe they will help with dinner, but they won’t have to do it all.
It follows this same format and I have found this is the easiest way to teach students to write paragraphs. When an action potential reaches the axon terminal, the depolarization causes voltage-dependent calcium gates to open. This article offers tips on how to keep track of references during the note taking and writing process while writing a paper. As calcium flows into the terminal, the neuron releases neurotransmitter into the synaptic cleft within 1-2 milliseconds.
Later experiments showed that the reinforcing brain stimulation almost exclusively activated tracts of axons that release dopamine, especially in an area called the nucleus accumbens.
I will let my kids drive as soon as they can reach the pedals and see over the steering wheel. Sherrington deduced the properties of the synapse from his experiments on reflexes (an automatic muscular response to stimuli). Many other reinforcing experiences will lead to increased DA activity including sexual excitement, gambling, and video games. At the axon or presynaptic terminal, the action potentials cause calcium to enter the cell, which leads to the release of neurotransmitters from the terminal into the synaptic cleft (space between the presynaptic and postsynaptic neuron).
After being released by the presynaptic neuron, the neurotransmitter diffuses across the synaptic cleft to the postsynaptic membrane, where it will attach to receptors.
Because of its role in reinforcement, the nucleus accumbens is regarded by many as the pleasure area and dopamine as the pleasure chemical.
Neurotransmitters, once released into the synaptic cleft, attach to receptors and alter activity of the postsynaptic neuron. However, several lines of evidence conflict with this interpretation and more recent studies suggest that dopamine and the nucleus accumbens play an important role in attention- getting or craving.C.
The neurotransmitters will separate from their receptors and (in some cases) are converted into inactive chemicals.

Several weak stimuli presented at slightly different times or locations produce a stronger reflex than a single stimulus does.
In some cells, much of the released neurotransmitter is taken back into the presynaptic neuron for recycling. Amphetamine increases dopamine release from presynaptic terminals by reversing the direction of the dopamine transporter.
Some postsynaptic cells send negative feedback messages to slow further release of the transmitter by the presynaptic cells C.
A neurotransmitter can have two types of effects when it attaches to the active site of the receptor: ionotropic or metabotropic effects. Chemicals that are released by one neuron at the synapse and affect another neuron are neurotransmitters.
The behavioral effects of cocaine are believed to be mediated primarily by dopamine and secondarily by serotonin.
Metabotropic effects: The neurotransmitter attaches to a receptor and initiates a cascade of metabolic reactions. The effects of amphetamine and cocaine are both short-lived, because of the depletion of dopamine stores and tolerance. Specifically, when the neurotransmitter attaches to the receptor it alters the configuration of the rest of the receptor protein; enabling a portion of the protein inside the neuron to react with other molecules. Prolonged use of cocaine can cause long-term changes in brain metabolism and blood flow, increasing the risk of stroke, epilepsy, and memory impairments.
Graded potentials: Either depolarization (excitatory) or hyperpolarization (inhibitory) of the postsynaptic neuron. Activation of the receptor by the neurotransmitter leads to activation of G-proteins which are attached to the receptor. A graded depolarization is known as an excitatory postsynaptic potential (EPSP) and occurs when Na+ ions enter the postsynaptic neuron. Acetylcholine: A chemical similar to an amino acid, with the NH2 group replaced by an N(CH3)3 group. The effects of methylphenidate are much longer lasting and less intense as compared to cocaine. EPSPs are not action potentials: The EPSP’s magnitude decreases as it moves along the membrane. Monoamines: Neurotransmitters containing an amine group (NH2) formed by a metabolic change of an amino acid. Methylenedioxymethamphetamine (MDMA, or “ecstasy”) is a stimulant that at low doses primarily increases the levels of dopamine; however, at higher doses it also releases serotonin and produces hallucinogenic effects.
Spatial summation: Several synaptic inputs originating from separate locations exerting a cumulative effect on a postsynaptic neuron. MDMA damages serotonin axons in laboratory animals by increasing body temperature and the production of hydrogen peroxide.

Inhibitory postsynaptic potential (IPSP): A temporary hyperpolarization of a postsynaptic cell (this occurs when K+ leaves the cell or Cl- enters the cell after it is stimulated). They are released from the neuron, often from the cell body or dendrites, following repeated stimulation.I. A hormone is a chemical that is secreted primarily by glands but also by other cells and is conveyed by blood to other organs whose activity it influences. Stimulates the nicotinic receptor (a type of acetylcholine receptor) in both the central nervous system and neuromuscular junction of skeletal muscles; can also increase dopamine release by attaching to neurons that release dopamine in the nucleus accumbens.
The probability of an action potential on a given neuron depends on the ratio of EPSPs to IPSPS at a given moment. Synthesis of neurotransmitters: Neurons synthesize neurotransmitters from precursors derived originally from food.
Repeated use of nicotine leads to decreased sensitivity in nucleus accumbens cells responsible for reinforcement. Unlike neurotransmitters, which are released directly to another neuron, hormones convey messages to any organ that can receive them. Catecholamines (dopamine, epinephrine, and norepinephrine): Three closely related compounds containing a catechol and an amine group. In most cases, synaptic transmission depends on chemical rather than electrical stimulation. Opiates have a net effect of increasing the release of dopamine by stimulating endorphin receptors.
This was demonstrated by Otto Loewi’s experiments where fluid from a stimulated frog heart was transferred to another heart.
Protein and peptide hormones bind to membrane receptors and activate a second messenger within the cell—exactly the same process as at a metabotropic synapse.
Some chemicals can act as both neurotransmitters and hormones, such as epinephrine, norepinephrine, insulin, and oxytocin.
The pituitary gland is attached to the hypothalamus and consists of two distinct glands, the anterior pituitary and the posterior pituitary.
Certain neurotransmitters, such as acetylcholine, are synthesized in the presynaptic terminal.
However, larger neurotransmitters, the neuropeptides, are synthesized in the cell body and transported down the axon to the terminal.
Transporting neurotransmitters from the cell body to the axon terminal can take hours or days in long axons. Neurotransmitters are stored in vesicles (tiny nearly spherical packets) in the presynaptic terminal.

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