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Chapter 3

PSYC62H3 Chapter Notes - Chapter 3: Mesocortical Pathway, Brain-Derived Neurotrophic Factor, Vasopressin


Department
Psychology
Course Code
PSYC62H3
Professor
Zachariah Campbell
Chapter
3

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Chapter 3: Neurotransmission Wajiha Afaq 2015
Neurotransmission is the transmission of information between neurons, typically
involving the neurons to release a chemical called neurotransmitters into a synapse,
allowing them to act on sites on another neurons.
Electrical Events Within a Neuron and the Release of Neurotransmitters
Electrical transmissions are a series of electrical events that begin at an axon
hillock and proceed down then length of the axon. These events must happen
before neurotransmitters can be released, and they depend on electrical potential,
which is the difference between the electric charges within a neuron vs the
electrical charge of the environment outside of it. Normally, - within neuron, +
outside, leaving the neurons membrane polarized. Depolarization is the reduced
difference between the + and- charges on each side of a membrane.
Hyperpolarization is the increased difference between the + and- charges on
each side of a membrane.
Local potential is the electrical potential on a specific part of a neuron, and it
changes according to events within neurons, as ions move in and out of the ion
channels, which are pores in the membranes that allow passage of ions into the
neuron. The influence of local potentials from other neurons is either excitatory
postsynaptic potential, (EPSP) which is a stimulus that depolarizes a local
potential, or an inhibitory postsynaptic potential,(IPSP) which hyperpolarises
the local potential.
Nerve Impulses: Electrical Potential Changes in Neurons
Nerve impulses are electrochemical signals in which neurons release
neurotransmitters from axon terminal
Resting Potential
A resting potential is the negatively charged local potential that precedes an
action potential; the charge can vary between species, structures, and
concentration of ions within or outside neuron. It exists bc of negatively charged
proteins within the neuron and closed ion channels that prevent Na+ ions to
pass. Although the channels let K+ pass, it isn’t enough to affect the resting
potential, because they are just attracted to the negative charge within the neuron,
called electrostatic attraction. At some point, they stop entering the neuron
because ions of the same type resist being concentrated, known as concentration
gradient. So as K+ becomes more concentrated within neuron, some of these ions
follow a concentration gradient and exit the neuron. The balance between the
electrostatic attraction and concentration gradient repulsion facilitates a
resting potential.
Na+ channels aren’t open during resting potential, but they still find a way in. To
prevent the excess Na from changing the resting potential, neuronal membranes
have sodium-potassium pumps, which brings two K+ ions into the neuron while
removing 3 Na out of it. By doing so, a net negative effect is achieved. Na+
channels are voltage gate ion channels, meaning they open or close, depending

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on local potential changes, and they open due to depolarization. Thus, when an
EPSP occurs, the depolarization causes the NA channels to open, allowing them
to enter. If no other EPSP occurs, then depolarization ends and resting potential
continues. Combined EPSP produces greater depolarization in two ways:
temporal summation: short succession of EPSP from the same source
spatial summation : EPSP occurring from multiple sources. If a series of EPSP
causes depolarization to reach a certain threshold, then action potential will occur.
Action Potential
An action potential is a rapid depolarization, causing the potential in the
neuron to become temporarily more positive than the outside environment,
and occurs when all Na+ channels are open (1-3 milliseconds)
all-or-none law states that a magnitude of an action potential is independent form
the magnitude of potential change that elicited the action potential. It will happen
regardless. Action potential immediately ends after Na+ channels close.
Refractory Period
Period following an action potential when the neuron resists producing another
action potential. It is divided into 2 phases:
- Absolute refractory period (1-2mil):. K+ channels are opened, and
concentration of positively charged ions causes K+ to exit neuron, making the
potential negative once again, and is now more negative than resting potential
charge. No amount of depolarization can produce another action potential bc Na
is closed bro.
- Relative refractory period: (2-4m)L greater depolarization is
necessary to reach threshold and produce another action potential. Na can be
opened, and local potential remains hyperpolarized, thus, greater
depolarization is necessary to reach threshold and produce another action
potential. Unless EPSP happens, membrane returns to resting potential.
Propagation of Action Potentials Down Axons
a series of action potentials occurring in succession down an axon, beginning at
axon hillock. Once it begins, each depolarization causes another action
potential to occur further down the axon until an action potential occurs at
the axon terminal. Action potentials propagate in only one direction bc
preceding portion is in refractory period.
Myelin sheathing increase speed of conductance down axon, the uncovered
sections of axons between sheaths is the nodes of ranvier, which contains Na+
and K+ channels. Thus, when an action potential happens at one node,
depolarization is carried through sheathing to next node, where another occurs,.
This jumping of action potentials from one node to another is saltatory
conduction. The firing rate, is the number of action potentials occurring per unit
of time, usually in milliseconds.

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Chapter 3: Neurotransmission Wajiha Afaq 2015
Neurotransmitters: Signaling Molecules for Neuronal Communication
Neurotransmitters are signalling chemicals that are synthesized within neurons,
released from neurons, and have effects on neurons or other cells
Neurotransmitter Synthesis
- Enzymes help, and synthesis occurs anywhere within neuron. Usually
(acytocholine, dopamime) smaller neurotransmitters are synthesised in axon
terminal, larger ones are in the soma.
Neurotransmitter Storage
- after synthesis, they are stored in a vesicular transporter a channel located on a
vesicle that allows passage of neurotransmitters. Synaptic vesicles protect the
neurotransmitter by enzymes, prevent it from being released prematurely, and
allow them to be pooled in axon terminal, for immediate release during
neurotransmission. But not every neurotransmitter is stored after synthesis. E.g.
endocannabinoid neurotransmitter anandamide isn’t , and without storage
mechanism, it escapes from the neuron immediately after synthesis.
Calcium Influx and Neurotransmitter Release
- once AP happens in axon terminal, Ca channels open and allow CA to enter.
Calcium causes exocytosis, which is the fusing of synaptic vesicles to the axon
membrane and release of stored neurotransmitters into the synaptic cleft. After
fusing, vesicles are brought back into terminal and refilled with neurotransmitters,
but this doesn’t occur for neuropeptide neurotransmitters, which is stored in
vesicles produced in soma.
Neurotranismitters Bind to Receptors
- Neurotransmitters released into synaptic cleft bind to receptor proteins, which
are located on postsynaptic terminal, axon terminal or both. They can also
bind to receptors outside of synapse, which is a process called volume
neurotranismission. This occurs from the overflow of neurotransmitters form a
synaptic cleft, resulting from high neuronal activity.
Termination of Neurotransmission
- after neurotransmitter releases from a receptor, enzymes break down
neurotransmitter into different molecules, known as catabolism, and bc these new
molecules don’t match to a neurotransmitter receptor, the transmission stops
-Reuptake also happens, when transporter channels on axon terminals return
neurotransmitters to axon terminal. Then the vesicles store them for later release,
like a recycling basically.
- Sometimes they’re moved from synaptic cleft to astrocyte glial cells, whose
enzymes catabolize it.
Neurotransmission: Neurotransmitter Binding to Receptors
Receptors are proteins in the neuron membranes that are bounded and activated
by neurotransmitters, and they match to a specific one. i.e. dopamine cant bind to
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