HDTenEightyP/NetNews huggingface dataset:
From: wcalvin@stein.u.washington.edu (William Calvin)
Newsgroups: bionet.neuroscience
Subject: Re: What are neural columns?
Date: 19 Jan 93 18:58:46 GMT
Distribution: bionet
Organization: University of Washington
NNTP-Posting-Host: stein.u.washington.edu

tbrannon@CSEE.Lehigh.Edu (tbrannon) writes:
>Can someone provide a brief overview of what neural columns are?

The newer parts of cerebral cortex seem to have two levels of "modular"
organization, about 300 minicolumns (about 30-50 microns in diameter, possibly
corresponding to those lined-up cells you see in Nissl stains, radiating
up from the white matter) nestled inside a macrocolumn (maybe 0.5 mm in size).

Physiologically, they are defined by clustering of response types:  a
typical minicolumn is the orientation column of visual cortex, all of
whose neurons seemingly interested in lines/edges at about the same
(within 10 degrees) orientation.  A typical macrocolumn is the ocular
dominance column, best defined in layer IVc whose cells are only
responsive to one eye; move laterally and you find another 0.5mm wide
group that are interested in the other eye.

Some other collections have been called "columns" such as Hubel & Wiesel's
hypercolumns (essentially two ocular dominance columns, left and right,
taken together, each of which has a full range of orientation columns
embedded in it).  Somatosensory cortex is where macrocolumns were
discovered in the first place by Mountcastle in 1957, where modalities
(skin vs joint sensation, for instance) cluster.  They have been seen in
several of the secondary visual areas, specializing in various kinds of
feature detection.  There is no general theory for what association cortex
might be doing with this kind of organization, though I find myself working
on one (and NO, there is nothing on this in my books such as CEREBRAL
SYMPHONY or ASCENT OF MIND; it's all happened recently, e.g., Soc. Neurosci.
Abstr. 18:214.18, 1992).

    William H. Calvin   WCalvin@U.Washington.edu
    University of Washington  NJ-15
    Psychiatry & Behavioral Sciences
    Seattle, Washington 98195 FAX:1-206-720-1989
Newsgroups: bionet.neuroscience
From: lieke@sonne.zedat.fu-berlin.de (Dr. E. Lieke)
Subject: PST-Histogram
Organization: Free University of Berlin, Germany
Date: Mon, 25 Jan 1993 08:43:40 GMT

Hi,
does anybody know of a simple and inexpensive (not necessarily very acurate) wayhow to obtain a Post-Stimulus-Time-Histogram from extracellular recordings?

I need this for course in which I want to record muscle potentials. We are both
equipped with analog and digital oscilloscops and PC-clones (i386). I thought
about a combination of some simple hardware connected to a serial (COM) or
parallel (LPT) port and a piece of software (assembler, C or C++ or Basic, 
doesn't matter).

Can anybody help me with this problem?
Please reply via email to: lieke@sonne.zedat.fu-berlin.de

Newsgroups: bionet.neuroscience,comp.sys.mac.misc,sci.psychology
From: green@ie.utoronto.ca (Marc Green)
Subject: Re: MACs for psychophysics
Organization: University of Toronto, Department of Industrial Engineering
Date: Mon, 25 Jan 1993 12:59:44 GMT

davis@pacific.mps.ohio-state.edu ("John E. Davis") writes:


>I am posting this for a friend.  I have no idea of the proper group in which
>to post this article. 

>                        ------------------------------
>Our laboratory is interested using a Mac to display simple and complex 
>images as stimuli in human psychophysical experimentation.  We would need 
>control of the timing and need synch pulses to control auxiliary equipment. 
> Is anyone aware of commercial hardware/software packages to do this?  
>Please respond directly to duffyfr@a1.tch.harvard.edu.  Thank you.
>Frank H. Duffy




>--
>     _____________
>#___/John E. Davis\_________________________________________________________
>#
># internet: davis@amy.tch.harvard.edu
>#   bitnet: davis@ohstpy
>#   office: 617-735-6746
>#

Yes, there is a package called VideoToolBox which has these functions and a
lot more. It is available from ftp.stolaf.edu in pub/macpsych.

Marc Green
Trent University

Newsgroups: bionet.neuroscience,sci.med
From: senseman@lucy.brainlab.utsa.edu (David M. Senseman)
Subject: Re: primary afferent depolarization
Organization: University of Texas at San Antonio
Distribution: bionet
Date: Tue, 26 Jan 1993 12:36:42 GMT

In article <9301251254.AA21883@xray1.cshl.org> anderson@CSHL.ORG (John Anderson) writes:
>I have been reading 
>
>  Sykova E. (1991) "Activity-related ionic and volume changes in
>  neuronal microenvironment" in _Volume Transmission in the Brain_ (K.
>  Fuxe, L.F. Agnati, Eds.), pp 317-336, Raven Press, New York.
>
>In that article, the following statement is made:
>
>  "[Extracellular] K+ accumulation has been accepted as one of two
>  causal factors (together with GABA) in primary afferent
>  depolarization, which is the mechanism underlying presynaptic
>  inhibition.  It is assumed that the increase in [K+]e that is
>  associated with repetitive neuronal activity reduces transmitter
>  release by curtailing the presynaptic spike amplitude by presynaptic
>  depolarization."
>
>Could someone please explain this statement?  How does presynaptic
>depolarization reduce the presynaptic spike amplitude?  Seems like it
>should enhance it.
>

PAD (primary afferent depolarization) isn't all that mysterious.
Why would expect depolarization to ENHANCE transmitter release?
Assuming that the axonal spike completely invades all the terminals,
(probably a reasonable assumption for most systems Eva was 
referring to), then depolarization would DECREASE syanptic release
simply because the membrane potential of the presynaptic terminal
would be closer to V    which is going to be somewhere above +100 mv.
                    Ca

(Hard to do subscripts :)

That means the electrical force driving Ca inward would be reduced 
so that calcium entry during the terminal spike would be reduced.
Since transmitter release is dependent on entry of external Ca,
less transmitter release would occur.

If you get enough PAD so that the terminal membrane is really
depolarized, then additional factors could come into to play
such as channel inactivation.


-- 
David M. Senseman, Ph.D.              | Imagine the Creator as a low 
(senseman@lonestar.utsa.edu)          | comedian, and at once the world 
Center for Information Visualization  | becomes explicable.
University of Texas at San Antonio    |               H.L. Mencken 
Newsgroups: bionet.neuroscience
From: aankrom@nyx.cs.du.edu (Anthony Ankrom)
Subject: Re: Questions about methylphenidate (Ritalin)
X-Disclaimer: Nyx is a public access Unix system run by the University
	of Denver for the Denver community.  The University has neither
	control over nor responsibility for the opinions of users.
Keywords: stimulant, pharmacology, ciba
Organization: Nyx, Public Access Unix at U. of Denver Math/CS dept.
Date: Sat, 23 Jan 93 20:23:01 GMT

In article <1jqqqkINNprd@overload.lbl.gov> herzog@ux5.lbl.gov (Hanan Herz
g) writes:
>Hi,
>	What are the effects of Ritalin on the central nervous system
>(technically, speaking)? What makes it a stimulant (i.e. how does it
>increase vigilance)? What are the long term effects of its use?
>Finally, what are its side-effects (command and rare)?
>
>Please reply by e-mail or e-mail me a copy of your post.
>
>Thanks,
>
>Hanan


 Ritalin is more like cocaine in its action than an amphetamine. It has
been shown to be a dopamine uptake inhibitor of similar potency to cocaine.
 I'm not sure of the side effects, but they can be found in a PDR.

St. Anthony
From: w0285@desire.wright.edu
Newsgroups: bionet.neuroscience
Subject: Thank you
Date: 28 Jan 93 02:07:08 GMT
Organization: Wright State University

Dear members,
	Thanks for helping me with my paper on schizophrenia.  I am still
working on it.  Unfortunately, I feel like I could write a book on this topic
alone.  So I have more journal articles than I can handle.  
				Tracy Craft
Newsgroups: bionet.neuroscience
From: YHADEISH@biomed.med.yale.edu (Yukiharu Hadeishi)
Subject: Re: Schizophrenia and the immune system
Organization: Yale University
Date: Sun, 24 Jan 1993 01:08:01 GMT
X-News-Reader: VMS NEWS 1.20

In a previous article, jxj24@po.CWRU.Edu (Jonathan Jacobs) says that:
> In a previous article, mitchm@casbah.acns.nwu.edu (Mitchell Maltenfort) says:
>>
>>       I was recently watching a PBS "Frontline" on schizophrenia, and was
>>struck by an idea when it was mentioned that schizophrenics have certain
>>white blood cell abnormalities.  Is it possible that schizophrenia is an
>>autoimmune disease?
> ...
>It is an interesting question alright.  It certainly seems plausible
>enough, and god knows that there are about a zillion ways your immune
>system can turn on you when you least expect it.  And there are about
>a zillion more ways that your brain can unravel on you when you least
>realize it.

I couldn't agree more.  In fact, there are probably many more ways than a
merely a zillion for the immune system to go wrong--- but my understanding is
that it cannot be a conventional, plain vanilla, lymphocyte-mediated autoimmune
response, if schitzophrenia is an autoimmune-mediated disease.  I may very well
be wrong here, not being directly involved in research in this area, but my
understanding is that there are no post-capillary venules feeding into the
brain, and thus no way for immune cells to penetrate into brain tissue (don't
ask me how microglia do it; maybe they truly are resident monocytes...).  Since
lymphocytes are unable to cross the blood-brain barrier, there is no way
(within the current model, of course...  ;-)  ) for there to be an autoimmune
reaction.

The fact that the brain is an immune-privileged area makes sense, from a
teleological perspective:  since the fine connectivity of the brain is
extremely important, and since most of your brain cells are no longer dividing
for most of your life, one cannot afford to have bloody wars going on in there,
pushing neurons this way and that, or worse, killing off neurons in the heat of
phagocytosis--- it would be a real mess.  We, meaning all life forms advanced
enough to have brains, are better off suffering from the occasional slow brain
virus than going through repeated inflammation responses and who knows what all
causing irreparable damage in the effort to save the brain from minor mishap.

Anyway, that's my understanding of the situation.  Please correct me if I am
wrong, all those who know more than I out there, I beg of you.

  -- yh.


------------------------------------------------------------------------------
Yukiharu "Yuki" Hadeishi   ---   Lurker at Large
Internet:  yhadeish@biomed.med.yale.edu
The Interdepartmental Neuroscience Program will have
absolutely nothing to do with any of my opinions...
From: anderson@CSHL.ORG (John Anderson)
Newsgroups: bionet.neuroscience
Subject: neural net simulators
Date: 24 Jan 93 20:50:21 GMT
Distribution: bionet

I tried several times to reply directly to the poster, but bounced
every time, so I'm posting to the newsgroup, since others may be
interested as well.

tbrannon@csee.lehigh.edu wrote:

>   Could you fill me in on GENESIS? Ie, obtaining, features?

GENESIS is a biological neural net simulator developed by Jim Bower's
group at Caltech.  It uses X Windows and has a nice graphical user
interface called XODUS.  You can model individual neurons or networks
of them.  There are a number of neural net simulators available.
Several of them are discussed and compared in an article in the
November 1992 issue of Trends in Neurosciences:

	E. De Schutter (1992) "A consumer guide to neuronal modeling
	software" TINS 15:462-464.

There is a table in that article giving addresses for the people
responsible for the packages it discusses.  The GENESIS contact is 

	C. Ploegaert
	Division of Biology
	216-76
	California Institute of Technology
	Pasadena, CA 91125
	FAX 818-795-2088
	genesis@cns.caltech.edu

By the way, that whole issue of TINS is about modeling the nervous
system, so you might want to check it out.

John
-------
John E. Anderson
W. M. Keck Structural Biology Laboratory
Cold Spring Harbor Laboratory
From: YHADEISH@biomed.med.yale.edu (Yukiharu Hadeishi)
Newsgroups: bionet.neuroscience
Subject: CO as retrograde messenger
Date: 27 Jan 93 05:01:00 GMT
Organization: Yale University
X-News-Reader: VMS NEWS 1.20

Okay, now that nitric oxide has finally made the cover of several national
magazines--- what's this I hear about carbon monoxide?  Sorry if I've been a
bit myopic, but I just heard about the existence of a carbon monoxide synthase
that's located in hippocampal pyramidal cells among other places.  Moreover, I
understand that carbon monoxide blocks LTP in slices.  Is this true?  Can
anybody give me a citation on this stuff?  I scanned through our miniMedline
and found no mention of any article yet.  I checked under Solomon Snyder,
Charles Stevens, and Ajay Verma.

Can anyone help me out with this?  A free smilie to the first person to get me
the correct citation!  ;-)  I think Stevens did the slice experiments.  Thanks
to all in advance!

  -- yh.

P.S.  Apologies to all those who might be infuriated by requests such as this
  one, but I think pretty much everybody is interested by this new class of
  neurotransmitters...


-----------------------------------------------------------------------------
Yukiharu "Yuki" Hadeishi   ---  Lurker at Large
Internet:  yhadeish@biomed.med.yale.edu
The Interdepartmental Neuroscience Program will have
absolutely nothing to do with any of my opinions...
From: mvcy@vax5.cit.cornell.edu
Newsgroups: bionet.neuroscience
Subject: Re: primary afferent depolarization
Date: 28 Jan 93 17:04:46 EST
Distribution: bionet
Organization: Cornell University

In article <1993Jan26.123642.11726@ringer.cs.utsa.edu>,
senseman@lucy.brainlab.utsa.edu (David M. Senseman) writes: 
> 
> PAD (primary afferent depolarization) isn't all that mysterious.
> Why would expect depolarization to ENHANCE transmitter release?
> Assuming that the axonal spike completely invades all the terminals,
> (probably a reasonable assumption for most systems Eva was 
> referring to), then depolarization would DECREASE syanptic release
> simply because the membrane potential of the presynaptic terminal
> would be closer to V    which is going to be somewhere above +100 mv.
>                     Ca
> 
> (Hard to do subscripts :)
> 
> That means the electrical force driving Ca inward would be reduced 
> so that calcium entry during the terminal spike would be reduced.
> Since transmitter release is dependent on entry of external Ca,
> less transmitter release would occur.
> 
> If you get enough PAD so that the terminal membrane is really
> depolarized, then additional factors could come into to play
> such as channel inactivation.
> 
> 
> -- 
> David M. Senseman, Ph.D.              | Imagine the Creator as a low 
> (senseman@lonestar.utsa.edu)          | comedian, and at once the world 
> Center for Information Visualization  | becomes explicable.
> University of Texas at San Antonio    |               H.L. Mencken 

You are forgetting that when the terminal membrane is depolarized, Calcium
channels would tend to open (It is, after all voltage sensitive, and that's
the mechanism for normal release when the AP invades the terminals).  So
your reasons are not valid, since there would be a steady calcium inward
current at rest.

The reason PAD seems to work is thought to be due to the property of Calcium
channels (at least some type of calcium channels anyway).  They seem to be
inactivated by a high concentration of internal calcium concentration.
This calcium dependent inactivation of calcium channels would keep the resting
currents low.

Review your Hille.

Sat Amagai
mvcy@cornella.cit.cornell.edu

Xref: sparky bionet.neuroscience:682 sci.med:24329 alt.drugs:21316 alt.psychoactives:1788
From: herzog@ux5.lbl.gov (Hanan Herzog)
Newsgroups: bionet.neuroscience,sci.med,alt.drugs,alt.psychoactives
Subject: Questions about methylphenidate (Ritalin)
Followup-To: bionet.neuroscience
Date: 23 Jan 1993 07:07:00 GMT
Organization: Lawrence Berkeley Laboratory
NNTP-Posting-Host: ux5.lbl.gov
Keywords: stimulant, pharmacology, ciba

Hi,
	What are the effects of Ritalin on the central nervous system
(technically, speaking)? What makes it a stimulant (i.e. how does it
increase vigilance)? What are the long term effects of its use?
Finally, what are its side-effects (command and rare)?

Please reply by e-mail or e-mail me a copy of your post.

Thanks,

Hanan
From: kristoff@NET.BIO.NET (David Kristofferson)
Newsgroups: bionet.neuroscience
Subject: BIOSCI/bionet Frequently Asked Questions
Date: 22 Jan 93 10:00:02 GMT
Distribution: bionet


New users of BIOSCI/bionet may want to read the "Frequently Asked
Questions" or "FAQ" sheet for BIOSCI.  The FAQ provides details on how
to participate in these forums and is available for anonymous FTP from
net.bio.net [134.172.2.69] in pub/BIOSCI/biosci.FAQ.  It may also be
requested by sending e-mail to biosci@net.bio.net (use plain English
for your request).  The FAQ is also posted on the first of each month
to the newsgroup BIONEWS/bionet.announce immediately following the
posting of the BIOSCI information sheet.

				Sincerely,

				Dave Kristofferson
				BIOSCI/bionet Manager

				kristoff@net.bio.net
Xref: sparky bionet.neuroscience:698 comp.ai.neural-nets:4983
From: mitchm@casbah.acns.nwu.edu (Mitchell Maltenfort)
Newsgroups: bionet.neuroscience,comp.ai.neural-nets
Subject: glitches compiling SNNS on RS6000
Date: 26 Jan 93 17:56:04 GMT
Organization: Northwestern University, Evanston Illinois.


	I've FTP'd and unarchived the Stuttgart NN simulator successfully, but
I keep having an error compiling the xgui interface: compiling funcdispl.c, it
told me that "printf" cannot be redeclared.  Now the RS6000 has some odd ways
of doing things, so I expect there's a simple, fixable bug.  Could someone
please tell me what it is?  Thanks.  


Mitchell Maltenfort	Northwestern Unversity	Chicago, Illinois

mgm@nwu.edu		|:* Studying simulations or simulating studies *:|
From: knowled@ccsmtp.ccf.org (Doug Knowles)
Newsgroups: bionet.neuroscience
Subject: Re: primary afferent depolarization
Date: 26 Jan 93 18:06:52 GMT
Distribution: bionet
Organization: Cleveland Clinic Foundation

In article <1993Jan26.123642.11726@ringer.cs.utsa.edu> senseman@lucy.brainlab.utsa.edu (David M. Senseman) writes:
>From: senseman@lucy.brainlab.utsa.edu (David M. Senseman)
>Subject: Re: primary afferent depolarization
>Date: Tue, 26 Jan 1993 12:36:42 GMT
>In article <9301251254.AA21883@xray1.cshl.org> anderson@CSHL.ORG (John Anderson) writes:

>>Could someone please explain this statement?  How does presynaptic
>>depolarization reduce the presynaptic spike amplitude?  Seems like it
>>should enhance it.
>>
>
>PAD (primary afferent depolarization) isn't all that mysterious.
>Why would expect depolarization to ENHANCE transmitter release?
>Assuming that the axonal spike completely invades all the terminals,
>(probably a reasonable assumption for most systems Eva was 
>referring to), then depolarization would DECREASE syanptic release
>simply because the membrane potential of the presynaptic terminal
>would be closer to V    which is going to be somewhere above +100 mv.
>                    Ca
>That means the electrical force driving Ca inward would be reduced 
>so that calcium entry during the terminal spike would be reduced.
>Since transmitter release is dependent on entry of external Ca,
>less transmitter release would occur.
>

	I don't agree.  The driving force on Ca++ is determined by the
	voltage *during* the spike when the voltage-sensitive Ca channels 
	are opened.  Besides, the driving force on Ca++ is so large that
	a few millivolts depolarization from rest wouldn't make much 
	difference.


>If you get enough PAD so that the terminal membrane is really
>depolarized, then additional factors could come into to play
>such as channel inactivation.
	
	This is probably more important--inactivation can occur
	near resting membrane potential.
	
>
>
>-- 
>David M. Senseman, Ph.D.              | Imagine the Creator as a low 
>(senseman@lonestar.utsa.edu)          | comedian, and at once the world 
>Center for Information Visualization  | becomes explicable.
>University of Texas at San Antonio    |               H.L. Mencken 

W. Douglas Knowles, Ph.D.            E-mail: knowled@ccsmtp.ccf.org
Department of Neurosciences          voice:  (216) 444-3870
Cleveland Clinic Foundation          FAX:    (216) 444-7927
9500 Euclid Avenue                   
Cleveland, OH 44195 USA              other:   hey, you!
 
quote: "We need not all give our whole time to the currently more glamorous
"molecular biology"; it will doubtless come soon enough."  I.H. Page 1962
   
Newsgroups: bionet.neuroscience
From: ddoherty@ics.uci.edu (Donald Doherty)
Subject: Re: Neural Columns
Reply-To: ddoherty@ics.uci.edu (Donald Doherty)
Organization: Univ. of Calif., Irvine, Info. & Computer Sci. Dept.
Date: Sat, 23 Jan 1993 01:27:38 GMT

In article <1jfig7INNf8o@shelley.u.washington.edu> wcalvin@stein.u.washington.edu (William Calvin) writes:
>erwin@trwacs.fp.trw.com (Harry Erwin) writes:
>
>>I'm looking for a good reference on the functions and dynamics of neural
>>columns. 
>
>>-- 
>>Harry Erwin
>>Internet: erwin@trwacs.fp.trw.com
>
>Vernon Mountcastle's chapter in THE NEUROSCIENCES FOURTH STUDY PROGRAM
>(MIT Press 1979) is a good summary.  Shaw, Harth and Scheibel in
>Experimental Neurology 77:324-358 (1982) is a good theoretical take on the
>subject.
>    William H. Calvin   WCalvin@U.Washington.edu
>

Hi Harry,

  Dr. Calvin's suggestion by Vernon Mountcastle is your best bet (Mouncastle
is one of the originators of the idea).  FYI, the same chapter is contained
in a book titled "The Mindful Brain: Cortical Organization and the Group-
Selective Theory of Higher Brain Function," by Gerald Edelman and Vernon
Mountcastle (1978) MIT press.

  Also what you are refering to as neural columns are more commonly refered to
as "cortical columns."  And it is good to keep in mind that cortical columns
are an idea that may have positive heuristic value but may or may not
actually exist.

Don

-------------------------------------------------------------------------------
Donald Doherty
Dept. of Psychobiology		Email:	    ddoherty@ics.uci.edu
University of California	CompuServe: 76646,1321
Irvine, CA  92717-4550		FAX:	    (714) 725-2447
U.S.A.				Voice:	    (714) 856-1776

Newsgroups: bionet.neuroscience
From: dbrown@newssun.med.miami.edu (Daniel Brown)
Subject: Request for Human Computational Models
Organization: University of Miami, School Of Medicine
Distribution: bionet
Date: Fri, 22 Jan 1993 14:14:40 GMT

Previously there was a request for information about human computational
models.  I tried to respond to the poster, but my mailer couldn't find his
address.  Here's the reply, slightly condensed:

There are many neural net human, computational models, particularly in 
the study of vision.  Because I'm not sure what kind of model you're
interested in (derived from empirical data, functional equivalency, etc.)
I won't list any articles.  However, a good overview of the use of NN
models of the human brain can be found in

	Patricia Churchland and Terrence Sejnowski, 
	_THE_COMPUTATIONAL_BRAIN_, (Cambridge: MIT Press, 1992).

For articles about neurocomputational models, look in

	_THE_JOURNAL_OF_COGNITIVE_NEUROSCIENCE_

	_NEURAL_NETWORKS_

	_NEURAL_COMPUTATION_

and I think that there's a new one called

	_THE_JOURNAL_OF_COMPUTATIONAL_NEUROSCIENCE_

Look for articles by

	Zipser, Sereno, Sejnowski, Lynch, Granger, Poggio, Hinton,
	Cohen, Grossberg, Carpenter, McNaughton, etc.

These authors have written about anything from hippocampal STM to
hyperacuity in vision.

Hope that helps!

Dan