This word document contains the essential, basic aspects of the Purves Neuroscience chapter(s) covered during the Neuroscience course at the Vrije Universiteit Amsterdam. Written in an extensive, explanatory, story-like style at a high level of English. The exact chapter's content for this summary ...
Test Bank for Neuroscience 6th Edition Purves • Augustine • Fitzpatrick • Hall LaMantia • Mooney ,Platt ,White (Chapter 1-34 complete )
Test Bank - for Neuroscience 6th Edition by Dale Purves, All Chapters 1- 34 | Complete Guide A+
Test Bank For Neuroscience, 6th Edition By Purves • Augustine • Fitzpatrick, Consists Of 34 Complete Chapters, ISBN: 978-1605353807
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Neurosciences 6
HC 6
There are many different kinds of neurotransmitters, generating tremendous diversity in chemical
signalling between neurons. The two major families include:
- Small-molecule neurotransmitters:
o Acetylcholine
o Amino acids: glutamate, aspartate, GABA, glycine
o Purines: ATP
o Biogenic amines:
Catecholamines: dopamine, noradrenaline, adrenaline
Indole-amine: serotonin
Imidazole-amine: histamine.
- Peptide neurotransmitters
When it comes to receptors, there are also many different subtypes. There are the ionotropic and
metabotropic receptors; the former inducing a fast response, the latter activating second
messengers that amplify the signal and trigger an intracellular response. Second messengers, like
cAMP or calcium, may induce cellular responses like protein phosphorylation, gene transcription
or the opening of ion channels. They amplify the neurotransmitter signal on three levels:
- One receptor activates many G-proteins, which activates adenylyl cyclase.
- One adenylyl cyclase may produce many cAMP particles, which activates protein kinase.
- One protein kinase phosphorylates many target prpteins.
On top of this, metabotropic receptors initiate multiple cascades simultaneously, along various
pathways, able to induce a wide-ranging response within a cell.
Acetylcholine
- Site of action: This neurotransmitter works primarily at neuromuscular junctions in skeletal
muscles, but also between the vagus nerve and cardiac muscle fibres, in synapses of the
visceral motor system ganglia and at various sites in the CNS. At every site, it induces a
different response depending on the tissue and receptors present.
- Synthesis: it is synthesised from the precursors acetyl-CoA and choline. Choline
acetyltransferase (ChAT) catalyses the reaction, which occurs in the nerve terminals. After
ACh has been synthesised, vesicular ACh transporter (VAChT) loads each molecule into
cholinergic vesicles. It loads the vesicles using antiport with hydrogen ions, of which the
concentration is kept high within the vesicle using active transport.
- Removal: the hydrolytic enzyme, acetylcholinesterase (AChE), breaks down ACh directly
ensuring a rapid decrease of ACh concentrations. This breakdown occurs in the synaptic
cleft, where there are high concentrations of the enzyme. So, this transmitter is not as other
transmitters taken up again, but degraded directly. The products of the degradation
reaction, include acetate and choline, whereby the latter is taken up and re-used for new
ACh synthesis. Inhibiting AChE leads to ACh accumulation in the cleft, which continuously
depolarises the postsynaptic muscle cell and induces the refractory period subsequent to
ACh release, leading to muscle paralysis.
- Receptors:
o Ionotropic: nicotinic receptors (nAChR), these are non-selective ligand-gated cation
channels that generate an excitatory postsynaptic response. These receptors are
large protein complexes with five subunits. However, not every nAChR has the same
combination of subunits; there are also many types of subunits of which different
, combinations may give rise to a receptor. All ionotropic receptors actually work like
this, many different types of possible subunits, of which 3-5 ought to be combined
for each receptor type. At the neuromuscular junction, for example, the receptor has
2alpha:1beta:1delta:1gamma/epsilon. Neuronal nAChRs consist of 3alpha:2beta.
Having different subunits, causes different responses to agonists or drugs as well.
Although both recognise ACh, the neuronal receptors are insensitive to e.g. a snake
toxin, while the muscular ones are. Each subunit has large extracellular regions and
four transmembrane domains which associate and hence form a channel. The
channel though does not discriminate between ligands or different cations; if a drug
binds to one of the alpha subunits, the receptor transmembrane domains tilt to open
the channel gate and permit various ions to diffuse through.
o Metabotropic: muscarinic receptors (mAChR), these mediate effects in the brain,
after ACh stimulation. They exist of seven helical membrane-spanning domains, but
ACh binds to one site only deep within the extracellular surface of the mAChR.
Binding causes a conformational change that permits G-proteins to bind the
intracellular domain of the receptor. There are five subtypes of domains known, each
coupled to a different G-type protein thus having a different postsynaptic response.
mAChR are especially expressed in the corpus striatum where the cause an inhibitory
influence of dopamine-mediated motor effects. However, in other brain parts, they
are excitatory again. They are also active in autonomic effector organs like the heart
and smooth muscle (inhibit vagus nerve).
Glutamate
- Site of action: nearly all excitatory neurons in the CNS are glutaminergic. Because this
actually is an amino acid, it resides in extremely high concentrations within cells. Upon a
brain trauma, and there is blood vessel and cell rupture, the excess glutamate spilled out
may cause exocitotoxicity. The glutamate overlay excites postsynaptic neurons, leading to
prolonger calcium influx which activates the breakdown of lipid and proteins, so induces
apoptosis. Hence, brain tissue is degraded.
- Synthesis: glutamate itself is a non-essential amino acid which cannot pass the blood brain
barrier, so is synthesised in neurons from local precursors, like glutamine. A transporter
(SAT2) takes up glutamine in presynaptic terminals which is metabolised into glutamate by
the mitochondrial enzyme glutaminase. Or, glutamate is synthesised from alpha-keto-
glutarate from the TCA cycle. Afterwards, various types of vesicular glutamate transporters
(VGLUTs) are involved in vesicular packaging (which again requires a proton gradient).
- Removal: the glutamate signal is terminated by excitatory amino acid transporters (EAATs)
which removes glutamate from the synaptic cleft by promoting re-uptake in the presynaptic
terminal or in glial cells. If glial cells take up glutamate, they convert it to glutamine and by a
different transport system, the glutamine ends up in the presynaptic terminal again.
Glutamine is transported, not glutamate, because otherwise the glutamate may diffuse back
to the cleft and induce a response again. Hence, there is a glutamate-glutamine cycle, so to
maintain and adequate supply of glutamate and to rapidly terminate postsynaptic glutamate
action.
- Receptors:
o ionotropic: AMPA, NMDA or kainate receptors, which are all glutamate-gated cation
channels that allow passage of both sodium and potassium, just like the nAChRs. So,
these as well, produce excitatory postsynaptic responses. Central excitatory synapses
express mainly AMPA and NMDA receptors, whereby the former react faster and
with a larger response than the latter. Kainate receptors turn out to be auto-
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