Volume 1 Issue 2 July 1997

Newletter Sponsored by Avenue Hospital, Nairobi, Kenya
 

This was the largest meeting devoted to neuroscience in Africa surpassing attendance at the past congresses of the Pan African Association of Neurological Sciences. Convened at the Civic Center near the foothills of the famed Table Mountain, in downtown Cape Town, it was also the occasion for the Second IBRO Regional Congress on Neuroscience. The meeting held under the auspices of the Southern African Neuroscience Society (SANS), was officially opened at the Mayoral reception on 21 April 1997. Alter a message of welcome to the Mother City and the bid city for the 2004 Olympic Games, Councillor Jacobs reminded the delegates to look confidently forward in their scientific endeavors, unlike past circumstances, which had repressed multicultural South Africa. The Secretary-General of IBRO, Professor David Ottoson, stressed the important role of IBRO in uniting and promoting co-operation in global neuroscience.

The SONA 97 week was attended by delegates from 39 countries. The conveners and IBRO-UNESCO provided 30 full or partial travel fellowships to African researchers from Cote D’ Ivoire, Egypt, Ethiopia, Ghana, Kenya, Morocco, Nigeria, Senegal, Sudan, Tanzania, and Zimbabwe.

The conference was preceded by three workshops held over two days. There was a workshop on communication skills by Michael Zigmond (USA) and Beth Fisher (USA) covering writing research articles, designing graphics and visual aids, giving presentations and advancing research careers. Marina Bentivoglio (Italy) and Francoise Omlin (South Africa) organized a workshop on neuroanatomy demonstrating current immunohistochemical and light microscope techniques. Finally, there was a behavioral neuroscience workshop or ganised by Terje Sagvolden (Norway).
 

The main scientific program comprised of about 260 presentations representing 10 plenary and special lectures, 25 symposia, and special interest sessions, over 100 free communications and posters. These represented an increase of 20% in content and participation compared to the 2nd SONA conference in Marrakesh, Morocco. There was a wealth of excellent information embracing modern aspects of cellular, molecular, systems, behavioral, and computational neuroscience offered by participants within and outside the African continent. Delegates were impressed that profound neuroscience research prevails in South Africa. Various laboratories from South Africa represented at meeting reported novel findings in both basic and clinical neuroscience. These presentations also rnade it obvious the strong investment in neurological sciences in Southern Africa.

A large portion of the programme entailed the mechanism of cell death. Areas covered by eminent international speakers (M. Zigmond, 1. Creese, D. Reis, K. P. Mohanakumar, and J. B. Clark) involved the primary and secondary factors that caused neuronal dysfunction in alcohol addition, Alzheimer's disease, Parkinson's disease, stroke, motorneuron disease, AIDS dementia complex, and demyelinating disorders.

From South Africa, F. Potocnik (University of Stellenbosch) presented work on Alzheimer's disease and C. de Villiers (Groote Schuur Hospital, Cape Town) on the problems of assessing the degree of dementia in local populations. J. Temlett (University of Wittswaterrand) reported the findings of sterotactic lesions in the treatment Parkinson's disease.

Behavioral neuroscience comprised several presentations describing animal models of obsessive compulsive disorders and attention deficit disorders by R. Emsley, D. J. Stein, and V. Russell (University of Stellenbosch). C.M. Masimirembwa (University of Zimbabwe) presented an intriguing finding that certain African populations may carry unique polymorphism of CYP2D6 resulting in diminished capacity to metabolise neuroleptic drugs.

Report of the study in Kenya and Tanzania by J. Sayi, S. Gatere, N. Patel, and R. Kalaria appeared to indicate a lack of correlation between dementia and apolipoprotein E4 in persons from that region of Africa. There were several presentations on the neurobiology of pineal gland and its secretory product, melatonin, by S. Daya and his group from Rhodes University.

Potential of African flora for therapeutic was illustrated by P. A. Akah (University of Nigeria) in the treatment of infantile convulsions with local herbs. S. Kombian and Yao Fiagbe (University of Ghana) showed the electrophysiology actions of extracts from the African shrub Vocanga africana claimed to be effective in reducing morphine and psychostimulant withdrawal symptoms.

African fauna offers intriguing studies in neuroscience. One symposium covered the neurobiology of the naked mole rat. H. Gamrani and the group from Marrakesh described the serotinnergic innervation in the semi-desert rodent, Meriones shawi. While N. Bourhin (Faculty of Science, Casablanca) presented work on the opioid receptors in the jerboa.

As in previous years, the meeting was generously subsidized by IBRO and UNESCO. Support was also received from several other organisations including the Third World Academy of Sciences, Medical Research Council of South Africa, South African Airways, and the City of Cape Town. In addition the organisation was helped by the continued support from the Society for Neuroscience (USA). Bristol Meyer Squibb and other South African pharmaceutical companies also provided generous support. The time and effort of individuals of the various local committee involved in making SONA 97 a success is also to be conurtended.

SONA meetings provides a unique venue for Afr,ican scientist. Besides the scientific aspect, these meetings also serve as social gatherin~s for Africa based neuroscientist to meet one another. By these contacts a network of colleagues has developed which provides support and opportunity to engage in collaborative work. In the long run, this cotnradship wlll aid in creating a self sustaining neuroscience community on this continent.
 
 

CHAIRPERSON A. G. Diop (Senegal)

PASTCHAIRPERSON V. Russell (South Africa)

SECRETARY GENERAL J. K. Kimani (Kenya)

ASST SECRETARY GENERAL E. P. Mtui(Tanzania)

TREASURER N. Lakdar-Ghazal (Morocco)

West Africa I. O. Adeoshun

East & Central Africa A. M. Kaduri

South Africa V. Russell
 

USA R. Kalana (CWRU, Cleveland)

Europe A. Adem (Karolinska Insitute. Stockholm)
 

Neuroscience Society of Nigeria was started by a meeting of the steering committee in Nairobi, Kenya in 1989. The committee consisted of Drs S. Asala, 1. Adesoun, K Adeniyi, and Prof. G. Osuide.

The objective of Neuroscience Society of Nigeria was to establish the presence of neuroscience in the West African sub-region with Nigeria as the social point. Inaugural meeting of the society was held the following year. Dr. S. Asala was elected the president. The enthusiasm was so high that the first scientific conference of the society was held the same year at the Ahmadu Bello University, Zaria, Nigeria. Scientific papers were presented by 42 registered participants. The proceeding of the meeting was published in the Nigerian Journal of Neuroscience which is the official publication of the society.

In 1991, the society held its 2nd Annual Conference at the University of 3Os. The meeting witnessed more participants than the previous one. Due to logistic and operational problems, the society was scientifically inactive for the next three years. However, in 1995, the society held a pre workshop meeting in Abuja. rn attendance were the executives, SONA regional representative and the patron of the society. The decision taken at the meeting included among others (a) to revive Neuroscience Society of Nigeria activities, (b) compile a directory of the Nigerian neuroscientists, (c) revive the constitution of the meeting, (d) to organize the 1996 meeting at Abuja and (e) update Neurosicence Society of Nigeria status with SONA.

The 3rd Annual Conference was held at the Natural Institute for Pharmaceutical Research and Development, Abuja between November 14-16, 1996. The theme of the conference was "The Role of Traditional Medicine in Neuropsychiatric Disorders". The conference was attended by more than 50 delegates. Four plenary lectures and 20 scientific papers were presented. New executives were elected at that meeting. The current president is Prof. U. A. Osunkwo, Department of Pharmacology, Usmanu Danfodio University, Sokoto while the secretary is Dr. S. A. Salawu, Department of Pharmacology and Clinical Pharmacy, Ahmadu Bello University, Zaria.

The 4th Annual Conference of Neurosicence Society of Nigeria is scheduled for October 15-18 1997 at Ahmadu Bello University, Zaria.

The society publishes a bi-annual newsletter and an almual journal - Nigerian Journal of Neurosciences. Inforrnation concerning these publications can be obtained from the editor-in-chief, Dr. Peter A. Akah, Department of Pharmocology and Toxicology, University of Nigeria, Nsukka, Nigeria. (Tel: +234-42770696, Fax: +234-9-5231043).
 

Since independence in the 1960's, the average life expectancy has increased in East Africa. In Kenya, it has gone from 48 to 58 years. With increase in life expendency comes the increase in ageing-related disorders. The East African Dementia Project is a collaborative effort involving the University of Nairobi, Kenya, Muhimbili Medical Center, Tanazania, and Case Western Reserve University, USA. The group objective is to determine the type and prevelence of age related dementia in East Africa. I

Currently the focus is on Alzheimer's Disease and recently a three year research grant was received from the National Alzheimer’s Association (USA)for a study entitled "Genetic and enviromental factors for Alzhelmer s disease in Kenya: A population based prevalence study". The principal investigators are Drs Robert Friedland and Thel Raj Kalaria (CWRU, USA) and Dr. Samuel Gatere (Kenya) with Dr Nilesh Patel (Kenya) as project manager. The project will involve screening 3,000 persons over 65 years living in the Nyeri District, Kenya, uslng a modified mini-mental state examination instrument based on the Indiana University Study and genotyping for the apolipoprotein E (ApoE).

In Tanazania Prof. Kitinya and Jane Sayi have found high ApoE₄ frequency, however the prevalence and incidence of AD in Tanzania is not known.
 
 

Many African neuroscientists attend international conferences, and a number of international congresses are held in beautiful resorts in the African continent. However, the Congress of the SONA provides a unique opportunity for a fruitful exchange among African neuroscientists, and also provides an opportunity to gain an insight in neuroscience research in Africa and to contact African colleagues. On the occasion of the Third Congress of the SONA, which was held in Cape Town (South Africa) in April 1997, as a member of SONA and Section Editor of Brain Research Bulletin, I have proposed to three African colleagues, Abdu Adem, Rajesh Kalana and Vivienne Russell (here listed in alphabetical order), to prepare a special issue of the journal dedicated to African neuroscience. With the invaluable help of these friends and colleagues, who are the guest editors of this special issue, we have selected from the abstracts submitted to the SONA Congress, articles focusing on African neurobiological models and African diseases. The editorial board of Brain Research Bulletin has approved and encouraged the initiative. The special issue on African Neuroscience of Brain Research Bulletin has now been sent to the Publisher and will appear soon. All the papers were peer-reviewed following the editorial policy of the journal. so that the manuscripts have been sent to referees for blind review (i.e. without the names of the authors and their affiliations). All the authors have carefully undertaken revision of their articles responding to the reviewers suggestions and criticisms.

In their editorial for the special issue. the guest editors state: In this Decade of the Brain we are privileged to evidence the growth of neuroscience research in Africa. This special issue of Brain Research Bulletin presents a taste of African neuroscience and research activities which involve the use of products from the vast continent. We gain a sense of the research activities that Africa can accord the advancement of modern brain research. The collection of papers in this issue also demonstrates the range of interesting basic and clinical neuroscience activities ongoing in African countries. Neuroscience research in Africa lives on despite little funding and limited technical proficiency. The distinctive type of African neuroscience is manifest in essentially two ways. One, by the use of animals and materials for scientific investigation as tools for technical advances, and two by the investigation of neurological and psychiatric illnesses that are characteristic to the African environment. Both of these approaches have impacted on modern neuroscience.

The guest editors also emphasis that a "large number of African neuroscientists simply cannot keep pace with the technical developments and new findings in various areas of neuroscience. It is anticipated that current advances in communications technology and availability of the Internet services will prove to be cost-effective and time-saving to African laboratories. Readers will note the type of collaborative neuroscience that has been already achieved within many laboratories in the continent. We hope that this issue serves to further stimulate neuroscience exchange between individuals or institutions within Africa and those outside in the developed world. Notwithstanding the financial backing provided by various organizations, it is also heartening to know that in recent years African neuroscience has been promoted and fostered by recently established organizations such as SONA and the Federation of the Pan African Association of Neurological Sciences (PAANS). We hope this issue of Brain Research Bulletin will not only expose the international community to African neuroscience in the face of challenging problems, but also encourage our African colleagues to continue, especially as they delve into resolving issues that relate to this rich continent."

The board of editors of Brain Research Bulletin welcome this opportunity to provide a forum to communicate a valuable selection of African neuroscience to a wide international audience. We will be pleased t~ receive further suggestions for future special issues, as well as submission of high quality original research manuscripts and review articles from the membership of the SONA.

Having personally followed the fate of this special issue on African neuroscience, I wish to emphasis that I have greatly enjoyed the exchange with the guest editors and the authors of the issue articles and I have received from them professional stimuli and inspiration. Finally, I also wish that this issue will encourage African neuroscientists not only to exploit the uniqueness of their environment, but also to impose to the international neuroscience community their priorities in terms of scientific communication, collaboration and interest on African neurobiological models and neurological disorders.
 

Contact: Dr. A.G. Diop, Chairman, SONA, Department of Neurology, University Hospital of Fann, BP 5035, Dakar, Senegal Fax: (+221) 259227; Email: gallo@ucad.refer.sn

Dr. R. N. Kalaria,( Liason 0fficer, USA), Department of Neurology, Case Western Reserve University, 2109 Adebert Rd, Cleveland, Ohio 441106, USA. Fax: 216-368-1144; email: rxk5@po.cwru.edu
 
 

What do humans have in common with worms, flies, and rodents? If you said, "not much", you're right. But not as "right" as you might think.

During the early 1980s, scientists discovered that most of the genes in fruit flies that control the identity of different body parts - a head, wing, or other structure - are remarkably identical. The genes contain short sequences of deoxyribonucleic acid (DNA), which is found in every living cell and forms the blueprint for all organisms. Surprisingly, researches discovered that the DNA sequence they had found in flies, called the homeobox, was common to genes that direct development of body structure in virtually all animals, including worms, flies, bids, mice and humans.

"Homeo" is derived form the Greek word for similiar; box refers to the clearly defined sequence, as though in a box.

Since the homeobox sequence stayed very similar during the millions of years of evolution in many species, scientists suspected it must be important to life. They soon learned that the part of the protein it encodes can bind to DNA in a way that turns other genes on and off,

Even more surprising, scientists found that many genes containing the homeobox sequence, called hox genes, are lined up in clusters along chromosomes - large strands of genetic material - in an order that parallels the body part they control. On a fly chromosome, hox genes closest to one end control formation of the head, while the next ones in line control the upper body. At the other end of the cluster are genes controlling abdomen formation. When all these genes work correctly, the proteins they produce act together to ensure that each organism’s body parts are made in correct locations. Hox genes also control development of parts of the central nervous system, including different regions of the brain.

Researchers concluded that hox genes are master regulators for the organization of the body. When the function of one of these genes is changed due to a genetic mutation or other factor, the wrong body part will develop in a given place. A fly, for example, might grow a leg in the middle of the head.

Because hox genes are so important to development, scientists realized that changes in how they work could lead to abnormal development in mammals. In mice, for example, changes in hox genes cause head abnormalities and other problems. This suggested that hox genes may also be altered in some human birth defects.

Some 150,000 Americans infants are born annually with birth defects, which
 

include cleft palate and brain abnormalities. Most of these disorders cannot be prevented, but hox genes are providing tantalizing clues about underlying causes. Scientists recent found that abnormally high amounts of retinoic acid, a well known cause of birth defects. can alter the normal function hox genes particularly those controlling the head and face.

While retinoic acid is commonly used to treat acne and is important for normal development, excessive amounts during pregnancy can cause spontaneous abortions, cleft palate, and brain abnormalities. Genetically - engineered mice with absent or overactive hox genes often have similar defects. This supports the idea that retinoic acid causes defects by acting on hox genes.

Most hox genes have a counterpart in a variety of organisms which may serve as models to study human disorders. Research in mice, for example, has shown that changes in a specific hox gene results in defects in the head, heart, and face that resemble Di George syndrome, a rare inherited human disease. Thus, the for Di George syndrome may interact with hox genes in some way.

Scientists are exploring the functions of many hox genes and how their malfunction affects development. These efforts may lead to safer drugs, genetic screening, and other methods to prevent or treat many birth defects.

(Brain Briefings. Society for Neuroscience, USA)
 
 

Society of Neuroscienist of Africa (SONA) objective is to foster and promote neuroscience teaching and research in Africa. Your memberships dues support this activities. We encourage you to join and support SONA activities.
 

Contributions and donations are welcome.

Membership applications and dues should be sent to your regional respresentative or the SONA Treasurer, Dr. N. Lakhdar-Ghazal, Department de Biologie, Faculte des Sciences, Mohammed V Universite, Boite Postale 314, Batouta Avenue, Rabat, Morocco. (Fax: (+212) 7 774561).

For those who live in countries that have foreign exchange restriction, please contact the treasurer for advice on payment of dues.
 

Cuts. Sunburn. Stubbed toes. Arthritis. We say that all of these things cause pain. But what do they have in common? What is the basis for this sensation?

In the last three decades, scientists have finally begun to understand the body systems that underlie pain. Recent discoveries:

• Show that pain results from activation of specific receptors for tissue damaging stimuli.
• Reveal special pathways and chemicals involved in pain.
• Point to new ways to treating acute and persistent pain.

Since other sensations, such as smell and sight organs, have unique sense organs, investigators began to look for sense organs that contribute to pain. They also linked pain to stimuli strong enough to be noxious, or harmful, and proposed that the body must contain unique receptors that signal pain. Though these receptors were difficult to find, scientists began calling them nociceptors (noci is a form of the word noxious).

In the 1960s, researchers described nerve fibers outside the brain and spinal cord that respond and send signals to the brain only with strong stimulation. The showed that these were nociceptors.

Unlike most other receptors, nociceptors become increasingly sensitive with continuing or repeated stimulation. When tissues become injured or inflamed, as with a sunburn or infection, they release chemicals called prostaglandins and leukotrienes that make nociceptors much more sensitive. Sensitized nociceptors react to even gentle stimuli, such as a breeze or caress, causing pain. Aspirin and related drugs interfere with prostaglandin production and can reduce sensitization.
 

Some research suggests that nerve injury can alter the way nociceptors respond to normal levels of noradrenaline, an important chemical used by nerve cells, or neurons. to communicate. This change makes nociceptors more sensitive after injury and may lead to some kinds of chronic pain. This discovery may lead to new ways of treating certain chronic pain syndromes that affect thousands of people.

Scientists are also beginning to understand the chemicals that affect transmission and regulation of nociceptor signals in the brain and spinal cord. They have learned that a chemical called capsaicin, found in hot peppers, can reduce pain by stimulating nerves in a way that exhausts the supply of substance P - another chemical that normally boosts transmission of pain signals. Opioid chemicals, which include morphine and natural body substances such as endorphins, block the transmission of some pain signals by spinal neurons and the connections that carry signals from the brain back to the spinal cord.

Pain research now focuses on the genes and molecules active in damaged an inflamed tissue. Agents that block the actions of leukotrienes and similar chemicals are now undergoing preliminary tests in humans. These and other new therapies promise to markedly improve our ability to treat pain.

(Brain Briefings.Society for Neuroscience,USA)
 

Chairman

Dr. A. G. Diop

Department of Neurology

University Hospital of Fann

BP 5035

Dakar, Senegal

Tel: (+221) 253678/252067

Fax: (+221) 259227

Email: gallo@ucad.refer.sn
 
 
 
 

SONA Secretariat

Prof J. K. Kimani

Department of Human Anatomy

University of Nairobi

P. O. Box 30197

Nairobi, Kenya

Tel: 254- 728116/726837

Fax: 254-717665

Email: kimani@nbnet.co.ke

SONA Treasurer

Dr. N. Lakhdar-Ghazal

Department of Biologie

Faculte des Sciences

Mohammed V Universite

Boite Postale 314

Batouta Avenue

Rabat, Morocco

Fax: (+212) 7 774561

SONA Newsletter Editor

Dr. N. B. Patel

Department of Medical Physiology

University of Nairobi P. O. Box

30197 Nairobi, Kenya

Fax: 254-2-750154