TY - JOUR
T1 - Activity-dependent regulation of substance P expression and topographic map maintenance by a cholinergic pathway
AU - Tu, Shichun
AU - Butt, Christopher M.
AU - Pauly, James R.
AU - Debski, Elizabeth A.
PY - 2000/7/15
Y1 - 2000/7/15
N2 - We have assessed the role of activity in the adult frog visual system in modulating two aspects of neuronal plasticity: neurotransmitter expression and topographic map maintenance. Chronic treatment of one tectal lobe with the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione decreased the percentage of substance P-like immunoreactive (SP-IR) tectal cells in the untreated lobe while disrupting topographic map formation in the treated one. Treatment with the NMDA receptor antagonist D-(-)-2,amino-5- phosphonovaleric acid (D-AP-5) disrupted the topographic map but had no affect on SP-IR cells. These results indicate that maintenance of the topographic map is dependent on direct input from the glutamatergic retinal ganglion cells, whereas substance P (SP) expression is being regulated by a pathway that relays activity from one tectal lobe to the other. Such a pathway is provided by the cholinergic nucleus isthmi, which is reciprocally connected to the ipsilateral tectum and sends a projection to the contralateral one. Mecamylamine and atropine, antagonists of nicotinic and muscarinic receptors, respectively, were used together to block all cholinergic activity or alone to block receptor subclass activity. All three treatments decreased SP expression and disrupted the topographic map in the treated tectal lobe. We conclude that both SP expression and topographic map maintenance in the adult optic tectum are activity-dependent processes. Although our results are consistent with the maintenance of the topographic map through an NMDA receptor-based mechanism, they suggest that SP expression is regulated by a cholinergic interaction that depends on retinal ganglion cell input only for its activation.
AB - We have assessed the role of activity in the adult frog visual system in modulating two aspects of neuronal plasticity: neurotransmitter expression and topographic map maintenance. Chronic treatment of one tectal lobe with the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione decreased the percentage of substance P-like immunoreactive (SP-IR) tectal cells in the untreated lobe while disrupting topographic map formation in the treated one. Treatment with the NMDA receptor antagonist D-(-)-2,amino-5- phosphonovaleric acid (D-AP-5) disrupted the topographic map but had no affect on SP-IR cells. These results indicate that maintenance of the topographic map is dependent on direct input from the glutamatergic retinal ganglion cells, whereas substance P (SP) expression is being regulated by a pathway that relays activity from one tectal lobe to the other. Such a pathway is provided by the cholinergic nucleus isthmi, which is reciprocally connected to the ipsilateral tectum and sends a projection to the contralateral one. Mecamylamine and atropine, antagonists of nicotinic and muscarinic receptors, respectively, were used together to block all cholinergic activity or alone to block receptor subclass activity. All three treatments decreased SP expression and disrupted the topographic map in the treated tectal lobe. We conclude that both SP expression and topographic map maintenance in the adult optic tectum are activity-dependent processes. Although our results are consistent with the maintenance of the topographic map through an NMDA receptor-based mechanism, they suggest that SP expression is regulated by a cholinergic interaction that depends on retinal ganglion cell input only for its activation.
KW - Autoradiography
KW - Elvax
KW - Muscarinic receptor
KW - NMDA receptor
KW - Neuropeptides
KW - Neurotransmitter expression
KW - Nicotinic receptor
KW - Non-NMDA receptor
KW - Nucleus isthmi
KW - Optic tectum
KW - Pipiens
KW - Retinotectal topography
KW - Visual plasticity
UR - http://www.scopus.com/inward/record.url?scp=0034661797&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034661797&partnerID=8YFLogxK
U2 - 10.1523/jneurosci.20-14-05346.2000
DO - 10.1523/jneurosci.20-14-05346.2000
M3 - Article
C2 - 10884319
AN - SCOPUS:0034661797
SN - 0270-6474
VL - 20
SP - 5346
EP - 5357
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 14
ER -