242
J. S. GRIFFITH
are artificially caused to be innervated by inappropriate motoneurons are
capable of transforming the character of the latter into that of the appropriate ones (WEISS [56], though see ref. [53]). This phenomenon, which is
called "specific modulation" or the "myotypic response", could have a very
similar mechanism to the one I have hypothesized above.
In relating memory at the cellular level to the overall nervous integration it is easiest, though not necessarily correct, to suppose that it involves a change in the strength of connections which already exist, rather
than the formation of completely new ones [10, 30]. This would be possible
according to the present hypothesis. One need only suppose that the switching involved in memory is, usually at least, between categories which
produce identically the same set of growth substances, but in different
amounts. This could occur if the structural genes were repressed to different
extents, or if several structural genes coded for the same mRNA and different
numbers were switched on.
Finally, note that although it is appealing to hope that the whole basis
of long-term memory might depend upon a single mechanism which has a
simple description at the molecular level, it may well be that Nature is
more complicated than this. Even if the present hypothetical mechanism
were correct, it might well act alongside others, such as the servomechanism I have discussed previously [29, 30].
References
1. AGRANOFF, B. W., R. E. DAVIS and J. J. BRINK: Brain Research 1,303 (1966).
2. BARNETT, W. E., D. H. BROWN and J. L. EPLER: Proc. Nat. Acad. Sci. 57,
1775 (1967).
3. BARONDES, S. H., and H. D. COHEN: Science 151, 594 (1966).
4. - - Brain Research 4, 44 (1967).
5. -, and M. E. JARVIK: J. Neurochem. 11, 187 (1964).
6. BOHDANECKA, M., Z. BOHDANECKY and M. E. JARVIK: Science 157, 334
(1967).
7. BONNER, J.: The Molecular Biology of Development. Oxford: University
Press 1965.
8. BORST, P., A. M. KROON and G. J. c. M. RUTTENBERG: In: Genetic Elements. Properties and Function, (SHUGAR, Ed.) p. 81. Academic Press 1967.
9. BYRNE, W. L., and 22 others: Science 153, 658 (1966).
10. CAJAL, S. R. Y.: Histologie du Systeme Nerveux. Paris 1910.
11. CHERKIN, A.: Proc. Nat. Acad. Sci. 55, 88 (1966).
12. COHEN, H. D., and S. H. BARONDES: J. Neurochem. 13, 207 (1966).
13. - - Science 157, 333 (1967).
14. DAVIS, R. E., and B. W. AGRANOFF: Proc. Nat. Acad. Sci. 55, 555 (1966).
15. DINGMAN, W., and M. B. Sporn: Science 144, 26 (1964).
16. DIXON, K. c.: Lancet 7 Jan., p. 27, (1967).
17. EDSTROM, A.: J. Neurochem. 11, 309 (1964).
18.
J. Neurochem. 13, 315 (1966).
19. - J. Neurochem. 14, 239 (1967).
J. S. GRIFFITH
are artificially caused to be innervated by inappropriate motoneurons are
capable of transforming the character of the latter into that of the appropriate ones (WEISS [56], though see ref. [53]). This phenomenon, which is
called "specific modulation" or the "myotypic response", could have a very
similar mechanism to the one I have hypothesized above.
In relating memory at the cellular level to the overall nervous integration it is easiest, though not necessarily correct, to suppose that it involves a change in the strength of connections which already exist, rather
than the formation of completely new ones [10, 30]. This would be possible
according to the present hypothesis. One need only suppose that the switching involved in memory is, usually at least, between categories which
produce identically the same set of growth substances, but in different
amounts. This could occur if the structural genes were repressed to different
extents, or if several structural genes coded for the same mRNA and different
numbers were switched on.
Finally, note that although it is appealing to hope that the whole basis
of long-term memory might depend upon a single mechanism which has a
simple description at the molecular level, it may well be that Nature is
more complicated than this. Even if the present hypothetical mechanism
were correct, it might well act alongside others, such as the servomechanism I have discussed previously [29, 30].
References
1. AGRANOFF, B. W., R. E. DAVIS and J. J. BRINK: Brain Research 1,303 (1966).
2. BARNETT, W. E., D. H. BROWN and J. L. EPLER: Proc. Nat. Acad. Sci. 57,
1775 (1967).
3. BARONDES, S. H., and H. D. COHEN: Science 151, 594 (1966).
4. - - Brain Research 4, 44 (1967).
5. -, and M. E. JARVIK: J. Neurochem. 11, 187 (1964).
6. BOHDANECKA, M., Z. BOHDANECKY and M. E. JARVIK: Science 157, 334
(1967).
7. BONNER, J.: The Molecular Biology of Development. Oxford: University
Press 1965.
8. BORST, P., A. M. KROON and G. J. c. M. RUTTENBERG: In: Genetic Elements. Properties and Function, (SHUGAR, Ed.) p. 81. Academic Press 1967.
9. BYRNE, W. L., and 22 others: Science 153, 658 (1966).
10. CAJAL, S. R. Y.: Histologie du Systeme Nerveux. Paris 1910.
11. CHERKIN, A.: Proc. Nat. Acad. Sci. 55, 88 (1966).
12. COHEN, H. D., and S. H. BARONDES: J. Neurochem. 13, 207 (1966).
13. - - Science 157, 333 (1967).
14. DAVIS, R. E., and B. W. AGRANOFF: Proc. Nat. Acad. Sci. 55, 555 (1966).
15. DINGMAN, W., and M. B. Sporn: Science 144, 26 (1964).
16. DIXON, K. c.: Lancet 7 Jan., p. 27, (1967).
17. EDSTROM, A.: J. Neurochem. 11, 309 (1964).
18.
J. Neurochem. 13, 315 (1966).
19. - J. Neurochem. 14, 239 (1967).