why are there multiple neurotransmitters?  why are some
neurotransmitters the same as hormones?

There are multiple neurotransmitters because these neurotransmitters
do different things to neurons.

There are exitatory neurotransmitters such as Glutamate, Aspartate
which potentiate Sodium and calcium currents (making the neuron more
depolarized, and hence more likely for an action potential to occur -
this is an EPSP or an excitatory post synaptic potential).

There are inhibitory neurotransmitters, such as GABA which increase
Cl- currrent, further hyperpolarizing the neuron, decreasing the
likelyhood of an action potention -- this is an IPSP, inhibitory post
synaptic potential.

There are also a class of NT's we call neuromodulators. These NTs can
have different effects depending on the receptor type, the target
neuron, and the colocalization of other NT's to that neuron.  Such NTs
include seratonin, dopamine, acetylcholine, and norepinepherine.

By having a wide variety of NT's the nervous system is capable of
presenting a more diverse set of messages.  If you think about
neurotransmission, it could have been all electrical - as some is.
This would involve the potentiation of current directly from one cell
to another through gap junctions, but this limits the information sent
in the message. The neurotransmitters help to add content to the
message being sent.

Some neurotransmitters are the same chemicals as hormones.  Typically
we talk of NT's as being produced in the nervous system and acting
within it, and hormones as acting outside of it.  A good example is
CRF aka CRH (cortiotropin releasing factor/hormone), which has a role
in affective regulation as well as an endocrine control.  The
redundancy here is useful, because a cell can respond to stimulus by
releasing CRF to a variety of areas that might affect - conveying that
information, and release CRF to the anterior pituitary, so that the
pituitary knows to release ACTH which will stimulate the adrenal
cortex to produce cortisol.

So, in the first case, its useful to have different chemicals
conveying different signals (fire  or dont fire), and in the latter
case it is useful to provoke multiple responses with one chemical.

Hope that helps, if you'd like more, let me know.

- Patrick

My take on "why" there are multiple neurotransmitters is somewhat
different.  There are multiple neurotransmitters because nature has
"found" multiple ways to solve the chemical signaling problem during
the course of evolution.  We happen to have the set of
neurotransmitters that we have because that combination has been found
to impart some selective advantage to our distant ancestors. (The
enzymes responsible for neurotransmitter release are very similar in
all vertebrates, so this set has been around for a while.)  The
particular set that we and our fellow vertebrates have is a result of
a long series of "experiments" involving mutations and lateral gene
transfers.

As to why some neurotransmitters are also act as hormones, it is
useful to be able to use the same compound for multiple purposes,
particularly if that compound is metabolically "expensive" to make.  
In everyday terms, if I'm running a factory, it will generally be
economically advantageous if I can use the same part in a number of
different processes or products.

Ok, i would like to accept Patrick's answer-- how do i do this?  

Also, my daughter has the following additional hypothesis/
clarificaion of how nt's might add content to the message-- perhaps
different transmitters used at the same synapse may provide a message
like "the consensus of A, B and C is yes, but the consensus of E and F
is no".

About the same chemical being used as an nt and a hormone, is it known
whether there is any direct connection between the 2 systems, say
hormones in the bloodstream directly stimulating neurons?  is that
what happens in the CRF example?

Thanks!

Sorry, but you can let your daughter know that's just not how the
system works.  Neurotransmitters generally potentiate or depotentiate
a neuron, making them more or less likely to fire.  They do not, by
themselves, encode a message with as much content as you desribed,
they merely represent the information, "this neuron X" fired.  The
actual higher-order information they represent is encoded in the
pattern of firing across the local network of neurons.  I am currently
a neuroscience student, and although research is being done, to my
knowledge we do not know exactly how information is represented in the
brain at the multi-cellular level, only the means by which neurons
interact and may possibly give rise to the information system.

This is a page about "neural networks" which gives a little
information about how this cellular process works, however is mostly
about computer modeling of this behavior, but it may prove helpful:
http://www.doc.ic.ac.uk/~nd/surprise_96/journal/vol4/cs11/report.html#Introduction%20to%20neural%20networks

Regards,
Andrewxmp

Lets see where to start....

First with a little vocab - there is no word "depotentiate", the
correct terms set of terms would be potentiate and inhibit, or excite
and inhibit, or depolarize and hyperpolarize.

Yes, the reason we have multiple neurotransmitters is due to selective
advantage.  No, this is not unique to vertebrates.  ACh, DA, and GABA
are some great examples. There is a huge body of literature using
Aplysia as a model for human learning and memory. So while taking the
stance that there are multiple NT's because nature selected for it is
correct, but it isn't good enough.  The interesting question is WHY
nature selected for it (see my original answer). With regrads to NT
release - its not enzymatically controlled per se.  NT synthesis is
another story - and the synthetic pathways for the monoamines are very
similar - they all involve hydroxylation (adding an -OH group) and
decarboxylation (removing a COOH group). Dopamine, Norepinepherine,
and Epinepherine all share the same pathway.  NT release is regulated
quite simply by calcium concentration.  The binding of calcium to
synaptotagmin is the crucial key in the release of the SNARE-SNARE
complex (proteins that attach a vessicle filled with NT to the cell
membrane) resulting in exocytosis of the NT.

It is not correct to speak of NT's encoding information in and of
themselves. They as I said either cause an IPSP or an EPSP (or in some
cases the transcription of a protein).  Their results do sum though. 
This is part of the interesting relationship seen in the Striatum
between D1, D2 dopamine receptors on neurons with colocalized
Glutamate receptors. In the case where a cell is heavily stimulated
via Glutamate, dopamine acting on D1 receptors will potentiate the
current, while acting on D2 receptors will decrease the current. So in
some regard information can be conveyed by the NTs.  For example,
cofiring of neurons in the locus corouleus and cortex to certain other
neurons can result in the synthesis of Substance P, a peptide NT,
wheras had only the glutamatergic info from cortex been received,
Substance P would not have been synthesised.

Ultimately though, the summation of IPSPs and EPSPs is the important
part of the system - its either GO or NO-GO. So certainly given a
neuron X, that recieves excitatory input from A, B, and C and
inhibitory input from D and E will integrate the information - the net
result being either an action potential or not.

The idea that "neurons that fire together, wire together" as proposed
by Donald Hebb is the theory that underlies a lot of neural
processing.  So, the point is, neurons do integrative work - A neuron
in the amygdala for example might be reciving thalamic sensory input
about a fearful stimuli, this same neuron could also be getting info
from the cortex to inhibit the firing - hence blocking the fear
response.

Don't think that its all clear, because it isn't, but we do know a lot
more than Andrew might have you believe.

A great example is the visual system.  The work that won Hubel and
Weisel thier nobel prize was on the structural organization of the
visual pathway.  They show through single cell recording (where an
electrode measures the firing of a single neuron) the differential
responses from photoreceptors, retinal ganglion cells, magno and
parvocellular layers of the lateral geniculate nucleus (the nucleus in
the thalamus where visual information is relayed) and from striate
cortex.  The visual system shows a clear hierachical processing that
is relativly straight forward to understand. We can see clearly how
the interactions allow us to be sensative to points of light, to
lines, to line orientation, to line movement. Its really quite
amazing.

With regards to your question about circulating hormones and
corralaries in the nervous system - its a really interesting one. 
Andrew is correct that it is likely that part of the reason NTs and
hormones are sometimes the same is efficiency. However, do not
underestimate the utility of divergent targets of release. Again, CRF
in the locus coeruleus and CRF in the pituitary may have different
results, but they both deal with stress reactivity.

I will first point out that elevated levels of CRF are present in the
CSF of depressed individuals - however, this correlation isn't
causation.

It is dangerous to think of peripheral hormones as an indicator of
brain state. Let me give an example. CRF is released from the
hypothalamus to the pituitary, but it is also released by nuclei in
the brainstem and in other areas including the amygdala.  When a
stressor is presented, these neurons do not necessarily co-fire. Now
that it is clear that the two don't necessarily have to be connected
in terms of firing and release, it is important to realize that yes,
circulating hormones can and do have an effect on the brain. CRF
doesn't provide negative feedback, but the product that it ultimately
results in does - Cortisol rapidly crosses the blood brain barrier
inhibiting CRF release and ACTH release at the levels of the
hypothalamus and anterior pituitary.  So circulating hormones can
directly have effects on central neurons.


So a final summary if I may.  Neurons that are recipients of NTs can
have specifically encoded information from those NTs but the general
case is that they are responding to a summation of IPSPs and EPSPs.
Circulating hormones can act on the nervous system, but just because a
circulating level of hormone is high, and that hormone also acts as an
NT at times doesn't mean the two are linked.

Well, I've slightly lost track of what I've said thus far, so I'm
going to go ahead and post this response. FYI, I am not a google
answerer, this information comes at no charge, I enjoy teaching what I
can about neuroscience - as a neuroscience student my eventual goals
are to continue my research, get an MD and PhD and eventually teach,
practice and research. So, I am more than willing to respond further.

All the best;

Patrick