From: langston@memstvx1.memst.edu (Mark C. Langston)
Newsgroups: alt.cyberpunk.tech
Subject: Neuropolis - v.92.01
Date: 25 Aug 92 21:57:58 -0600
Organization: Memphis State University






		           PsychoNaut Labs
		             Presents...
		  _________________________________
		 /                                 ]
		[ *     o                  o     * ]
		[       |       _          | `  _  ]
		[     |\| E {/ |  [] |] [] | | |_  ]
		[     | |            |     '    /  ] 
		[  o__|______________|_________/   ] 
		[     !              |             ]   
		[     ;              ;             ]
		[     o              o             ]
		[         ..increase your          ]
		[ *          bandwidth.          * ]
		[_________________________________/   
                            ___________
			   [__v.92.01__]
                                 _       _
		    NEUROPOLIS (nu rahp' o lis) 
                 A medium to advance the utility of
                      information technology.


+--------------------------------------------------------------
|
; The purpose of Neuropolis:
:   
|   Many advances have been made in information technology, most
!  notably the InterNet.  Many scientists, philosophers, entrepreneuers,
:  educators, writers, and techophiles of all sorts delight in 
.  speculation about the possibilities of cutting-edge technology.
.   However, the denser the signal, the greater the possibility for
   noise.  Neuropolis (city of the mind), is presented as a medium
   to advance the utility of information technology, through the
   dissemination of research summaries, news bites, and references
   for the latest in both high-tech and street-tech.
    Bluntly, our goal is to keep you informed, and allow you to become
   more informed.  To feed you a strong, clean signal.
    NEUROPOLIS will be transmitted on a quarterly basis, or more 
   frequently, depending on available time and material.  Any opinions
   expressed in neuropolis are solely those of the _cited_ author, and
   not those of the authors of neuropolis, as we are not here to form 
   opinions, but merely to supply information.  Neuropolis has no
   connection to Memphis State University, other than being one of the
   many nodes that this transmission may visit.


+--------------------------------------------------------------
|                         _________________
;                        [__Contributions__]
:
|    The authors would be more than willing to accept any written works,
!  either fiction or nonfiction, for consideration.  If the submission
:  is nonfiction, references, data ( if applicable), and publication site
.  must be included, since we strive to provide a clean signal. 
.  Anyone wishing to contribute to future issues can submit to:
   langston@memstvx1.memst.edu.  Comments and suggestions are also welcome.






 
			 ___________________
			[__Available_Bands__]

		    [1]	Cognitive-Enhancing Drugs
                    [2] Nerve-On-A-Chip
                    [3] Neural-interface Street Tech




+--------------------------------------------------------------
|		     _____________________________	 
; 		    [__Cognitive-Enhancing_Drugs__]
:
| [ The following article was written by Karen Moline, and originally
!  appeared in _HeadLines_, May/June 1992.  Reprinted w/o permission ]
:
.   Over the past decade, a myriad of drugs has been examined for their
. potential to improve cognitive deficits.  because learning is a 
  biochemically-mediated process that depends upon a unique interrelation
  -ship between neurotransmitters -- certain ones of which play a key role
  in the acquisition of information, learning, and memory -- researchers 
  have focused their studies on drugs that influence these neurotransmitters
  and neurotransmitter systems. 
  A balancing act...
    As evidenced by patients with brain injury and Alzheimer's disease (AD),
  any interference in the functioning of the neurotransmitters can upset the 
  delicate balance and ultimately cause learning and memory dysfunction.  In
  the case of traumatic brain injury (TBI), the cognitive impairment results
  when the neurotransmitter network is disrupted, while in patients with AD, 
  the associated memory loss is thought to be due to a breakdown of neuro-
  transmitters.  Researchers believe that several neurotransmitter systems
  may participate collectively in the pathologic process of cognitive impairment.
  Biochemically enhancing these compromised neurotransmitter systems may be
  necessary to facilitate remediation in attention, memory, and learning 
  impairments.
    To date, much of the experimental research has involved animals and aged 
  humans with dementias (particularly AD), as well as persons with attention-
  deficit disorders and psychiatric conditions.  The extent to which the findings
  are generalizable and relevant to the treatment of attention and memory 
  deficits in individuals with TBI is unclear.  Theoretically, however, 
  understanding the basic underlying biochemical mechanisms of cognition can
  assist in the development of pharmacologic treatments with a potential to
  enhance attention, memory, and learning.

  Development of cognitive-enhancing drugs...
    "Traumatic brain injury is a very broad indication involving a considerable
  heterogeneous group of disorders," acknowledges Elkan Gamzu, PhD, a neuro-
  pharmacologist and president of Massachusetts-based Cambridge neuroScience.
  "The nature of the injury and where the injury occurs can influence the type
  of cognitive dysfunction and how it is treated.  In actual practice, little
  is being used for the long-term treatment of cognitive dysfunction in patients
  with TBI because of these various problems."
    Similar problems exist in the search for specific pharmacologic agents to 
  treat the memory loss associated with AD.  Gary Wenk, PhD, a psychopharmo-
  cologist in the division of neural systems, memory, and aging at the University 
  of Arizona in Tuscon, points out that "we don't know enough yet about aging
  to be able to develop a single compound that addresses the problem of
  cognitive dysfunction.  Everyone ages so differently, and multiple body systems
  degenerate in unique ways.  As a result, drugs may need to be targeted to a 
  specific system that has become compromised with age, and cognitive dysfunction
  may have a relatively unique etiology in different people."
    Although no single cognitive-enhancing drug under investigation consistently
  improves memory, attention, or cognitive function in all clinical and
  experimental settings, four pharmacologic groups have demonstrated varying 
  degrees of potential for cognitive enhancement.  However, overall results have
  been mixed.

  Cholinergic Agonists
    The colinergic system has been studied most extensively by researchers 
  because of a demonstrated role in the neural processes that underlie learning
  and memory.  Evidence suggests that augmenting colinergic transmission 
  appears to facilitate short-term memory function in animals and humans,
  whereas anticholinergic activity disrupts memory storage.  Much of the
  research has involved patients with AD;  the short-term memory loss in AD
  and geriatric dementias has been associated with impaired cholinergic function.
    Researchers also believe that cholinergic stimulation may assist in the
  incorporation of new information into long-term memory storage.  They note 
  that this function may have important implications for the treatment of TBI
  because similar deficits in transferring from short-term memory into long-term
  memory are common in both conditions.
    A compromised cholinergic system may not be solely responsible for 
  cognitive impairments.  Wenk has studied this system in rats and reports that
  behavioural performance suggestive of learning and memeory function is not
  disrupted when rats are given a toxic substance that destroys all cholinergic
  transmission.  The finding suggests that cholinergic dysfunction may be just 
  one aspect of biochemical memory impairment.
    Physostigmine is one cholinergic agonist that is being increasingly
  evaluated in TBI.  Primarily studied in Alzheimer's disease, this drug has
  produced modest outcomes in memory improvement.  Researchers at the University
  of Washington reported improved memory function in patients with brain damage
  due to carbon monoxide poisoning by combining memory training with adminis-
  tration of oral physostigmine (_Brain_Injury_ 1987;1,2:145-149).  Increasing
  the availability of acetylcholine may promote a greater state of arousal that
  enhances the patient's ability to benefit from memory training.  The research-
  ers also determined individual therapeutic levels of physostigmine and followed
  patient progress over time.  Although only two patients were studied, these
  findings contribute to a greater understanding of the narrow therapeutic
  range of physostigmine and the variable long-term cognitive performance after
  brain injury.
    Researchers believe that THA (tetrahydroaminoacridine), or tacrine, an anti-
  cholinesterase, may have potential for improving memory performance in AD and
  ultimately may find utility in TBI.  Tacrine is being investigated in a 
  multicenter study to determine efficacy, safety, and optimal dosage range.
  Earlier studies suggest improved cognitive function in AD, but results are 
  not conclusive.

  Catecholamine Agonists
    Catecholamine agonists, which increase the activity of norepinephrine or
  dopamine at the postsynaptic receptor, appear to have an important role in
  facilitating learning in patients with TBI by stimulating arousal and 
  attention.  Gregory O'Shanick, MD, a neurophyciatrist at the Center for
  Neurorehabilitation Services in Richmond, Virginia indicates that "L-dopa,
  bromocriptine, and amantadine are used most frequently in clinical 
  practice to treat cognitive impairments after brain injury."  Although these
  drugs have a primary indication in other therapeutic areas, they have been
  found to be clinically useful for trating learning and memory deficits
  associated with TBI.

  Neuropeptides
    Vasopressin, a neuropeptide compound, has been studied extensively in 
  animals and humans with regard to memory and attention, and apparently is 
  the only neuropeptide to be evaluated in patients with TBI, with mixed
  results.  Improvements in memory initially were thought to be the primary
  effect of vasopressin.  More recent studies, however, suggest that attention
  and motivation also may be positively influenced.  Clinical application of 
  this compound may be limited by the effects of vasopressin on electrolytes 
  and sodium homeostasis.
    Results from current animal research of Org2766 indicate improved 
  behavioural performance on spatial orientation tasks.  This neuropeptide
  appears to facilitate recovery of function after brain injury and to 
  counteract age-related decreases in performance in rats (_Brain_Research_
  1990;527:192-197).

  Nootropics
    The nootropics are relatively new compounds with unique chemical 
  structures and unproven mechanisms of action that have demonstrated
  cognitive-enhancing properties.  Nootropics improve general functioning of
  the central nervous system by stabilizing impaired homeostatic functions
  and protecting against various types of insults.  Evidence suggests that 
  information acquisition and performance may be enhanced through a normal-
  ization of disruption in basic functioning in the brain.  "Nootropics 
  demonstrate reliable effects in animals that can be relevant for humans, but
  the beneficial effects are not clear at this time," says Gamzu, who suggests
  that the cognitive-enhancing properties of nootropics are yet to be proven
  in humans.  Most nootropic compounds are not available for clinical use in
  the US, although they are used in various European countries for the 
  cognitive enhancement of patients with AD and stroke-related memory loss.
    In a recent double-blind study, the nootropic, pramiracetam, was 
  evaluated against placebo to determine its effectiveness in treating memory
  and other cognitive problems in four adult males with severe brain injuries
  (_Brain_Injury_ 1991;5,4:375-380).  Clinically significant improvements in
  delayed recall and information retrieval were observed during treatment
  phases.  The improvements were maintained for up to six months after the
  study ended and for one month following the discontinuation of pramiracetam.
    Phosphatidylserine, a nootropic with a phospholipid structure, was given to
  149 patients with age-associated memory impairment in another recent placebo-
  controlled study (_Neurology_ 1991;41,5:644-649).  Treated patients displayed
  greater improvements in learning and memory tasks of daily life than patients
  who received placebo.  A subsample analysis revealed that patients whose
  pretreatment performance level was relatively low were most likely to 
  respond.  The encouraging results, although not conclusive, suggest that this
  compound may be useful in treating memory loss associated with aging.

  Development considerations...
    Although promising results are anticipated in the development of cognitive
  enhancers, it may be wise to heed caution in being overly optimistic for 
  immediate application in TBI.  "Drugs that demonstrate effectiveness in 
  treating memory loss in Alzheimer's disease may find secondary application
  for TBI," proposes Gamzu.  "A [more] rational search for drugs to treat
  Alzheimer's disease is possible because reasonable hypotheses exist about
  the cause of the symptoms and how to treat them."
    Because of the unique nature of the therapeutic area of TBI and cognitive
  dysfunction, special considerations are necessary for effective drug
  development.  Such concerns include suboptimal routes of administration,
  toxic side effects, and lack of standardized measurements of memory improve-
  ment, says O'Shanick.  In addition, the poor correlation between animal and 
  human models of cognitive dysfunction must be addressed.  Evidence also
  suggests that the extent of inter-individual variability in dosing is likely
  to be greater than in other therapeutic areas, requiring the identification
  of a specific therapeutic range for individual patients.  Finally, researchers
  note that time may be a limiting factor in determining the clinical efficacy
  of these compounds because the beneficial effects may not be observed until
  after many weeks of treatment, thus necessitating longer-term clinical trials.
    Regarding the future of pharmacologic intervention for cognitive enhancement,
  Wenk believes that research may reveal an underlying interaction between 
  multiple neurotransmitter systems, rather than one critical neurotransmitter.
  Enhancement of an assumed deficiency via new drugs or, potentially, a form
  of nutritional therapy, ultimately will assist in improving memory and
  learning.  Proposes Wenk, "One day we will have an effective cognitive-
  enhancing drug to treat compromised patients, and perhaps even improve
  memory in normal, healthy individuals."


+------------------------------------------------------------
|                           ___________________
; 			   [__Nerve-On-A-Chip__]
: 
| [ author: E. Pennisi, reprinted from Science News, December 21 & 28, 1991
!  reprinted w/o permission...]
: 
. New analog chip acts just like a nerve cell
    It may look like an ordinary computer chip, but the 'silicon neuron' is
  nothing like those that run even the most avant-garde machines.
    Two computational neuroscientists have made a new chip that brings re-
  searchers a step closer to creating a machine that mimics the nervous
  system.  Because the device uses a new type of analog technology, its
  transistors act like nerve-cell membranes, says Misha Mahowald, a graduate
  student at the California Institute of Technology in Pasadena.  She and
  Rodney J. Douglas of the University of Oxford in England designed the chip
  so that its circuits replicate the electrical currents that affect cell
  membranes and cause nerve cells to fire.  They describe the device in the 
  Dec. 19/26 _Nature_.
    Mahowald and Douglas are now working out the technical details for
  putting many neurons onto one chip and interconnecting a series of chips to
  create 'megacircuits' that can model brain function, Douglas says.
    In addition, the researchers plan to link the silicon neurons to existing
  analog chips that mimic sensory nerve cells in the ear (SN: 1/6/90, p7) or
  in the retina, Mahowald says.
    Scientists currently simulate small groups of neurons by using neural
  networks, but the computer programs take a long time to run, even on very
  powerful machines.  "[silicon] neurons could solve these kinds of 
  problems very easily'" says Douglas.  Even with thousands hooked together,
  silicon neurons should work at least as fast as the nerve cells they
  emulate and with little power consumption, he says.
    Douglas and Mahowald hope to make an easy-to-use system that neurobio-
  logists can put to work testing ideas about neural circuitry.  "We'd like 
  to make a cheap, fast tool for the 'neuroscientist in the street,'" Douglas
  says.
    Because even a network of silicon neurons operates in real time and requires
  little power, Douglas thinks robotics may find these neurons more useful
  than artificial intelligence computers for controlling robots that must
  maneuver on their own.
    Computer chips typically use digital signals to operate; thus, a signal is
  either on or off, but never partly on.  Analog devices need less power to run,
  and they operate very rapidly.  Their signals exhibit a continuum of res-
  ponses, so they lack the precision of their digital counterparts.  "But a
  very important characteristic of the brain,' notes Douglas, "is that it
  doesn't do things very precisely."
    For years, Douglas has studied the electrical properties of brain cells
  involved in vision.  His research provided the details necessary to design
  the circuitry in the silicon enuron.  "It all rests on the fact that trans-
  istors in this subthreshhold regime have physical characteristics of a 
  real membrane," Douglas says.
    For example, in a nerve cell, the membrane serves a function similar to
  the gate in a transistor.  To conduct a current, a transistor lets elec-
  trons through its gate.  Likewise, a cell membrane's current results when
  channels in the membrane open briefly to let ions move into and out of the
  cell.  The types of membrane channels and the rate at which they open 
  result in the different impulses that let nerve cells communicate with 
  each other.
    Douglas and Mahowald designed the silicon neuron so that each of its 
  circuits represents a different kind of membrane channel.  With these
  circuits, they can recreate the various types of currents that make a nerve
  fire.
    According to Mahowald, several neurobiologists have had trouble dis-
  tinguishing between the patterns generated on oscilloscopes by real
  neurons and their silicon counterparts.
    "It comes closer than anything I could ever imagine," says Oxford
  neurobiologist Kevan A. C. Martin.  "It does in an electronic way what a
  biological neuron is doing.  That's tremendously exciting."  
  
  
  
  
+------------------------------------------------------------------  
|                    ________________________________
;                   [__Neural-interface_Street_Tech__]
:
|  [ reprinted from Science News, Nov. 30, 1991, p361, w/o permission.
!    original author: E. Pennisi ]
:
.  [ excerpted]
  
    [Christopher P.] Stone, a 17-year old tinkerer from Bloomington, Ind.,
  combines [various] perspectives in his approach to research.  As a high
  school freshman, he built an insect robot, in part by scavenging syringes
  for pistons and removing voltage converters from old computer printers for
  use in his robot.  Last year, he got interested in how crayfish walk and
  began probing their nervous systems.  For his junior year science project
  he pinpointed crayfish nerve cells involved in walking and connected them
  to his computer via very thin copper wires.  He then modified the computer
  program that coordinated the robot's legs.  With this new version, he 
  stimulated a living crayfish by sending very tiny voltages down the copper
  wires.  The voltages made the animal amble across a table.

    "I want to help make [paralyzed] people walk, and for quadriplegics to
  sign their names," says Stone about his long-term goals.
  
  
  
+-----------------------------------------------------------------
|                           ____________________
;                          [__End_Transmission__]
:
|
!
.