www.cerebral.org/neurotransmitters
Glutamate in the CNS:
The
Glutamatergic System
Glutamate Alzheimers connection http://www.memantine.com/inhalte/s2.html
- Glutamate Migraine connection
-
- Cananzi
AR, et al. [See
Related Articles]
- Platelet and plasma levels of glutamate and glutamine in migraine with and without aura.
Cephalalgia. 1995 Apr;15(2):132-5.
PMID: 7641248; UI: 95368693.
- Storer
RJ, et al. [See
Related Articles]
- Trigeminovascular nociceptive transmission involves N-methyl-D-aspartate and
non-N-methyl-D-aspartate glutamate receptors.
Neuroscience. 1999;90(4):1371-6.
PMID: 10338304; UI: 99268626.
-
- Glutamate ADD connection
-
- Boast
C, et al. [See
Related Articles]
- 5HT antagonists attenuate MK801-impaired radial arm maze performance in rats.
Neurobiol Learn Mem. 1999 May;71(3):259-71.
PMID: 10196105; UI: 99214500.
- Glutamate Mood Disorder connection
-
- Costa
E. [See
Related Articles]
- Building a bridge between neurobiology and mental illness.
J Psychiatr Res. 1992 Oct;26(4):449-60. Review.
PMID: 1337107; UI: 93148187.
-
- Pangalos
MN, et al. [See
Related Articles]
- Effect of psychotropic drugs on excitatory amino acids in patients undergoing
psychosurgery for depression.
Br J Psychiatry. 1992 May;160:638-42.
PMID: 1350494; UI: 92274134.
- Ongur
D, et al. [See
Related Articles]
- Glial reduction in the subgenual prefrontal cortex in mood disorders.
Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13290-5.
PMID: 9789081; UI: 99007307.
-
Glutamate MS connection http://www.drkoop.com/news/stories/january/ms_research.html
On how altered glutamate homeostasis may contribute to demyelinating diseases of the
CNS.
Matute C, Domercq M, Fogarty DJ, Pascual de Zulueta M, Sanchez-Gomez MV
Departamento de Neurociencias Universidad del Pais Vasco, Vizcaya, Spain.
onpmaalc@lg.ehu.es
Glial cells communicate reciprocally with neurons in multiple ways, both in synaptic
and non-synaptic regions of the central nervous system. In the latter, neuron to glial and
glial to glial signals can be mediated by neurotransmitters. Here, we review the presence
and some of the functional properties of glutamate transporters and receptors in
oligodendrocytes. In addition, we present data illustrating that alterations in glutamate
homeostasis can be excitotoxic to oligodendroglia and that the tissue lesions caused by
overactivation of glutamate receptors resemble those observed in demyelinating diseases
such as multiple sclerosis. Overall, this information indicates that aberrant glutamate
signaling may contribute to the development of some white matter pathologies.
Publication Types:
- Pitt
D, et al. [See
Related Articles]
- Glutamate excitotoxicity in a model of multiple sclerosis.
Nat Med. 2000 Jan;6(1):67-70.
[MEDLINE record in process]
PMID: 10613826; UI: 20081025.
- Barkhatova
VP, et al. [See
Related Articles]
- [Neurotransmitter changes in multiple sclerosis].
Zh Nevropatol Psikhiatr Im S S Korsakova. 1997;97(5):7-10. Russian.
PMID: 9245166; UI: 97342086.
-
Abnormal glutamic acid metabolism in multiple sclerosis.
Westall FC, Hawkins A, Ellison GW, Myers LW
We have found extensive amino acid abnormalities in multiple sclerosis sera. The most
consistent abnormality is an elevation in serum glutamate, which is most striking during
relapses. The increase in glutamate in the patients does not occur sharply during the
onset of the relapse. Instead it appears to rise gradually within a month or two prior to
the onset of the clinical relapse, to reach a peak during the relapse and then to slowly
decline.
PMID: 7420112, UI: 81027549
- Gade-Andavolu
R, et al. [See
Related Articles]
- Association between the gamma-aminobutyric acid A3 receptor gene and multiple sclerosis.
Arch Neurol. 1998 Apr;55(4):513-6.
PMID: 9561979; UI: 98220446.
"These results suggest the GABRA3 gene may be a risk
factor for MS. As with the DRD2 gene, the effect may be mediated through its regulation of
prolactin release".
NeuroInvestment
Daxanabinol-
US: Press Release on Patent For Analogs Of Cannabinoid
January 27, 2000 -- Pharmos
Announces Record Quarterly Revenues in 1999 Fourth Quarter
November 1, 1999
-- Pharmos Corporation Receives Additional Patents For Novel Drug
Delivery Technologies
March 23, 1999 - Pharmos Corporation Receives Notice of Allowance on Dexanabinol Patent for Use in
the Treatment of Multiple Sclerosis
October 7, 1998 -
Pharmos Announces Sucessful Phase II Head Trauma Study - Marijuana Analog Benefits Brain
Injured Patients
June 3, 1998 --
U.S. Army Finds Pharmos' Dexanabinol Effective In Treating Damage Caused by Nerve Gas
Exposure
May 21, 1998
-- Pharmos Corporation's Dexanabinol May Provide Treatment for
Ulcerative Colitis: Study Suggests Additional Application for Drug
LONG-TERM BENEFICIAL EFFECT OF DEXABINOL (HU-211) IN RAT BRAIN TRANSIENT FOCAL
ISCHEMIA. A. Bar-Joseph, V. Lavie, A. Weksler, Y. Berkovitch, and A Biegon. Pharmos,
Kiryat Weizmann, Rehovot 76326, Israel
Dexanabinol (HU-211) is a nonpsychotropic cannabinoid which acts as a noncompetitive NMDA
receptor antagonist. It also has anti-oxidant and cytokine-inhibitory properties. The
compound was previously shown to be neuroprotective in models of head trauma, rat optic
nerve injury, global and focal ischemia. The purpose of the present study was to
investigate the long-term effects of single and multiple doses of Dexanabinol and MK-801
on the prevention of degeneration and on sprouting in transient focal ischemia induced by
middle cerebral artery (MCA) occlusion. The MCA was occluded for 90 minutes in
Sprague-Dawley rats by intraluminal suture. Dexanabinol (5mg/kg i.v.) or MK-801 (1 mg/kg
s.c.) And their vehicles were administered seventy-five minutes after the initiation of
the ischemic insult once or once daily for seven days. The success of the MCA occlusion
was clinically tested sixty minutes post insult initiation. Eight weeks later, brains were
fixed, serially sectioned and stained with Hematoxyline and Eosin. The infarct volumes
evaluated by a blind investigator, were measured using a computerized image analyzer.
Parallel sets of sections were immunocychemically stained with anti GAP-43 to evaluate
sprouting. Results demonstrated that the mean infarct volume of the single Dexanabinol
treatment animals was reduced by about 70% in comparison to vehicle treated animals. The
effect of repeated treatments with Dexanabinol and MK-801 as well as the GAP-43 staining
is still undergoing analysis. Thus, a single dose of Dexanabinol given more than an hour
after MCAO, produced a long term (eight weeks) neuroprotective effect on infarct volume.
This finding further supports the clinical development of Dexanabinol for stroke.
NEUROPROTECTIVE EFFECTS OF HU-211 ON BRAIN DAMAGE RESULTING FROM SOMAN-INDUCED
SEIZURES. M.G. Filbert, J. S. Forster, C. D. Smith, M. C. kovalenko, M.J. Jaworski, and G.
P. H. Ballough. Neurotoxology Branch, Pharmacology Division, US Army Medical research
Institute of Chemical Defenses, Aberdeen proving Ground, MD, USA 21010- 5245 and LaSalle
University, Department of Biology, Philadelphia, PA 19141-1199.
The present study was undertaken to examine the possible neuroprotective effects of HU-
211 on brain damage resulting from the soman-induced seizures. Male Sprague-Dawley rats
were challenged with 180 ug/kg Soman (i.e., 1.6 LD50). They were subsequently given a
single intraperitoneal injection of 25 mg/kg HU-211 at either 5 or 40 minutes post onset
of seizures. HI- 6 (126mg/kg) and atropine methylnitrate (2 mg/kg) were administered to
protect against the peripheral effects of soman. Electrocorticographic (EcoG) recordings
were monitored via indwelling cortical electrodes. Rats were euthanized 27hr after soman
administration. Alternate brain hemispheres were processed for microtubule-associated
protein 2 (MAP2) and glial fibrillary acidic protein (GFAP) immunocytochemical staining or
hematoxylin and eosin (H&E) histochemical staining. Morpohometric image analysis was
used to assess the cross-sectional areas of temporal lobe necrosis (MAP2 negative) and
reactive astrocytosis (GFAP positive) resulting from soman exposure. H&E stained
sections were examined for classical histopathology. All rats that received soman showed
EcoG evidence of sustained seizures and status epilepticus for several hours. Treatment
with HU-211 had no apparent effect on the strength or duration of these seizures.
Interestingly, HU-211 administration 5-minutes post onset of seizures significantly
reduced (by 75.8%) the mean cross-sectional areas of temporal lobe necrosis. These
findings were corroborated by H&E histopathological assessments which showed a
significant reduction in piriform cortical damage in the HU-211 5 minute group ("mild
damage", i.e., 11-25% neuronal loss) compared to soman controls ("severe
damage", i.e., greater than 45% neuronal loss). It is concluded that HU-211 provides
considerable neuroprotection against brain damage resulting from soman-induced seizures,
despite having no apparent effect on the seizures themselves.
5) NEUROPATHIC PAIN
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uid
s=1663228&dopt=Abstract
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Link&db=PubMed&dbFrom=PubMe
d&from_uid=1663228
7) MULTIPLE SCLEROSIS:
http://www.pharmoscorp.com/news/currentnews/pr030600.htm
http://www.pharmoscorp.com/news/currentnews/pr032399.htm
http://www.ifmss.org.uk/Research/Dexanabinol.htm
http://www.mapinc.org/drugnews/v99/n336/a08.html
http://www.neuroinv.com/Pharmos.html
http://www.acmed.org/english/1999/bulletin040499.html
http://geocities.com/TheTropics/Shores/1244/teranews13.htm
8) NERVE GAS:
http://messages.yahoo.com/bbs?action=m&board=7077174&tid=pars&sid=7077174&mid=17
347
http://www.mapinc.org/drugnews/v98/n417/a14.html
http://marijuananews.com/could_medical_marijuana_have_pre.htm
http://www.tty.com/news/9806/980605il.html
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1
0668456&dopt=Abstract
9) PARKINSON:
http://www.nimh.nih.gov/events/prcann.htm
http://www.geocities.com/Area51/Stargate/1792/page2.html
10) SEPTIC SHOCK:
http://164.195.100.11/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&u=netahtml/sear
ch-adv.htm&r=1&p=1&f=G&l=50&d=curr&S1=5932610&OS=5932610&RS=5932610
11) SPINAL CORD INJURY:
http://www.neuroinv.com/Pharmos.html
12) STROKE:
http://www.neuroinv.com/Pharmos.html
http://www.mapinc.org/drugnews/v98/n571/a02.html
http://sciencenews.org/sn_arc98/7_11_98/fob2.htm
13) ULCERATIVE COLITIS:
http://www.cannabinoid.com/wwwboard/medical/messages/134.shtml
MISC:
14) ANANDAMIDE http://www.mapinc.org/find?K=anandamide&COL=Body&T=All+words&MAX=50&Y=1999&DE=Lo
w
15) http://www.fgi.net/~lstevens/cannabis/reports.htm
16) http://www.geocities.com/Area51/Stargate/1792/page2.html
This transdermal delivery system was developed to enhance
bio-availability for non-water soluble substances such as cannibinoids.
"Iselin, NJ, November 1, 1999 - Pharmos Corporation (Nasdaq: PARS) announced that
it has recently received, jointly with the U.S. Army, a new patent from the U.S. Patent
and Trademark Office. The patent covers Submicron Emulsion (SME), a novel drug delivery
technology developed by Pharmos, as vaccine adjuvants. Pharmos announced it has also
received a Notice of Allowance for a new patent with claims covering SMEs as topical and
transdermal delivery systems."
Society for Neuroscience
